Background No current treatment for obesity reliably sustainsweight loss, perhaps because compensatory metabolic processesresist the maintenance of the altered body weight. We examinedthe effects of experimental perturbations of body weight onenergy expenditure to determine whether they lead to metabolicchanges and whether obese subjects and those who have neverbeen obese respond similarly.
Methods We repeatedly measured 24-hour total energy expenditure,resting and nonresting energy expenditure, and the thermic effectof feeding in 18 obese subjects and 23 subjects who had neverbeen obese. The subjects were studied at their usual body weightand after losing 10 to 20 percent of their body weight by underfeedingor gaining 10 percent by overfeeding.
Results Maintenance of a body weight at a level 10 percent ormore below the initial weight was associated with a mean (±SD)reduction in total energy expenditure of 6±3 kcal perkilogram of fat-free mass per day in the subjects who had neverbeen obese (P<0.001) and 8±5 kcal per kilogram perday in the obese subjects (P<0.001). Resting energy expenditureand nonresting energy expenditure each decreased 3 to 4 kcalper kilogram of fat-free mass per day in both groups of subjects.Maintenance of body weight at a level 10 percent above the usualweight was associated with an increase in total energy expenditureof 9±7 kcal per kilogram of fat-free mass per day inthe subjects who had never been obese (P<0.001) and 8±4kcal per kilogram per day in the obese subjects (P<0.001).The thermic effect of feeding and nonresting energy expenditureincreased by approximately 1 to 2 and 8 to 9 kcal per kilogramof fat-free mass per day, respectively, after weight gain. Thesechanges in energy expenditure were not related to the degreeof adiposity or the sex of the subjects.
Conclusions Maintenance of a reduced or elevated body weightis associated with compensatory changes in energy expenditure,which oppose the maintenance of a body weight that is differentfrom the usual weight. These compensatory changes may accountfor the poor long-term efficacy of treatments for obesity.
Obesity is a common and intractable problem in some modern societies.Body weight is normally regulated by integrated, coordinateeffects on food intake and energy expenditure.1 The high rateof recidivism among obese people who lose weight may reflectthe operation of such regulatory processes.2,3,4
In humans, total energy expenditure is accounted for by restingenergy expenditure (approximately 60 percent of total energyexpenditure), which is the metabolic cost of processes suchas the maintenance of transmembrane ion gradients and restingcardiopulmonary activity; the thermic effect of feeding (approximately10 percent of total energy expenditure), which is the energyexpended in the digestion, transport, and deposition of nutrients;and nonresting energy expenditure (approximately 30 percentof total energy expenditure), which is all the remaining expenditureof energy, mainly in the form of physical activity.5 In an earlierstudy, we found a persistent 28 percent decrease in the energyexpended per unit of body-surface area in formerly obese patientswith a stable reduced weight,6 suggesting a metabolic resistanceto the maintenance of a reduced body weight. The present studywas designed to examine the components of energy expenditureduring the maintenance of usual and altered body weight in obesesubjects and subjects who had never been obese.
Methods
Subjects
Eighteen obese subjects (11 women and 7 men; mean [±SD]age, 29±10 years [range, 21 to 45]) and 23 subjects whohad never been obese (7 women and 16 men; mean age, 26±10years [range, 19 to 41]) were recruited through physicians'referrals or advertisements (Table 1). All subjects were attheir maximal lifetime weight and had maintained this weightwithin a range of 2 kg for at least six months. None were takingmedications or on special diets. Subjects whose body-mass index(expressed as the weight in kilograms divided by the squareof the height in meters) was higher than 28.0 were classifiedas obese.7 All subjects had normal findings on physical examinationand laboratory evaluations, including thyroid-function tests,complete blood count, tests for hepatitis A and B and humanimmunodeficiency virus infection, biochemical tests, and urinalysis.Six of the obese subjects and two of those who had never beenobese smoked 2 to 10 cigarettes daily throughout the study.The protocol was approved by the Rockefeller University HospitalInstitutional Review Board, and written informed consent wasobtained from all the subjects.
Table 1. Characteristics and Body Composition of Subjects at Initial and Altered Weights.
Study Design
The subjects were admitted to the Clinical Research Center atRockefeller University and fed a liquid formula (40 percentfat [corn oil], 45 percent carbohydrate [glucose polymer], and15 percent protein [casein hydrolysate]) supplemented with 5.0g of iodized sodium chloride, 1.9 g of potassium ions as a potassiumsalt, and 2.5 g of calcium carbonate per day, 1 mg of folicacid twice weekly, and 36 mg of ferrous iron every other day.The mean caloric content of this formula, measured with a bombcalorimeter, was 1.36 kcal per gram. With the use of standarddigestibility quotients, the content of metabolizable calorieswas 1.25 kcal per gram.8 Fecal calorie and urinary nitrogenlosses were measured at all weight plateaus to confirm thatthey did not change (see below). The caloric intake was adjusteduntil the body weight was constant (slope of the regressionline of body weight [grams] vs. time [days], <10 g per day)for at least 14 days. All subjects then underwent studies ofenergy expenditure and body composition during approximatelya 10-day period while continuing to ingest the same quantityof dietary formula. Body composition was analyzed by hydrodensitometry9;stool and urine samples, collected for eight days, were analyzedto determine fecal calorie loss (by bomb calorimetry) and urinarynitrogen excretion10; and resting energy expenditure and thethermic effect of feeding were determined by indirect calorimetrywith the use of a Beckman MMC Horizon Metabolic Cart (BeckmanInstruments, Fullerton, Calif.) with a ventilated hood fittedsnugly around the subject's neck11 (and unpublished data).
Resting energy expenditure at 8 a.m. in the postabsorptive statewas calculated from oxygen consumption corrected for the respiratoryquotient and the daily rate of nitrogen excretion based on thenitrogen content of the dietary formula and the rate of urinarynitrogen excretion. To measure the thermic effect of feeding,at 9 a.m. the subjects were given dietary formula with a caloriccontent equal to 60 percent of the 24-hour resting energy expendituremeasured that morning. Oxygen consumption and carbon dioxideproduction were measured in the hood calorimeter for 30 minutes2 and 4 hours after the feeding. The area of the polygon whosebase is the prefeeding value of resting energy expenditure andwhose other vertexes are resting energy expenditure at 9 a.m.,11 a.m., and 1 p.m. represents the increase in energy expenditureduring the four hours after ingestion of food; this area wasused to calculate the percentage of calories oxidized afteringestion of the formula.
Since no technique is available for the direct measurement ofnonresting energy expenditure, we calculated this componentof energy expenditure as the difference between total energyexpenditure and the sum of the resting components of total energyexpenditure: nonresting energy expenditure = total energy expenditure- (resting energy expenditure + thermic effect of feeding).In a subgroup of subjects studied at multiple weight plateaus,total energy expenditure was also determined by the differentialexcretion rates12 of two stable isotopes of water (2H2O andH218O) and by indirect calorimetry performed at the ClinicalDiabetes and Nutrition Section, National Institute of Diabetesand Digestive and Kidney Diseases (Phoenix, Ariz.), in a respirationchamber equipped with wall-mounted radar detectors to monitorphysical activity.13 These subjects also underwent measurementof body composition by isotope dilution12 and by dual-photonabsorptiometry14 to validate the caloric titration and hydrodensitometricmethods used in the study (unpublished data).
