Plasma Ghrelin Levels after Diet-Induced Weight Loss or Gastric Bypass Surgery
David E. Cummings, M.D., David S. Weigle, M.D., R. Scott Frayo, B.S., Patricia A. Breen, B.S.N., Marina K. Ma, E. Patchen Dellinger, M.D., and Jonathan Q. Purnell, M.D.
Background Weight loss causes changes in appetite and energyexpenditure that promote weight regain. Ghrelin is a hormonethat increases food intake in rodents and humans. If circulatingghrelin participates in the adaptive response to weight loss,its levels should rise with dieting. Because ghrelin is producedprimarily by the stomach, weight loss after gastric bypass surgerymay be accompanied by impaired ghrelin secretion.
Methods We determined the 24-hour plasma ghrelin profiles, bodycomposition, insulin levels, leptin levels, and insulin sensitivityin 13 obese subjects before and after a six-month dietary programfor weight loss. The 24-hour ghrelin profiles were also determinedin 5 subjects who had lost weight after gastric bypass and 10normal-weight controls; 5 of the 13 obese subjects who participatedin the dietary program were matched to the subjects in the gastric-bypassgroup and served as obese controls.
Results Plasma ghrelin levels rose sharply shortly before andfell shortly after every meal. A diet-induced weight loss of17 percent of initial body weight was associated with a 24 percentincrease in the area under the curve for the 24-hour ghrelinprofile (P=0.006). In contrast, despite a 36 percent weightloss after gastric bypass, the area under the curve for theghrelin profile in the gastric-bypass group was 77 percent lowerthan in normal-weight controls (P<0.001) and 72 percent lowerthan in matched obese controls (P=0.01). The normal, meal-relatedfluctuations and diurnal rhythm of the ghrelin level were absentafter gastric bypass.
Conclusions The increase in the plasma ghrelin level with diet-inducedweight loss is consistent with the hypothesis that ghrelin hasa role in the long-term regulation of body weight. Gastric bypassis associated with markedly suppressed ghrelin levels, possiblycontributing to the weight-reducing effect of the procedure.
Obesity represents a global epidemic1 and is a leading causeof illness and death worldwide.2,3 Weight reduction achievedby dieting, exercise, or medical therapy often elicits compensatorychanges in appetite and energy expenditure4,5 that make weightloss of more than 5 to 10 percent unlikely to be sustained.6,7,8,9,10In contrast, gastric bypass surgery, in which most of the stomachand duodenum are bypassed with the use of a gastrojejunal anastomosis,typically causes substantial, long-term weight loss.11,12,13The operation appears to undermine the normal compensatory physiologicresponses to energy deficit. This effect is unlikely to resultfrom gastric restriction alone, and it has been proposed thata disruption of gut-derived factors that regulate eating behavioris involved, although no such factors have been identified.14,15
Ghrelin is a recently discovered16 orexigenic hormone that issecreted primarily by the stomach and duodenum17 and has beenimplicated in both meal-time hunger and the long-term regulationof body weight.18,19,20,21,22,23,24 In humans, plasma ghrelinlevels rise shortly before and fall shortly after every meal,a pattern that is consistent with a role in the urge to begineating.24 If circulating ghrelin participates in long-term regulationof body weight, its level should increase with weight loss aspart of the compensatory response to an energy deficit. In contrast,gastric bypass may disrupt ghrelin secretion by isolating ghrelin-producingcells from direct contact with ingested nutrients, which normallyregulate ghrelin levels,18,24 and this effect may contributeto the efficacy of the procedure in reducing weight. To testthese hypotheses, we determined the 24-hour plasma ghrelin profilesin subjects before and after diet-induced weight loss, and comparedthese values with those in subjects who had lost weight afterproximal gastric bypass surgery.