After the completion of studies at their initial weight, 11of the obese subjects and 13 of the subjects who had never beenobese (hereafter referred to as nonobese) were given the maximallytolerated amount of self-selected foods (generally 5000 to 8000kcal per day) until they had gained 10 percent of their initialbody weight (Figure 1). No formula was ingested during the periodof weight gain, which ranged from 4 to 6 weeks in the nonobesesubjects and from 6 to 10 weeks in the obese subjects. At thenew weight plateau, the dietary formula was reinstated, andthe quantity of formula was titrated to maintain the weight.When the weight had been stable for at least 14 days, the studiesof energy expenditure and body composition, described above,were repeated. Eight obese women who had undergone and maintaineda 10 percent weight gain were then fed 800 kcal per day of theformula until they had returned to their initial weight. Theywere given the same number of kilocalories of formula that hadbeen required to maintain their initial weight, and the studiesof energy metabolism were repeated once their weight had beenstabilized.
All subjects were studied at their initial weight and after at least one change in weight.
After the initial-weight studies described above, 9 obese subjectsand 11 nonobese subjects were fed 800 kcal of the dietary formulaper day until their body weight had been reduced to a levelthat was 10 percent below their initial weight (Figure 1). (Eightof the obese and one of the nonobese subjects had previouslyundergone studies after a 10 percent gain in weight.) The periodof weight loss ranged from 4 to 7 weeks for the nonobese subjectsand from 6 to 14 weeks for the obese subjects. When the subjectshad lost 10 percent of their initial weight, the formula wasreinstated and adjusted to maintain the weight for at least14 days; the studies described above were then repeated. Tenobese subjects who had undergone initial-weight studies (sevenof whom were also studied after a 10 percent weight loss) werefed 800 kcal of dietary formula per day until they had lost20 percent of their initial weight. The studies described abovewere performed after their weight had stabilized at the lowerlevel.
Resting energy expenditure was determined in some subjects atthe end of each period of weight gain or loss, when the intendedlevel of weight had been achieved (10 percent higher or lowerthan the initial weight or after a return to the initial weight)but the subjects were still gaining or losing weight. Thesestudies were performed to assess the degree to which the metabolicstatus was carried over from a period of changing weight toa period of stable weight.
Statistical Analysis
The results are presented as means ±SD. Energy expenditureat each weight plateau is expressed as the absolute number ofkilocalories per day, as well as the number per kilogram offat-free mass, to allow comparisons among different groups ofsubjects at the same weight plateau and among different weightplateaus for the same subject. The thermic effect of feedingand fecal calorie loss are expressed as percentages of ingestedcalories that were oxidized and lost in stool, respectively.Comparisons of energy expenditure in the same subjects at differentweight plateaus were made by a one-way analysis of variancewith repeated measures.15 The effects of sex and adiposity onmeasures of energy expenditure at different weight plateauswere determined by a multivariate analysis of variance withrepeated measures15 in which sex and adiposity were treatedas dichotomous variables (male vs. female and nonobese vs. obese).
At the usual body weight, resting energy expenditure is closelycorrelated with measures of metabolic mass (e.g., fat-free mass).13Regression lines relating energy expenditure to metabolic massdo not have zero intercepts.5 Thus, subjects with values onthe same regression line can have different values for the ratioof energy expenditure to metabolic mass. To correct for thispossibility, regression equations relating measures of energyexpenditure to fat-free mass and fat mass at the initial weightwere calculated at that weight and used to determine the predictedvalue of energy expenditure in the same subject at each newweight plateau. The observed-minus-predicted values were thentested against the null hypothesis that the observed-minus-predictedvalue was 0, to determine whether the observed values differedsignificantly from the predicted values for each subject. Allstatistical tests were two-tailed.
Results
Energy Expenditure
The rates of energy expenditure changed in both the obese andthe nonobese subjects after changes in body weight (Table 2and Figure 2 and Figure 3). A 10 percent increase or decreasein the usual weight was accompanied by a 16 percent increaseor 15 percent decrease, respectively, in 24-hour total energyexpenditure corrected for body composition. Fat-free mass wassignificantly related to total energy expenditure, resting andnonresting energy expenditure, and the thermic effect of feeding.Fat mass was significantly related to total and resting energyexpenditure.
Figure 2. Mean (±SD) Observed-minus-Predicted Total Energy Expenditure (Shaded Bars) Based on the Regression of Total Energy Expenditure in a Model with a Variable Combining Fat-free Mass and Fat Mass in the Same Subjects at Their Initial Weight.
The components of total energy expenditure are given in Table 2.
Figure 3. Total and Resting Energy Expenditure According to Fat-free Mass at the Initial Weight and after a Gain or Loss in Weight.
The results are presented in terms of fat-free mass to facilitate comparisons among subjects studied at different weights. The diagonal lines represent regression equations for energy expenditure as compared with fat-free mass at the initial weight and at an altered weight in the same subjects. For subjects studied at their initial weight and after a 10 percent gain in weight (left-hand graphs), total energy expenditure equaled 39.7 kg of fat-free mass plus 348.8 (r2 = 0.72, P<0.001), and resting energy expenditure equaled 13.1 kg of fat-free mass plus 670.1 (r2 = 0.42, P = 0.004). For subjects studied at their initial weight and after a weight loss (right-hand graphs), total energy expenditure equaled 56.8 kg of fat-free mass minus 496.1 (r2 = 0.74, P<0.001), and resting energy expenditure equaled 27.5 kg of fat-free mass plus 220.2 (r2 = 0.44, P = 0.004).
Plotted numbers denote individual subjects. Subjects 1 through 23 were not obese; subjects 24 through 38 were obese. Six women and two men studied after a 10 percent weight loss had previously been studied after a 10 percent weight gain; six women studied after a 20 percent weight loss had previously been studied after a 10 percent gain and a 10 percent loss. The number and direction of previous weight changes did not significantly affect any measures of energy expenditure at a given weight plateau.
In agreement with the results of other studies,16 total energyexpenditure and resting energy expenditure, expressed as kilocaloriesper kilogram of fat-free mass per day, were significantly higherin the obese subjects than in the nonobese subjects, whereasthe thermic effect of feeding was lower in the obese subjectsthan in the nonobese subjects.17,18 The higher resting energyexpenditure in the obese subjects probably reflects increasedcardiorespiratory work related to chest-wall weight and a largermass of adipose tissue. Smokers did not differ significantlyfrom nonsmokers for any of the measures. Fecal calorie and urinarynitrogen losses, expressed as percentages of ingested caloriesand protein, respectively, were not significantly affected bychanges in body weight and did not differ significantly accordingto sex or prior adiposity.
Effects of Weight Gain
Total energy expenditure, nonresting energy expenditure, andthe thermic effect of feeding were significantly higher aftera 10 percent gain in weight than at the initial weight. Stabilizationof body weight after a 10 percent gain resulted in significantincreases in observed-minus-predicted values for total energyexpenditure, nonresting energy expenditure, and the thermiceffect of feeding (Table 2). The magnitude of these changeswas not affected by sex or initial adiposity. In 14 subjects(7 obese and 7 nonobese), the percentage of time spent in motionduring a 23-hour period, measured in a respiration chamber,did not differ significantly between the initial weight (9.1±2.0percent) and the 10 percent higher weight (8.6±2.1 percent,P = 0.47).
Return to Initial Weight
Eight obese women were studied at their initial weight, at aweight 10 percent higher than their initial weight, and aftera return to their initial weight. No significant differencesin body composition or in any aspect of energy expenditure werenoted between the time of the initial-weight study and the returnto the initial weight (Table 1 and Table 2).