Methods
Study Subjects
Subjects in the dietary-weight-loss group and normal-weightcontrols were recruited through advertising in local newspapersand on the campus of the University of Washington. All subjectswere at least 18 years old and had had stable body weight forat least three months. Criteria for exclusion included chronicmedical or psychiatric illness, pregnancy, tobacco use, substanceabuse, consumption of more than two alcoholic drinks per day,aerobic exercise for more than 30 minutes three times per week,and previous gastrointestinal surgery. The Human Subjects ReviewCommittee at the University of Washington approved all proceduresand protocols, and written informed consent was obtained fromall subjects before enrollment. Studies were performed at theGeneral Clinical Research Center of the University of Washington.
Protocol for Diet-Induced Weight Loss and Stabilization
Through the Nutrition Research Unit of the research center,13 obese subjects (Table 1) received a low-fat, high-protein,liquid-formula diet of 1000 kcal per day, supplemented withdaily multivitamins and minerals, for three months. Subjectsthen underwent a gradual transition over the course of two weeksto a solid diet containing 30 percent fat, 15 percent protein,and 55 percent carbohydrates — a macronutrient compositionapproximating that of the average diet in the United States.25The total number of calories was adjusted to stabilize weight,and subjects were taught to continue this process at home inorder to maintain a stable, reduced weight for three months.Throughout the six months of the program of weight loss andstabilization, subjects met with research dietitians two tothree times per week and were weighed on a single scale.
At the beginning and end of the study, subjects were admittedto the research center after fasting overnight, and intravenouscatheters were placed in both arms. Blood was withdrawn formeasurement of insulin and leptin, followed by a tolbutamide-modifiedfrequently sampled intravenous glucose-tolerance test to determineinsulin sensitivity with the use of the minimal model of glucosekinetics.26 Blood was collected in EDTA tubes every 30 minutesbetween 8 a.m. and 9 p.m., then hourly until 8 the followingmorning (24 hours in all). Samples were stored at 4°C duringthe collection period, after which plasma was stored at –80°C.Breakfast, lunch, and dinner (based on the solid diet describedabove) were served at 8 a.m., noon, and 5:30 p.m., respectively.At the beginning and end of the study, the percentage of bodyfat was measured by underwater weighing,27 the volumes of subcutaneousand visceral fat were assessed by computed tomography,28 andthe adipocyte volume was determined by applying Goldrick's equationto the measured diameters of 400 adipocytes aspirated from theposterior superior iliac-crest region.29
Gastric-Bypass Study
The 24-hour plasma ghrelin profiles were determined as describedabove in subjects who had undergone a proximal Roux-en-Y gastricbypass 9 to 31 months previously (mean [±SE], 1.4±0.4years) (Table 1). These profiles were compared with the 24-hourghrelin profiles from two control groups without previous gastrointestinalsurgery: normal-weight subjects and a group of matched obesesubjects who had recently lost weight by dieting and were matchedto the subjects in the gastric-bypass group according to finalbody-mass index (the weight in kilograms divided by the squareof the height in meters), age, and sex. The latter group wasa subgroup of the dietary-weight-loss group and was includedto control for the effects of obesity, age, and sex on ghrelinlevels.
Subjects in all three groups had stable weight at the time of24-hour sampling, as defined by a change of no more than 5 percentin body weight during the preceding three months. We selectednormal-weight controls whose weight was at its lifetime maximumand who had maintained this weight for at least three months;during the two weeks preceding blood sampling, their caloricintake was adjusted twice weekly to maintain stability of weight.During this period, the average body-mass index of the groupvaried by only 0.4±0.3 percent.
Hormone Assays
Plasma immunoreactive ghrelin was measured in duplicate witha radioimmunoassay involving an iodine-125–labeled bioactiveghrelin tracer and a rabbit polyclonal antibody against full-length,octanoylated human ghrelin that recognizes the acylated anddesacyl forms of the hormone (Phoenix Pharmaceuticals). Thelower and upper limits of detection were 80 and 2500 pg permilliliter (24 and 740 pmol per liter), respectively, and in41 assays, the coefficient of variation was 6.9 percent withinassays and 12.8 percent between assays. Plasma insulin was measuredin duplicate with a double-antibody radioimmunoassay,30 andleptin was measured in duplicate with a commercial radioimmunoassaykit (Linco Research).
Statistical Analysis
Hormone levels are expressed as means ±SE. Values forthe area under the curve for the 24-hour ghrelin profile werecalculated with the use of the trapezoidal rule. End pointswere compared with the use of two-tailed, paired Student's t-tests,and exact binomial methods were used where indicated. Correlationswere determined by univariate linear regression.
Results
Effect of Diet-Induced Weight Loss on Plasma Ghrelin Levels
Thirteen obese subjects with stable weight underwent diet-inducedweight loss for three months, followed by three months of stabilizationat the reduced weight. At the end of this period, subjects hadlost a mean (±SE) of 17.4±1.5 percent of theirinitial body weight (P<0.001) (Table 2). A total of 84 percentof the lost weight came from fat and was derived relativelyevenly from intraabdominal and subcutaneous adipose tissue.Weight loss was associated with significant reductions in adipocytevolume, leptin levels, insulin levels, and blood pressure, aswell as with increased insulin sensitivity and improved lipidprofiles (Table 2).
The 24-hour plasma ghrelin profiles determined at the beginningand end of the study are shown in Figure 1. The temporal patternof the levels of circulating ghrelin was similar before andafter weight loss. Levels rose progressively for one to twohours before each meal and fell to trough levels within oneto two hours after the subjects began eating. The ghrelin levelincreased from premeal troughs by a mean of 20 percent beforebreakfast, 45 percent before lunch, and 51 percent before dinner.Between-meal ghrelin values rose gradually throughout the dayin a diurnal pattern, with a nadir between 9 a.m. and 10 a.m.and a peak between midnight and 2 a.m., as in normal-weightsubjects.24
Figure 1. Mean (±SE) 24-Hour Plasma Ghrelin Profiles in 13 Obese Subjects before and after Diet-Induced Weight Loss.
Breakfast, lunch, and dinner were provided at the times indicated. To convert ghrelin values to picomoles per liter, multiply by 0.296.
After weight loss, the mean plasma ghrelin level increased atevery time point throughout the 24-hour period (Figure 1), andthe mean (±SE) area under the curve in the ghrelin profileincreased by 24 percent (9365±1127 pg-days per milliliter[2772±334 pmol-days per liter] before weight loss, ascompared with 11,585±1449 pg-days per milliliter [3429±429pmol-days per liter] after weight loss, P=0.006). For each meal,the maximally suppressed postprandial mean ghrelin level afterweight loss was only slightly lower than the peak preprandiallevel before weight loss. Individual values for the area underthe curve increased with weight loss in 12 of the 13 subjects(P=0.003 by the exact binomial test). Among these 12, therewas a positive correlation between the percentage decrease ineither body weight or body-mass index and the percentage increasein the area under the curve (R=0.67, P=0.01). There were similartrends toward positive correlation between the magnitude ofthe increase in the area under the curve for the ghrelin profileand the magnitude of the decrease in all other measures of adiposityshown in Table 2.
Plasma Ghrelin Levels after Gastric Bypass Surgery
The 24-hour plasma ghrelin profile was determined for subjectsin three groups with stable weight (Table 1): obese subjectswho had undergone a proximal Roux-en-Y gastric bypass; normal-weightcontrols; and matched obese controls who had recently lost weightby dieting and were matched to the subjects in the gastric-bypassgroup according to the final body-mass index (at the end ofthe six-month period), age, sex, and fasting plasma leptin level(23.2±9.3 ng per milliliter [1.9±0.7 nmol permilliliter] in the matched obese controls and 21.1±9.8ng per milliliter [1.7±0.8 nmol per milliliter] in thegastric-bypass group).