Effects of Weight Loss
Total energy expenditure and nonresting and resting energy expenditurewere significantly lower at weights 10 and 20 percent belowthe initial weight than at the initial weight (Table 2). Stabilizationof body weight at a level 10 percent below the initial weightwas associated with negative observed-minus-predicted valuesfor total energy expenditure and nonresting and resting energyexpenditure. Stabilization of body weight at a level 20 percentbelow the initial weight was associated with negative observed-minus-predictedvalues for total energy expenditure and nonresting energy expenditure.The magnitude of these changes was not significantly relatedto sex or initial adiposity. There were no significant differencesin energy expenditure at weights 10 and 20 percent below theinitial weight, suggesting that the maximal adaptation to themaintenance of a reduced body weight was already attained atthe 10 percent level. Among eight subjects (six nonobese andtwo obese) the mean percentage of time spent in motion in therespiratory chamber was 9.2±2.0 percent at the initialweight and 9.4±1.8 percent after a 10 percent loss inweight (P = 0.52).
Static Weight Maintenance versus Dynamic Weight Change
The high degree of weight stability among the subjects (meanrate of weight change during the 10-day testing periods, -1.2g per day) suggests that body composition was constant duringweight maintenance. When weight and body composition are stable,the respiratory quotient reflects mainly the composition ofthe diet. As expected, the processes of weight gain and lossresulted in increases and decreases, respectively, in the respiratoryquotient. However, the respiratory quotient did not differ significantlyfrom the quotient for the dietary formula (0.85) at any of theweight plateaus, indicating that the subjects were in caloricbalance at each plateau, without a carryover effect of weightloss or gain on caloric requirements or substrate use.
The effects of weight gain and loss on energy metabolism werealso assessed by comparing resting energy expenditure at theend of the dynamic phase of weight change with that at the endof the period of maintenance of the same weight (Table 3). Theprocess of increasing weight by overfeeding was accompaniedby approximately 12 percent more resting energy expenditurethan a 10 percent weight gain maintained for 14 days. Conversely,the process of losing weight on a diet of 800 kcal per day resultedin 10 to 15 percent less resting energy expenditure than a stabilizedweight loss of 10 percent.
Table 3. Comparison of Resting Energy Expenditure and Respiratory Quotient at the End of a Period of Weight Gain or Loss and during Maintenance of the Altered Weight.
Body Composition
A 10 percent gain in weight resulted in increases in adiposetissue and fat-free body mass, and a weight loss of 10 percentresulted in significant decreases in both these measures. Thesechanges in body composition, expressed as the change in thepercentage of body fat, were statistically significant withinall subgroups of subjects. There was no evidence that sex orprior adiposity affected the distribution of weight gained orlost between fat mass and fat-free mass (Table 1). There wasa trend for the obese subjects to gain a lower percentage ofweight as fat than the nonobese subjects (P = 0.11) and to losea higher percentage of weight as fat (P = 0.13).
Discussion
We found that energy expenditure adjusted for metabolic massincreased with a weight gain and decreased with a weight loss.These changes in energy expenditure were evident during periodsof stable altered body weight and were in a direction tendingto return the subject to his or her initial weight; their magnitudewas similar in nonobese and obese subjects. After a 10 percentgain in weight, the increase in total energy expenditure reflecteda large increase in the absolute number of kilocalories of nonrestingenergy expenditure per day and a small increase in the absolutenumber of kilocalories per day attributed to the thermic effectof feeding. After a 10 or 20 percent loss in weight, the declinein total energy expenditure reflected similar decreases in bothnonresting and resting energy expenditure.
In some studies, energy expenditure has been higher than thatpredicted for metabolic mass during weight gain or maintenanceof a higher body weight in nonobese subjects.19 In other studies,20,21such an increase has not occurred. Resting energy expendituredeclines during a period of weight loss,22 but whether a similardecline occurs when weight loss has stabilized is the subjectof considerable debate.23,24,25,26 Likewise, there is a lackof agreement concerning the effect of weight reduction on totalenergy expenditure; both decreases (of 8 to 22 percent) andno change or increases (of approximately 9 percent, as comparedwith the values for weight-matched nonobese controls) have beenreported.27,28,29
Several considerations are important in drawing conclusionsfrom our findings. The alterations in energy expenditure donot reflect carryovers from the dynamic periods of weight change,since the measures of energy expenditure at the initial weightand after a return to that weight were similar, the anticipatedchanges in resting energy expenditure occurred during periodsof weight change, and respiratory quotients at the various weightplateaus equaled that predicted for a stable weight while subjectswere ingesting the dietary formula. Subtle shifts in body compositionduring periods of stable weight could have masked differencesin energy expenditure among the weight plateaus. Such changesare unlikely, since they would have led to discrepancies betweentotal energy expenditure as measured by formula titration andtotal energy expenditure as measured by elimination rates for2H2O and H218O. Yet these two measures were highly correlatedand did not differ significantly at any weight plateau (unpublisheddata). In addition, respiratory quotients during all periodsof stable weight equaled that predicted on the basis of thenutrient composition of the formula diet, suggesting that therewas no net storage or catabolism of fat.
Although we did not examine the permanence of these changesin rates of energy expenditure, a reduced level of energy expenditurehas been reported to persist in subjects who have maintaineda reduced body weight for periods ranging from six months tomore than four years.6 The aspect of body composition that mediatesor signals these changes in energy expenditure is not known.In our study, the largest changes in body composition with weightalteration occurred in fat mass. A substantial body of literaturesuggests that the mass of adipose tissue or the size of adipocytesis the aspect of body composition that is regulated,30 but thefeedback mechanism for the effect of fat mass on energy metabolismis not known. A candidate gene for such a signal from fat hasrecently been cloned.31
The metabolic variable most affected by weight change was nonrestingenergy expenditure. Since it was not measured directly, thenature of the changes in this variable cannot be identified.Differences in the energy needed to move a larger or smallerbody mass account for only some of the differences in energyexpenditure, as suggested by Weigle and Brunzell, in whose studylost weight was replaced with backpack loads.32 This cannotbe the entire explanation, however, since obese and lean subjectsat their usual body weight have nearly equal nonresting energyexpenditure, corrected for both fat-free mass and fat mass.One possibility is that the efficiency with which skeletal muscleperforms mechanical work is different at different weight plateaus(decreased with a 10 percent gain in weight and increased witha 10 percent loss). The efficiency of muscular work before andafter weight gain does not change, nor does the energy expenditureassociated with moderate exercise.33,34 The effect of a changein weight on the energy expended during mild physical exertion,however, has not been systematically studied, and this minimallevel of exertion may be most representative of the physicalactivity of sedentary adults. The possibility that changes inskeletal muscle have a role in mediating the alterations inenergy expenditure that occur with weight loss may be the reasonexercise is helpful in maintaining a reduced body weight.
Body weight in adults is remarkably stable for long periodsof time. In the Framingham Study the body weight of the averageadult increased by only 10 percent over a 20-year period.35Such a fine balance is evidence of the presence of regulatorysystems for body weight.4,36 Whatever the mechanism (or mechanisms),the weight at which regulation occurs differs from one personto another, and these differences are almost certainly due inpart to genetic37,38 and developmental39 influences.
Our results have immediate implications for the clinical managementof obesity. Many obese people who lose weight have metabolicalterations similar to those observed in our subjects. The reductionin energy expenditure to a level 15 percent below that predictedfor body composition, as a result of a 10 percent (or larger)decrease in body weight, is large when one considers that anaverage daily intake of 2500 kcal would be associated with apositive energy balance of approximately 375 kcal per day. Inaddition, the sense of hunger or dysphoria that may accompanythis state of reduced energy expenditure will promote increasedfood intake, further widening the gap between energy outputand intake.3 Physicians should be aware that for some obesepatients the achievement of what is considered to be a morehealthful body weight may be accompanied by metabolic alterationsthat make it difficult to maintain the lower weight. Nevertheless,the beneficial effect of even a modest weight loss on lipidand carbohydrate metabolism in obese patients40,41 justifiespersistent efforts at weight reduction and maintenance of areduced body weight for the treatment of obesity.