Plasma ghrelin levels were markedly lower in the gastric-bypassgroup than in either control group (Figure 2). The area underthe curve for the 24-hour ghrelin profile of subjects in thegastric-bypass group (3058±718 pg-days per milliliter[905±213 pmol-days per liter]) was 77 percent lower thanthat in the normal-weight controls (13,401±1785 pg-daysper milliliter [3967±528 pmol-days per liter], P<0.001)and 72 percent lower than that in the matched obese controls(10,803±3591 pg-days per milliliter [3198±1063pmol-days per liter], P=0.01). The ghrelin profile of subjectsin the gastric-bypass group showed neither the meal-relatedoscillations nor the diurnal rhythm that were found in the profilesof both control groups and the profiles displayed in Figure 1.Instead, ghrelin levels in subjects who underwent gastricbypass remained only slightly above the limit of detection throughoutthe day. We have previously shown that the temporal patternof circulating ghrelin is the reciprocal of that of insulinand in phase with that of leptin.24 Subjects in the gastric-bypassgroup had normal postprandial insulin spikes and an intact diurnalrhythm of leptin levels (Figure 3), indicating that physiologicchanges in the levels of these hormones are not sufficient tocause the normal daily variation in plasma ghrelin after gastricbypass.
Figure 2. Mean (±SE) 24-Hour Plasma Ghrelin Profiles in Subjects Who Underwent Gastric Bypass and in Controls.
The study groups represented are 5 obese subjects who underwent a proximal Roux-en-Y gastric bypass, 10 normal-weight controls, and 5 obese subjects who had recently lost weight by dieting and were matched to the subjects in the gastric-bypass group according to final body-mass index, age, and sex. Breakfast, lunch, and dinner were provided at the times indicated. To convert ghrelin values to picomoles per liter, multiply by 0.296.
Figure 3. Mean (±SE) 24-Hour Profiles of Plasma Ghrelin, Insulin, and Leptin in Five Subjects Who Underwent Gastric Bypass.
Breakfast, lunch, and dinner were provided at the times indicated. To convert values for ghrelin to picomoles per liter, multiply by 0.296. To convert values for insulin to picomoles per liter, multiply by 6. To convert values for leptin to nanomoles per milliliter, multiply by 0.08.
Discussion
Our data are consistent with the hypothesis that ghrelin hasa role in both mealtime hunger and the long-term regulationof body weight. We have confirmed in obese subjects our previousfindings in lean persons24 that plasma ghrelin levels rise shortlybefore and fall shortly after every meal. This pattern is consistentwith a model according to which ghrelin, a gut hormone withrapid, short-lived orexigenic effects in rodents,18,19,20,21has a causal role in mealtime hunger in humans.
Moreover, the levels of circulating ghrelin over a 24-hour periodincreased after diet-induced weight loss — a finding thatis consistent with a role for ghrelin in the long-term regulationof body weight in humans. Several observations from studiesin rodents provide further support for such a role. First, continuousadministration of ghrelin durably increases body weight.18,19,21Second, in addition to increasing food intake, exogenous ghrelindecreases the metabolic rate21 and the catabolism of fat,18thereby affecting all aspects of the system of energy regulationin such a way as to increase body weight. Finally, blockadeof ghrelin in the brain leads to a reduction in food intake,19suggesting that endogenous ghrelin signaling is required tomaintain normal appetite. Our finding that plasma ghrelin levelsrise with diet-induced weight loss suggests that increased levelsof circulating ghrelin may participate in the adaptive responsesthat constrain such weight loss.
Plasma ghrelin levels in subjects who underwent gastric bypassdid not oscillate in relation to meals and were markedly lowerthan those of both lean controls and matched obese controls,despite massive weight loss. Thus, whereas weight loss achievedby caloric restriction was associated with increased plasmaghrelin levels, that achieved by gastric bypass was associatedwith abnormally low levels. In addition to having altered gastrointestinalanatomy, subjects who underwent gastric bypass differed fromthe normal-weight controls in that they had lost substantialamounts of body weight and in that they were (still) obese.However, neither of these differences accounts for the suppressionof ghrelin in these subjects. Although it has been shown thatobesity is associated with mildly decreased levels of circulatingghrelin,31 the area under the curve for the 24-hour ghrelinprofile of the matched obese controls in our study was 3.5 timesthat of the subjects in the gastric-bypass group, even thoughthese groups had the same average body-mass index. Nor can thevery low ghrelin values in the gastric-bypass group be explainedby the fact that the subjects in that group had lost more weightthan the matched obese controls, since weight loss should increasethe plasma ghrelin level (Figure 1). Thus, it seems clear thatgastric bypass surgery is itself associated with decreased levelsof circulating ghrelin.
These findings raise the possibility that suppression of ghrelinis one mechanism by which gastric bypass reduces body weight.Gastric restriction after this operation should cause earlysatiety, and this effect has been clearly documented.13,32 However,if gastric restriction were the only important alteration, patientswho had undergone such surgery would be expected to eat morefrequent, small meals and to favor calorie-dense foods, especiallywith continued weight loss, which should elicit compensatoryhyperphagia. In contrast, patients who undergo gastric bypasshave been shown to feel hungry less often after the operation,32,33,34eat fewer meals and snacks per day,32 and voluntarily reducetheir intake of calorie-dense foods such as fats, high-caloriecarbohydrates, high-calorie beverages, red meat, and ice cream.32,34,35These alterations occur despite the fact that patients reportno change in their perception of the deliciousness of high-caloriecarbohydrates (i.e., sweets) or in their overall enjoyment offood.32 This finding suggests that other mechanisms beyond gastricrestriction contribute to the loss of appetite and body weightcaused by gastric bypass.
Our finding of markedly reduced ghrelin levels after gastricbypass suggests that suppression of ghrelin can now be studiedas a potential mechanism by which this procedure causes weightloss. This hypothesis offers a plausible explanation for theparadoxical reduction of hunger between meals that occurs aftergastric bypass, as well as for the observation that the procedureis more effective than gastroplasty in facilitating long-termweight loss.12,13,14,35,36,37,38,39,40 These operations produceequivalent gastric restriction,35,41 but only gastric bypassisolates ghrelin cells from contact with enteral nutrients.
The mechanism by which gastric bypass leads to a reduction inghrelin levels remains to be determined. Our data show thatingested nutrients powerfully regulate the level of circulatingghrelin. Although an empty stomach is associated with an increasedghrelin level in the short term, it is possible that the permanentabsence of food in the stomach and duodenum that results fromgastric bypass causes a continuous stimulatory signal that ultimatelysuppresses ghrelin production through the process of "overrideinhibition." By this mechanism, continuous gonadotropin-releasinghormone signaling initially stimulates but eventually suppressesgonadotropin secretion,42 and a similar desensitization occurswith the unabated stimulation of growth hormone by growth-hormone–releasinghormone.43 The possibility that override inhibition occurs inthe case of ghrelin is suggested by our data showing a progressivedecline in the circulating level during an overnight fast (Figure 1and Figure 2).24
In summary, 24-hour plasma ghrelin levels increase in responseto diet-induced weight loss, suggesting that ghrelin may playa part in the adaptive response that limits the amount of weightthat may be lost by dieting. We also found that ghrelin levelsare abnormally low after gastric bypass, raising the possibilitythat this operation reduces weight in part by suppressing ghrelinproduction. These data suggest that ghrelin antagonists maysomeday be considered in the treatment of obesity.
Supported by a Burroughs Wellcome Fund Career Award (80-1519,to Dr. Cummings); by a grant (to Dr. Cummings) from the AndrewW. Mellon Foundation; by grants (RO1 DK55460 [to Dr. Weigle],K24 DK02860 [to Dr. Weigle], K23 DK02689 [to Dr. Purnell], GeneralClinical Research Center grant MO1RR00037, and Diabetes EndocrineResearch Center grant P3ODK17047) from the National Institutesof Health; and by the Medical Research Service of the Departmentof Veterans Affairs.