Supported in part by grants from the National Institutes ofHealth (DK30583 and GCRCRR00102) and the Weight Watchers Foundation.During part of the study period, Dr. Rosenbaum was an AmparoRugarcia Clinical Scholar, and Dr. Leibel was an EstablishedInvestigator of the American Heart Association.
We are indebted to Drs. Elio Presta, Streamson C. Chua, andLisa C. Hudgins, Mr. David Markel, Ms. Rachael Kolb, Ms. EileenMullen, Ms. Jennifer Ziedonis, Ms. Alice Murphy, and the membersof the nursing staff of the Rockefeller University HospitalClinical Research Center for their help with the care of thesubjects; to Ms. Cynthia Seidman and her staff of research dietitiansfor supervising the preparation and testing of the dietary formula;to Drs. Steven Heymsfield and Steven Lichtman at St. Luke's–RooseveltHospital Medical Center for supervising the body-compositionstudies; to Dr. Eric Ravussin at the National Institute of Diabetesand Digestive and Kidney Diseases in Phoenix, Arizona, for supervisingthe chamber respirometry studies and for his helpful suggestionson the manuscript; and to Dr. Dwight Matthews and Mr. ChuckGilker for performing the mass spectrometric analysis of urinefor 2H2O and H218O.
Source Information
From the Laboratory of Human Behavior and Metabolism, Rockefeller University, 1230 York Ave., New York, NY 10021, where reprint requests should be addressed to Dr. Leibel.
References
Keesey RE, Corbett SW. Metabolic defense of the body weight set-point. In: Stunkard AJ, Stellar E, eds. Eating and its disorders. Vol. 62 of Research publications: association for research in nervous and mental disease. New York: Raven Press, 1984:87-96.
Leibel RL. A biologic radar system for the assessment of body mass: the model of a geometry sensitive endocrine system is presented. J Theor Biol 1977;66:297-306. [CrossRef][Medline]
Weigle DS. Appetite and the regulation of body composition. FASEB J 1994;8:302-310. [Abstract]
Leibel RL. Is obesity due to a heritable difference in `set point' for adiposity? West J Med 1990;153:429-431. [Medline]
Ravussin E, Bogardus C. Relationship of genetics, age and physical fitness to daily energy expenditure and fuel utilization. Am J Clin Nutr 1989;49:968-975.
Leibel RL, Hirsch J. Diminished energy requirements in reduced-obese patients. Metabolism 1984;33:164-170. [CrossRef][Medline]
Epstein FH, Higgins M. Epidemiology of obesity. In: Bjorntorp P, Brodoff BN, eds. Obesity. Philadelphia: J.B. Lippincott, 1992:330-42.
Department of Agriculture. Composition of foods: raw, processed, prepared. Agricultural handbook no. 8 series. Washington, D.C.: Government Printing Office, 1963:159-69.
Heymsfield SB, Wang J, Kehayias JJ, Heshka S, Lichtman S, Pierson RN Jr. Chemical determination of human body density in vivo: relevance to hydrodensitometry. Am J Clin Nutr 1989;50:1282-1289. [Free Full Text]
Benedict FG, Fox EL. A method for determination of the energy values of foods and excreta. J Biol Chem 1925;66:783-799. [Free Full Text]
Ferrannini E. The theoretical bases of indirect calorimetry: a review. Metabolism 1988;37:287-301. [CrossRef][Medline]
Schoeller DA, van Santen E. Measurement of energy expenditure in humans by doubly labeled water method. J Appl Physiol 1982;53:955-959. [Free Full Text]
Ravussin E, Lillioja S, Anderson TE, Christin L, Bogardus C. Determinants of 24-hour energy expenditure in man: methods and results using a respiratory chamber. J Clin Invest 1986;78:1568-1578.
Mazess RB, Peppler WW, Gibbons M. Total body composition by dual-photon (153Gd) absorptiometry. Am J Clin Nutr 1984;40:834-839. [Free Full Text]
SAS/STAT user's guide: version 6. 4th ed. Cary, N.C.: SAS Institute, 1990.
Ravussin E, Burnand B, Schutz Y, Jequier E. Twenty-four-hour energy expenditure and resting metabolic rate in obese, moderately obese, and control subjects. Am J Clin Nutr 1982;35:566-573. [Free Full Text]
Blondheim SH, Mendelson B. Dietary thermogenesis: why the conflicting results? In: Berry EM, Blondheim H, Eliahou HE, Shafrir E, eds. Recent advances in obesity research V. London: John Libbey, 1987:151-4.
Ravussin E, Swinburn BA. Energy metabolism. In: Stunkard AJ, Wadden TA, eds. Obesity: theory and therapy. 2nd ed. New York: Raven Press, 1993:97-123.
Sims EAH, Danforth E Jr, Horton ES, Bray GA, Glennon JA, Salans LB. Endocrine and metabolic effects of experimental obesity in man. Recent Prog Horm Res 1973;29:457-496.
Norgan NG, Durnin JVGA. The effect of 6 weeks of overfeeding on the body weight, body composition, and energy metabolism of young men. Am J Clin Nutr 1980;33:978-988. [Free Full Text]
Tremblay A, Despres JP, Theriault G, Fournier G, Bouchard C. Overfeeding and energy expenditure in humans. Am J Clin Nutr 1992;56:857-862. [Free Full Text]
Forbes GB, Welle SL. Lean body mass in obesity. Int J Obes 1983;7:99-107. [Medline]
Elliot DL, Goldberg L, Kuehl KS, Bennett WM. Sustained depression of the resting metabolic rate after massive weight loss. Am J Clin Nutr 1989;49:93-96. [Free Full Text]
Doré C, Hesp R, Wilkins D, Garrow JS. Prediction of energy requirements of obese patients after massive weight loss. Hum Nutr Clin Nutr 1982;36:41-48.
Froidevaux F, Schutz Y, Christin L, Jequier E. Energy expenditure in obese women before and during weight loss, after refeeding, and in the weight-relapse period. Am J Clin Nutr 1993;57:35-42. [Free Full Text]
Amatruda JM, Statt MC, Welle SL. Total and resting energy expenditure in obese women reduced to ideal body weight. J Clin Invest 1993;92:1236-1242.
deBoer JO, van Es AJH, Roovers LCA, van Raaij JM, Hautvast JG. Adaptation of energy metabolism of overweight women to low-energy intake, studied with whole-body calorimeters. Am J Clin Nutr 1986;44:585-595. [Free Full Text]
Weigle DS, Sande KJ, Iverius PH, Monsen ER, Brunzell JD. Weight loss leads to a marked decrease in nonresting energy expenditure in ambulatory human subjects. Metabolism 1988;37:930-936. [CrossRef][Medline]
Astrup A, Buemann B, Christensen NJ, Madsen J. 24-hour energy expenditure and sympathetic activity in postobese women consuming a high-carbohydrate diet. Am J Physiol 1992;262:E282-E288. [Free Full Text]
Faust IM. Role of the fat cell in energy balance physiology. In: Stunkard AJ, Stellar E, eds. Eating and its disorders. Vol. 62 of Research publications: association for research in nervous and mental disease. New York: Raven Press, 1984:97-107.
Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the mouse obese gene and its human homologue. Nature 1994;372:425-432. [CrossRef][Medline]
Weigle DS, Brunzell JD. Assessment of energy expenditure in ambulatory reduced-obese subjects by the techniques of weight stabilization and exogenous weight replacement. Int J Obes 1990;14:Suppl 1:69-77.
Weigle DS. Contribution of decreased body mass to diminished thermic effect of exercise in reduced-obese men. Int J Obes 1988;12:567-578. [Medline]
Geissler CA, Miller DS, Shah M. The daily metabolic rate of the post-obese and the lean. Am J Clin Nutr 1987;45:914-920. [Free Full Text]
Belanger AJ, Cupples LA, D'Agostino RB. Means at each examination and inter-examination consistency of specified characteristics: Framingham Heart Study, 30-year followup. In: Kannel WB, Wolf PA, Garrison RJ, eds. The Framingham Study: an epidemiological investigation of cardiovascular disease. Sect. 36. Washington, D.C.: Government Printing Office, 1988. (NIH publication no. 88-2970.)
Harris RB. Role of set-point theory in regulation of body weight. FASEB J 1990;4:3310-3318. [Abstract]
Bogardus C, Lillioja S, Ravussin E, et al. Familial dependence of the resting metabolic rate. N Engl J Med 1986;315:96-100. [Abstract]
Bouchard C, Perusse L. Genetics of obesity. Annu Rev Nutr 1993;13:337-354. [CrossRef][Medline]
Knittle JL, Timmers K, Ginsberg-Fellner F, Brown RE, Katz DP. The growth of adipose tissue in children and adolescents: cross-sectional and longitudinal studies of adipose cell number and size. J Clin Invest 1979;63:239-246.
Olefsky J, Reaven GM, Farquhar JW. Effects of weight reduction on obesity: studies of lipid and carbohydrate metabolism in normal and hyperlipoproteinemic subjects. J Clin Invest 1974;53:64-76.
Jimenez J, Zuniga-Guajardo S, Zinman B, Angel A. Effects of weight loss in massive obesity on insulin and C-peptide dynamics: sequential changes in insulin production, clearance, and sensitivity. J Clin Endocrinol Metab 1987;64:661-668. [Free Full Text]
King, N A, Hopkins, M, Caudwell, P, Stubbs, R J, Blundell, J E
(2009). Beneficial effects of exercise: shifting the focus from body weight to other markers of health. Br. J. Sports. Med.
43: 924-927
[Abstract][Full Text]
Keun, H. C., Sidhu, J., Pchejetski, D., Lewis, J. S., Marconell, H., Patterson, M., Bloom, S. R., Amber, V., Coombes, R. C., Stebbing, J.
(2009). Serum Molecular Signatures of Weight Change during Early Breast Cancer Chemotherapy. Clin. Cancer Res.
15: 6716-6723
[Abstract][Full Text]
Bosy-Westphal, A., Kossel, E., Goele, K., Later, W., Hitze, B., Settler, U., Heller, M., Gluer, C.-C., Heymsfield, S. B, Muller, M. J
(2009). Contribution of individual organ mass loss to weight loss-associated decline in resting energy expenditure. Am. J. Clin. Nutr.
90: 993-1001
[Abstract][Full Text]
Singh, A., Wirtz, M., Parker, N., Hogan, M., Strahler, J., Michailidis, G., Schmidt, S., Vidal-Puig, A., Diano, S., Andrews, P., Brand, M. D., Friedman, J.
(2009). Leptin-mediated changes in hepatic mitochondrial metabolism, structure, and protein levels. Proc. Natl. Acad. Sci. USA
106: 13100-13105
[Abstract][Full Text]
Savage, J. S, Hoffman, L., Birch, L. L
(2009). Dieting, restraint, and disinhibition predict women's weight change over 6 y. Am. J. Clin. Nutr.
90: 33-40
[Abstract][Full Text]
Teske, J. A., Kotz, C. M.
(2009). Effect of acute and chronic caloric restriction and metabolic glucoprivation on spontaneous physical activity in obesity-prone and obesity-resistant rats. Am. J. Physiol. Regul. Integr. Comp. Physiol.
297: R176-R184
[Abstract][Full Text]
Swinburn, B. A, Sacks, G., Lo, S. K., Westerterp, K. R, Rush, E. C, Rosenbaum, M., Luke, A., Schoeller, D. A, DeLany, J. P, Butte, N. F, Ravussin, E.
(2009). Estimating the changes in energy flux that characterize the rise in obesity prevalence. Am. J. Clin. Nutr.
89: 1723-1728
[Abstract][Full Text]
Rogge, M. M.
(2009). The Role of Impaired Mitochondrial Lipid Oxidation in Obesity. Biol Res Nurs
10: 356-373
[Abstract]
Gratze, P., Boschmann, M., Dechend, R., Qadri, F., Malchow, J., Graeske, S., Engeli, S., Janke, J., Springer, J., Contrepas, A., Plehm, R., Klaus, S., Nguyen, G., Luft, F. C., Muller, D. N.
(2009). Energy Metabolism in Human Renin-Gene Transgenic Rats: Does Renin Contribute to Obesity?. Hypertension
53: 516-523
[Abstract][Full Text]
Stroebele, N., de Castro, J. M., Stuht, J., Catenacci, V., Wyatt, H. R., Hill, J. O.
(2009). A Small-Changes Approach Reduces Energy Intake in Free-Living Humans. J. Am. Coll. Nutr.
28: 63-68
[Abstract][Full Text]
Leibel, R. L.
(2008). Energy In, Energy Out, and the Effects of Obesity-Related Genes. NEJM
359: 2603-2604
[Full Text]
Hall, K. D, Jordan, P. N
(2008). Modeling weight-loss maintenance to help prevent body weight regain. Am. J. Clin. Nutr.
88: 1495-1503
[Abstract][Full Text]
Trevaskis, J. L., Coffey, T., Cole, R., Lei, C., Wittmer, C., Walsh, B., Weyer, C., Koda, J., Baron, A. D., Parkes, D. G., Roth, J. D.
(2008). Amylin-Mediated Restoration of Leptin Responsiveness in Diet-Induced Obesity: Magnitude and Mechanisms. Endocrinology
149: 5679-5687
[Abstract][Full Text]
Rosenbaum, M., Hirsch, J., Gallagher, D. A, Leibel, R. L
(2008). Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight. Am. J. Clin. Nutr.
88: 906-912
[Abstract][Full Text]
Amati, F., Dube, J. J., Shay, C., Goodpaster, B. H.
(2008). Separate and combined effects of exercise training and weight loss on exercise efficiency and substrate oxidation. J. Appl. Physiol.
105: 825-831
[Abstract][Full Text]
Thomson, R. L., Buckley, J. D., Noakes, M., Clifton, P. M., Norman, R. J., Brinkworth, G. D.
(2008). The Effect of a Hypocaloric Diet with and without Exercise Training on Body Composition, Cardiometabolic Risk Profile, and Reproductive Function in Overweight and Obese Women with Polycystic Ovary Syndrome. J. Clin. Endocrinol. Metab.
93: 3373-3380
[Abstract][Full Text]
Larrouy, D., Barbe, P., Valle, C., Dejean, S., Pelloux, V., Thalamas, C., Bastard, J.-P., Le Bouil, A., Diquet, B., Clement, K., Langin, D., Viguerie, N.
(2008). Gene expression profiling of human skeletal muscle in response to stabilized weight loss. Am. J. Clin. Nutr.
88: 125-132
[Abstract][Full Text]
Mark, A. L.