We are indebted to Holly Callahan, Colleen Matthys, Pamela Yang,and Holly Edelbrock for their outstanding work with subjectsin the General Clinical Research Center; to Dr. George Merriamfor his important contribution to this research; and to Dr.Michael Schwartz for his insightful review of the manuscript.
Source Information
From the Departments of Medicine (D.E.C., D.S.W., R.S.F., P.A.B., M.K.M.) and Surgery (E.P.D.), University of Washington; the Veterans Affairs Puget Sound Health Care System (D.E.C., R.S.F., M.K.M.); the Harborview Medical Center (D.S.W., P.A.B.); and University Hospital (E.P.D.) — all in Seattle; and the Department of Medicine, Oregon Health and Science University, Portland (J.Q.P.).
Address reprint requests to Dr. Cummings at the Veterans Affairs Puget Sound Health Care System, Seattle Div., 1660 S. Columbian Way, S-111-Endo, Seattle, WA 98108, or at davidec{at}u.washington.edu.
References
Taubes G. As obesity rates rise, experts struggle to explain why. Science 1998;280:1367-1368. [Free Full Text]
Kopelman PG. Obesity as a medical problem. Nature 2000;404:635-643. [Medline]
Lew EA. Mortality and weight: insured lives and the American Cancer Society Studies. Ann Intern Med 1985;103:1024-1029. [Medline]
Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995;332:621-628. [Erratum, N Engl J Med 1995;333:399.] [Free Full Text]
Schwartz MW, Woods SC, Porte D Jr, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature 2000;404:661-671. [Medline]
Bray GA, Tartaglia LA. Medicinal strategies in the treatment of obesity. Nature 2000;404:672-677. [Medline]
Safer DJ. Diet, behavior modification, and exercise: a review of obesity treatments from a long-term perspective. South Med J 1991;84:1470-1474. [Web of Science][Medline]
Wadden TA, Sternberg JA, Letizia KA, Stunkard AJ, Foster GD. Treatment of obesity by very low calorie diet, behavior therapy, and their combination: a five-year perspective. Int J Obes 1989;13:Suppl 2:39-46.
Sjostrom L, Rissanen A, Andersen T, et al. Randomized placebo-controlled trial of orlistat for weight loss and prevention of weight regain in obese patients. Lancet 1998;352:167-172. [CrossRef][Web of Science][Medline]
Bray GA, Blackburn GL, Ferguson JM, et al. Sibutramine produces dose-related weight loss. Obes Res 1999;7:189-198. [Web of Science][Medline]
Mun EC, Blackburn GL, Matthews JB. Current status of medical and surgical therapy for obesity. Gastroenterology 2001;120:669-681. [CrossRef][Web of Science][Medline]
Hell E, Miller KA, Moorehead MK, Norman S. Evaluation of health status and quality of life after bariatric surgery: comparison of standard Roux-en-Y gastric bypass, vertical banded gastroplasty and laparoscopic adjustable silicone gastric banding. Obes Surg 2000;10:214-219. [CrossRef][Web of Science][Medline]
Trostler N, Mann A, Zilberbush N, Avinoach E, Charuzi I. Weight loss and food intake 18 months following vertical banded gastroplasty or gastric bypass for severe obesity. Obes Surg 1995;5:39-51. [CrossRef][Web of Science][Medline]
Kellum JM, Kuemmerle JF, O'Dorisio TM, et al. Gastrointestinal hormone responses to meals before and after gastric bypass and vertical banded gastroplasty. Ann Surg 1990;211:763-771. [Web of Science][Medline]