(2008). Dietary Therapy for Obesity: An Emperor With No Clothes. Hypertension
51: 1426-1434
[Full Text]
Lutfiyya, M. N., Garcia, R., Dankwa, C. M., Young, T., Lipsky, M. S.
(2008). Overweight and Obese Prevalence Rates in African American and Hispanic Children: An Analysis of Data from the 2003-2004 National Survey of Children's Health. J Am Board Fam Med
21: 191-199
[Abstract][Full Text]
Villaverde, C., Ramsey, J. J., Green, A. S., Asami, D. K., Yoo, S., Fascetti, A. J.
(2008). Energy Restriction Results in a Mass-Adjusted Decrease in Energy Expenditure in Cats That Is Maintained after Weight Regain. J. Nutr.
138: 856-860
[Abstract][Full Text]
Toledo, F. G.S., Menshikova, E. V., Azuma, K., Radikova, Z., Kelley, C. A., Ritov, V. B., Kelley, D. E.
(2008). Mitochondrial Capacity in Skeletal Muscle Is Not Stimulated by Weight Loss Despite Increases in Insulin Action and Decreases in Intramyocellular Lipid Content. Diabetes
57: 987-994
[Abstract][Full Text]
Jackman, M. R., Steig, A., Higgins, J. A., Johnson, G. C., Fleming-Elder, B. K., Bessesen, D. H., MacLean, P. S.
(2008). Weight regain after sustained weight reduction is accompanied by suppressed oxidation of dietary fat and adipocyte hyperplasia. Am. J. Physiol. Regul. Integr. Comp. Physiol.
294: R1117-R1129
[Abstract][Full Text]
Levine, J. A., McCrady, S. K., Lanningham-Foster, L. M., Kane, P. H., Foster, R. C., Manohar, C. U.
(2008). The Role of Free-Living Daily Walking in Human Weight Gain and Obesity. Diabetes
57: 548-554
[Abstract][Full Text]
Patterson, C. M., Dunn-Meynell, A. A., Levin, B. E.
(2008). Three weeks of early-onset exercise prolongs obesity resistance in DIO rats after exercise cessation. Am. J. Physiol. Regul. Integr. Comp. Physiol.
294: R290-R301
[Abstract][Full Text]
Rucker, D., Padwal, R., Li, S. K, Curioni, C., Lau, D. C W
(2007). Long term pharmacotherapy for obesity and overweight: updated meta-analysis. BMJ
335: 1194-1199
[Abstract][Full Text]
Roth, J. D., Coffey, T., Jodka, C. M., Maier, H., Athanacio, J. R., Mack, C. M., Weyer, C., Parkes, D. G.
(2007). Combination Therapy with Amylin and Peptide YY[3 36] in Obese Rodents: Anorexigenic Synergy and Weight Loss Additivity. Endocrinology
148: 6054-6061
[Abstract][Full Text]
Guijarro, A., Suzuki, S., Chen, C., Kirchner, H., Middleton, F. A., Nadtochiy, S., Brookes, P. S., Niijima, A., Inui, A., Meguid, M. M.
(2007). Characterization of weight loss and weight regain mechanisms after Roux-en-Y gastric bypass in rats. Am. J. Physiol. Regul. Integr. Comp. Physiol.
293: R1474-R1489
[Abstract][Full Text]
Levin, B. E.
(2007). Why some of us get fat and what we can do about it. J. Physiol.
583: 425-430
[Abstract][Full Text]
Dokken, B. B., Tsao, T.-S.
(2007). The Physiology of Body Weight Regulation: Are We Too Efficient for Our Own Good?. Diabetes Spectr.
20: 166-170
[Abstract][Full Text]
Craig, J.
(2007). How to Maintain Lost Weight. Diabetes Spectr.
20: 186-188
[Full Text]
Zhang, Y., Guo, K., LeBlanc, R. E., Loh, D., Schwartz, G. J., Yu, Y.-H.
(2007). Increasing Dietary Leucine Intake Reduces Diet-Induced Obesity and Improves Glucose and Cholesterol Metabolism in Mice via Multimechanisms. Diabetes
56: 1647-1654
[Abstract][Full Text]
Hunnell, N. A., Rockcastle, N. J., McCormick, K. N., Sinko, L. K., Sullivan, E. L., Cameron, J. L.
(2007). Physical activity of adult female rhesus monkeys (Macaca mulatta) across the menstrual cycle. Am. J. Physiol. Endocrinol. Metab.
292: E1520-E1525
[Abstract][Full Text]
Gentile, C. L., Orr, J. S., Davy, B. M., Davy, K. P.
(2007). Modest weight gain is associated with sympathetic neural activation in nonobese humans. Am. J. Physiol. Regul. Integr. Comp. Physiol.
292: R1834-R1838
[Abstract][Full Text]
Heymsfield, S. B, Harp, J. B, Reitman, M. L, Beetsch, J. W, Schoeller, D. A, Erondu, N., Pietrobelli, A.
(2007). Why do obese patients not lose more weight when treated with low-calorie diets? A mechanistic perspective. Am. J. Clin. Nutr.
85: 346-354
[Abstract][Full Text]
Loucks, A B
(2007). Refutation of "the myth of the female athlete triad". Br. J. Sports. Med.
41: 55-57
[Full Text]
Bossu, C., Galusca, B., Normand, S., Germain, N., Collet, P., Frere, D., Lang, F., Laville, M., Estour, B.
(2007). Energy expenditure adjusted for body composition differentiates constitutional thinness from both normal subjects and anorexia nervosa. Am. J. Physiol. Endocrinol. Metab.
292: E132-E137
[Abstract][Full Text]
Hill, J. O.
(2006). Understanding and Addressing the Epidemic of Obesity: An Energy Balance Perspective. Endocr. Rev.
27: 750-761
[Abstract][Full Text]
Foster-Schubert, K. E., Cummings, D. E.
(2006). Emerging Therapeutic Strategies for Obesity. Endocr. Rev.
27: 779-793
[Abstract][Full Text]
Hayes, C.
(2006). Meal Provision as a Strategy for Supporting Weight Loss and Improving Metabolic Parameters in Type 2 Diabetes. Clin. Diabetes
24: 182-185
[Full Text]
Moran, L. J, Noakes, M., Clifton, P. M, Wittert, G. A, Williams, G., Norman, R. J
(2006). Short-term meal replacements followed by dietary macronutrient restriction enhance weight loss in polycystic ovary syndrome. Am. J. Clin. Nutr.
84: 77-87
[Abstract][Full Text]
Hall, K. D.
(2006). Computational model of in vivo human energy metabolism during semistarvation and refeeding. Am. J. Physiol. Endocrinol. Metab.
291: E23-E37
[Abstract][Full Text]
Ramsey, J. J., Hagopian, K.
(2006). Energy Expenditure and Restriction of Energy Intake: Could Energy Restriction Alter Energy Expenditure in Companion Animals?. J. Nutr.
136: 1958S-1966S
[Abstract][Full Text]
MacLean, P. S., Higgins, J. A., Jackman, M. R., Johnson, G. C., Fleming-Elder, B. K., Wyatt, H. R., Melanson, E. L., Hill, J. O.
(2006). Peripheral metabolic responses to prolonged weight reduction that promote rapid, efficient regain in obesity-prone rats. Am. J. Physiol. Regul. Integr. Comp. Physiol.
290: R1577-R1588
[Abstract][Full Text]
Heilbronn, L. K., de Jonge, L., Frisard, M. I., DeLany, J. P., Larson-Meyer, D. E., Rood, J., Nguyen, T., Martin, C. K., Volaufova, J., Most, M. M., Greenway, F. L., Smith, S. R., Deutsch, W. A., Williamson, D. A., Ravussin, E., for the Pennington CALERIE Team,
(2006). Effect of 6-Month Calorie Restriction on Biomarkers of Longevity, Metabolic Adaptation, and Oxidative Stress in Overweight Individuals: A Randomized Controlled Trial. JAMA
295: 1539-1548
[Abstract][Full Text]
Orbach, S.
(2006). Commentary: There is a public health crisis--its not fat on the body but fat in the mind and the fat of profits. Int J Epidemiol
35: 67-69
[Full Text]
Lofgren, P., Andersson, I., Adolfsson, B., Leijonhufvud, B.-M., Hertel, K., Hoffstedt, J., Arner, P.
(2005). Long-Term Prospective and Controlled Studies Demonstrate Adipose Tissue Hypercellularity and Relative Leptin Deficiency in the Postobese State. J. Clin. Endocrinol. Metab.
90: 6207-6213
[Abstract][Full Text]
Hill, J. O., Wyatt, H. R.
(2005). Role of physical activity in preventing and treating obesity. J. Appl. Physiol.
99: 765-770
[Abstract][Full Text]
Kok, P., Roelfsema, F., Langendonk, J. G., Frolich, M., Burggraaf, J., Meinders, A. E., Pijl, H.
(2005). High Circulating Thyrotropin Levels in Obese Women Are Reduced after Body Weight Loss Induced by Caloric Restriction. J. Clin. Endocrinol. Metab.
90: 4659-4663
[Abstract][Full Text]
Pi-Sunyer, F. X.
(2005). Weight Loss in Type 2 Diabetic Patients. Diabetes Care
28: 1526-1527
[Full Text]
MacLean, P. S.
(2005). A peripheral perspective of weight regain. Am. J. Physiol. Regul. Integr. Comp. Physiol.
288: R1447-R1449
[Full Text]
Dixon, A. F. R., Dixon, J. B., O'Brien, P. E.
(2005). Laparoscopic Adjustable Gastric Banding Induces Prolonged Satiety: A Randomized Blind Crossover Study. J. Clin. Endocrinol. Metab.
90: 813-819
[Abstract][Full Text]
Schwartz, M. W., Niswender, K. D.
(2004). Adiposity Signaling and Biological Defense Against Weight Gain: Absence of Protection or Central Hormone Resistance?. J. Clin. Endocrinol. Metab.
89: 5889-5897
[Abstract][Full Text]
Avesani, C. M., Draibe, S. A., Kamimura, M. A., Dalboni, M. A., Colugnati, F. A. B., Cuppari, L.
(2004). Decreased resting energy expenditure in non-dialysed chronic kidney disease patients. Nephrol Dial Transplant
19: 3091-3097
[Abstract][Full Text]
Levin, B. E.
(2004). The drive to regain is mainly in the brain. Am. J. Physiol. Regul. Integr. Comp. Physiol.
287: R1297-R1300
[Full Text]
MacLean, P. S., Higgins, J. A., Johnson, G. C., Fleming-Elder, B. K., Donahoo, W. T., Melanson, E. L., Hill, J. O.
(2004). Enhanced metabolic efficiency contributes to weight regain after weight loss in obesity-prone rats. Am. J. Physiol. Regul. Integr. Comp. Physiol.
287: R1306-R1315
[Abstract][Full Text]
Pereira, M. A., Swain, J., Goldfine, A. B., Rifai, N., Ludwig, D. S.
(2004). Effects of a Low-Glycemic Load Diet on Resting Energy Expenditure and Heart Disease Risk Factors During Weight Loss. JAMA
292: 2482-2490
[Abstract][Full Text]
Swinburn, B., Egger, G.
(2004). The runaway weight gain train: too many accelerators, not enough brakes. BMJ
329: 736-739
[Full Text]
Speakman, J. R.
(2004). Obesity: The Integrated Roles of Environment and Genetics. J. Nutr.
134: 2090S-2105S
[Abstract][Full Text]
MacLean, P. S., Higgins, J. A., Johnson, G. C., Fleming-Elder, B. K., Peters, J. C., Hill, J. O.
(2004). Metabolic adjustments with the development, treatment, and recurrence of obesity in obesity-prone rats. Am. J. Physiol. Regul. Integr. Comp. Physiol.
287: R288-R297
[Abstract][Full Text]
Franks, P. W., Ekelund, U., Brage, S., Wong, M.-Y., Wareham, N. J.
(2004). Does the Association of Habitual Physical Activity With the Metabolic Syndrome Differ by Level of Cardiorespiratory Fitness?. Diabetes Care
27: 1187-1193
[Abstract][Full Text]
Levine, J. A.
(2004). Nonexercise activity thermogenesis (NEAT): environment and biology. Am. J. Physiol. Endocrinol. Metab.
286: E675-E685
[Abstract][Full Text]
Doucet, E., Pomerleau, M., Harper, M.-E.
(2004). Fasting and Postprandial Total Ghrelin Remain Unchanged after Short-Term Energy Restriction. J. Clin. Endocrinol. Metab.
89: 1727-1732
[Abstract][Full Text]
Levin, B. E., Dunn-Meynell, A. A.
(2004). Chronic exercise lowers the defended body weight gain and adiposity in diet-induced obese rats. Am. J. Physiol. Regul. Integr. Comp. Physiol.
286: R771-R778
[Abstract][Full Text]
Albert, S. G., Mooradian, A. D.
(2004). Low-Dose Recombinant Human Growth Hormone as Adjuvant Therapy to Lifestyle Modifications in the Management of Obesity. J. Clin. Endocrinol. Metab.
89: 695-701
[Abstract][Full Text]
Hays, N. P., Starling, R. D., Liu, X., Sullivan, D. H., Trappe, T. A., Fluckey, J. D., Evans, W. J.
(2004). Effects of an Ad Libitum Low-Fat, High-Carbohydrate Diet on Body Weight, Body Composition, and Fat Distribution in Older Men and Women: A Randomized Controlled Trial. Arch Intern Med
164: 210-217
[Abstract][Full Text]
Kelley, D. E., Kuller, L. H., McKolanis, T. M., Harper, P., Mancino, J., Kalhan, S.
(2004). Effects of Moderate Weight Loss and Orlistat on Insulin Resistance, Regional Adiposity, and Fatty Acids in Type 2 Diabetes. Diabetes Care
27: 33-40
[Abstract][Full Text]
Obici, S., Rossetti, L.
(2003). Minireview: Nutrient Sensing and the Regulation of Insulin Action and Energy Balance. Endocrinology
144: 5172-5178
[Abstract][Full Text]
Heilbronn, L. K, Ravussin, E.
(2003). Calorie restriction and aging: review of the literature and implications for studies in humans. Am. J. Clin. Nutr.
78: 361-369
[Abstract][Full Text]
Doucet, E., Tremblay, A., Simoneau, J.-A., Joanisse, D. R
(2003). Skeletal muscle enzymes as predictors of 24-h energy metabolism in reduced-obese persons. Am. J. Clin. Nutr.
78: 430-435
[Abstract][Full Text]
Ricci, M. R., Levin, B. E.
(2003). Ontogeny of diet-induced obesity in selectively bred Sprague-Dawley rats. Am. J. Physiol. Regul. Integr. Comp. Physiol.
285: R610-R618
[Abstract][Full Text]
Lowell, B. B., Bachman, E. S.
(2003). {beta}-Adrenergic Receptors, Diet-induced Thermogenesis, and Obesity. J. Biol. Chem.