Pappas TN. Physiological satiety implications of gastrointestinal antiobesity surgery. Am J Clin Nutr 1992;55:Suppl:571S-572S. [Free Full Text]
Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 1999;402:656-660. [CrossRef][Medline]
Date Y, Kojima M, Hosoda H, et al. Ghrelin, a novel growth hormone-releasing acylated peptide, is synthesized in a distinct endocrine cell type in the gastrointestinal tracts of rats and humans. Endocrinology 2000;141:4255-4261. [Free Full Text]
Tschop M, Smiley DL, Heiman ML. Ghrelin induces adiposity in rodents. Nature 2000;407:908-913. [CrossRef][Medline]
Nakazato M, Murakami N, Date Y, et al. A role for ghrelin in the central regulation of feeding. Nature 2001;409:194-198. [CrossRef][Medline]
Wren AM, Small CJ, Ward HL, et al. The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion. Endocrinology 2000;141:4325-4328. [Free Full Text]
Asakawa A, Inui A, Kaga T, et al. Ghrelin is an appetite-stimulatory signal from stomach with structural resemblance to motilin. Gastroenterology 2001;120:337-345. [CrossRef][Web of Science][Medline]
Wren AM, Small CJ, Abbott CR, et al. Ghrelin causes hyperphagia and obesity in rats. Diabetes 2001;50:2540-2547. [Free Full Text]
Wren AM, Seal LJ, Cohen MA, et al. Ghrelin enhances appetite and increases food intake in humans. J Clin Endocrinol Metab 2001;86:5992-5992. [Free Full Text]
Cummings DE, Purnell JQ, Frayo RS, Schmidova K, Wisse BE, Weigle DS. A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes 2001;50:1714-1719. [Free Full Text]
Bergman RN, Ider YZ, Bowden CR, Cobelli C. Quantitative estimation of insulin sensitivity. Am J Physiol 1979;236:E667-E677. [Free Full Text]
Goldman RF, Buskirk EK. A method for underwater weighing and determination of body density. In: Brozek J, Henschel A, eds. Techniques for measuring body composition. Washington, D.C.: National Academy of Sciences, 1961:78-9.
Shuman WP, Morris LL, Leonetti DL, et al. Abnormal body fat distribution detected by computed tomography in diabetic men. Invest Radiol 1986;21:483-487. [Web of Science][Medline]
Goldrick RB. Morphological changes in the adipocyte during fat deposition and mobilization. Am J Physiol 1967;212:777-782.
Morgan CR, Lazarow A. Immunoassay of insulin: two antibody system: plasma insulin levels of normal, subdiabetic and diabetic rats. Diabetes 1963;12:115-126. [Web of Science]
Tschop M, Weyer C, Tataranni PA, Devanarayan V, Ravussin E, Heiman ML. Circulating ghrelin levels are decreased in human obesity. Diabetes 2001;50:707-709. [Free Full Text]
Halmi KA, Mason E, Falk JR, Stunkard A. Appetitive behavior after gastric bypass for obesity. Int J Obes 1981;5:457-464. [Web of Science][Medline]
Rand CS, Macgregor AM, Hankins GC. Eating behavior after gastric bypass surgery for obesity. South Med J 1987;80:961-964. [CrossRef][Web of Science][Medline]
Hafner RJ, Watts JM, Rogers J. Quality of life after gastric bypass for morbid obesity. Int J Obes 1991;15:555-560. [Web of Science][Medline]
Kenler HA, Brolin RE, Cody RP. Changes in eating behavior after horizontal gastroplasty and Roux-en-Y gastric bypass. Am J Clin Nutr 1990;52:87-92. [Free Full Text]
Näslund I. Gastric bypass versus gastroplasty: a prospective study of differences in two surgical procedures for morbid obesity. Acta Chir Scand Suppl 1987;536:44-49.