278: 29385-29388
[Full Text]
Das, S. K., Roberts, S. B, McCrory, M. A, Hsu, L. G., Shikora, S. A, Kehayias, J. J, Dallal, G. E, Saltzman, E.
(2003). Long-term changes in energy expenditure and body composition after massive weight loss induced by gastric bypass surgery. Am. J. Clin. Nutr.
78: 22-30
[Abstract][Full Text]
Duggan, C., Bechard, L., Donovan, K., Vangel, M., O'Leary, A., Holmes, C., Lehmann, L., Guinan, E.
(2003). Changes in resting energy expenditure among children undergoing allogeneic stem cell transplantation. Am. J. Clin. Nutr.
78: 104-109
[Abstract][Full Text]
Rosenbaum, M., Vandenborne, K., Goldsmith, R., Simoneau, J.-A., Heymsfield, S., Joanisse, D. R., Hirsch, J., Murphy, E., Matthews, D., Segal, K. R., Leibel, R. L.
(2003). Effects of experimental weight perturbation on skeletal muscle work efficiency in human subjects. Am. J. Physiol. Regul. Integr. Comp. Physiol.
285: R183-R192
[Abstract][Full Text]
Berkowitz, R. I., Wadden, T. A., Tershakovec, A. M., Cronquist, J. L.
(2003). Behavior Therapy and Sibutramine for the Treatment of Adolescent Obesity: A Randomized Controlled Trial. JAMA
289: 1805-1812
[Abstract][Full Text]
Cummings, D. E., Shannon, M. H.
(2003). Roles for Ghrelin in the Regulation of Appetite and Body Weight. Arch Surg
138: 389-396
[Full Text]
Landry, N., Bergeron, N., Archer, R., Samson, P., Corneau, L., Bergeron, J., Deriaz, O.
(2003). Whole-body fat oxidation rate and plasma triacylglycerol concentrations in men consuming an ad libitum high-carbohydrate or low-carbohydrate diet. Am. J. Clin. Nutr.
77: 580-586
[Abstract][Full Text]
Schultes, B., Oltmanns, K. M., Kern, W., Fehm, H. L., Born, J., Peters, A.
(2003). Modulation of Hunger by Plasma Glucose and Metformin. J. Clin. Endocrinol. Metab.
88: 1133-1141
[Abstract][Full Text]
Friedman, J. M.
(2003). A War on Obesity, Not the Obese. Science
299: 856-858
[Abstract][Full Text]
Blanc, S., Schoeller, D., Kemnitz, J., Weindruch, R., Colman, R., Newton, W., Wink, K., Baum, S., Ramsey, J.
(2003). Energy Expenditure of Rhesus Monkeys Subjected to 11 Years of Dietary Restriction. J. Clin. Endocrinol. Metab.
88: 16-23
[Abstract][Full Text]
Levin, B. E., Dunn-Meynell, A. A.
(2002). Reduced central leptin sensitivity in rats with diet-induced obesity. Am. J. Physiol. Regul. Integr. Comp. Physiol.
283: R941-R948
[Abstract][Full Text]
Hirsch, J.
(2002). The search for new ways to treat obesity. Proc. Natl. Acad. Sci. USA
99: 9096-9097
[Full Text]
Rogge, M. M.
(2002). The Case for an Immunologic Cause of Obesity. Biol Res Nurs
4: 43-53
[Abstract]
Kaufman, B. A., Warren, M. P., Dominguez, J. E., Wang, J., Heymsfield, S. B., Pierson, R. N.
(2002). Bone Density and Amenorrhea in Ballet Dancers Are Related to a Decreased Resting Metabolic Rate and Lower Leptin Levels. J. Clin. Endocrinol. Metab.
87: 2777-2783
[Abstract][Full Text]
Cummings, D. E., Weigle, D. S., Frayo, R. S., Breen, P. A., Ma, M. K., Dellinger, E. P., Purnell, J. Q.
(2002). Plasma Ghrelin Levels after Diet-Induced Weight Loss or Gastric Bypass Surgery. NEJM
346: 1623-1630
[Abstract][Full Text]
Heitmann, B. L., Garby, L.
(2002). Composition (lean and fat tissue) of weight changes in adult Danes. Am. J. Clin. Nutr.
75: 840-847
[Abstract][Full Text]
Tershakovec, A. M, Kuppler, K. M, Zemel, B., Stallings, V. A
(2002). Age, sex, ethnicity, body composition, and resting energy expenditure of obese African American and white children and adolescents. Am. J. Clin. Nutr.
75: 867-871
[Abstract][Full Text]
Luscombe, N.D., Clifton, P.M., Noakes, M., Parker, B., Wittert, G.
(2002). Effects of Energy-Restricted Diets Containing Increased Protein on Weight Loss, Resting Energy Expenditure, and the Thermic Effect of Feeding in Type 2 Diabetes. Diabetes Care
25: 652-657
[Abstract][Full Text]
Wyatt, H. R, Hill, J. O
(2002). Let's get serious about promoting physical activity. Am. J. Clin. Nutr.
75: 449-450
[Full Text]
Weinsier, R. L, Hunter, G. R, Desmond, R. A, Byrne, N. M, Zuckerman, P. A, Darnell, B. E
(2002). Free-living activity energy expenditure in women successful and unsuccessful at maintaining a normal body weight. Am. J. Clin. Nutr.
75: 499-504
[Abstract][Full Text]
SCHRAUWEN, P., SARIS, W. H. M., HESSELINK, M. K. C.
(2001). An alternative function for human uncoupling protein 3: protection of mitochondria against accumulation of nonesterified fatty acids inside the mitochondrial matrix. FASEB J.
15: 2497-2502
[Abstract][Full Text]
O'Sullivan, A. J., Martin, A., Brown, M. A.
(2001). Efficient Fat Storage in Premenopausal Women and in Early Pregnancy: A Role for Estrogen. J. Clin. Endocrinol. Metab.
86: 4951-4956
[Abstract][Full Text]
Franz, M. J., Pastors, J. G., Warshaw, H., Daly, A. E.
(2001). Does "Diet" Fail?. The Diabetes Educator
27: 563-570
Franz, M. J.
(2001). The Answer to Weight Loss Is Easy--Doing It Is Hard!. Clin. Diabetes
19: 105-109
[Abstract][Full Text]
Weinsier, R. L.
(2001). Etiology of Obesity: Methodological Examination of the Set-Point Theory. JPEN J Parenter Enteral Nutr
25: 103-110
van Aggel-Leijssen, D. P., Saris, W. H., Hul, G. B, van Baak, M. A
(2001). Short-term effects of weight loss with or without low-intensity exercise training on fat metabolism in obese men. Am. J. Clin. Nutr.
73: 523-531
[Abstract][Full Text]
Weinsier, R., Hunter, G., Schutz, Y.
(2001). Metabolic response to weight loss. Am. J. Clin. Nutr.
73: 655-657
[Full Text]
Rosenbaum, M., Leibel, R. L
(2001). Reply to R Weinsier et al. Am. J. Clin. Nutr.
73: 657-658
[Full Text]
Fried, L. P., Tangen, C. M., Walston, J., Newman, A. B., Hirsch, C., Gottdiener, J., Seeman, T., Tracy, R., Kop, W. J., Burke, G., McBurnie, M. A.
(2001). Frailty in Older Adults: Evidence for a Phenotype. Journals of Gerontology Series A: Biological Sciences and Medical Sciences
56: 146M-157
[Abstract][Full Text]
A correction has been published: N Engl J Med 1995;333(6):399.