Howard L, Malone M, Michalek A, Carter J, Alger S, Van Woert J. Gastric bypass and vertical banded gastroplasty -- a prospective randomized comparison and 5-year follow-up. Obes Surg 1995;5:55-60. [CrossRef][Web of Science][Medline]
Pories WJ, Flickinger EG, Meelheim D, Van Rij AM, Thomas FT. The effectiveness of gastric bypass over gastric partition in morbid obesity: consequence of distal gastric and duodenal exclusion. Ann Surg 1982;196:389-399. [Web of Science][Medline]
Sugerman HJ, Starkey J, Birkenhauer R. A randomized prospective trial of gastric bypass versus vertical banded gastroplasty for morbid obesity and their effects on sweets versus non-sweets eaters. Ann Surg 1987;205:613-624. [Web of Science][Medline]
Lissner L, Lindroos AK, Sjostrom L. Swedish obese subjects (SOS): an obesity intervention study with a nutritional perspective. Eur J Clin Nutr 1998;52:316-322. [Medline]
Belchetz PE, Plant TM, Nakai Y, Keogh EJ, Knobil E. Hypophysial responses to continuous and intermittent delivery of hypothalamic gonadotropin-releasing hormone. Science 1978;202:631-633. [Free Full Text]
Rittmaster RS, Loriaux DL, Merriam GR. Effect of continuous somatostatin and growth hormone-releasing hormone (GHRH) infusions on the subsequent growth hormone (GH) response to GHRH: evidence for somatotroph desensitization independent of GH pool depletion. Neuroendocrinology 1987;45:118-122. [Web of Science][Medline]
Weight Loss and Plasma Ghrelin Levels
Rubino F., Gagner M., Camilleri M., Cremonini F., Geliebter A., Cummings D. E., Purnell J. Q., Weigle D. S.
Extract |
Full Text |
PDF
N Engl J Med 2002;
347:1379-1381, Oct 24, 2002.
Correspondence
This article has been cited by other articles:
Van Vugt, D. A.
(2009). Brain imaging studies of appetite in the context of obesity and the menstrual cycle. Hum Reprod Update
0: dmp051v1-dmp051
[Abstract][Full Text]
Lomenick, J. P., Melguizo, M. S., Mitchell, S. L., Summar, M. L., Anderson, J. W.
(2009). Effects of Meals High in Carbohydrate, Protein, and Fat on Ghrelin and Peptide YY Secretion in Prepubertal Children. J. Clin. Endocrinol. Metab.
94: 4463-4471
[Abstract][Full Text]
Stearns, A. T., Balakrishnan, A., Tavakkolizadeh, A.
(2009). Impact of Roux-en-Y gastric bypass surgery on rat intestinal glucose transport. Am. J. Physiol. Gastrointest. Liver Physiol.
297: G950-G957
[Abstract][Full Text]
Zheng, H., Shin, A. C., Lenard, N. R., Townsend, R. L., Patterson, L. M., Sigalet, D. L., Berthoud, H.-R.
(2009). Meal patterns, satiety, and food choice in a rat model of Roux-en-Y gastric bypass surgery. Am. J. Physiol. Regul. Integr. Comp. Physiol.
297: R1273-R1282
[Abstract][Full Text]
Taddei, S., Virdis, A.
(2009). Exogenous Ghrelin on Nitric Oxide-Endothelin 1 Imbalance in Metabolic Syndrome: Can We Kill 2 Birds With 1 Stone?. Hypertension
54: 960-961
[Full Text]
Kandil, M. E., Elwan, A., Hussein, Y., Kandeel, W., Rasheed, M.
(2009). Ghrelin Levels in Children with Congenital Heart Disease. J Trop Pediatr
55: 307-312
[Abstract][Full Text]
St-Pierre, D. H, Rabasa-Lhoret, R., Lavoie, M.-E., Karelis, A. D, Strychar, I., Doucet, E., Coderre, L.
(2009). Fiber intake predicts ghrelin levels in overweight and obese postmenopausal women. Eur J Endocrinol
161: 65-72
[Abstract][Full Text]
Beck, B, Richy, S
(2009). Dietary modulation of ghrelin and leptin and gorging behavior after weight loss in the obese Zucker rat. J Endocrinol
202: 29-34
[Abstract][Full Text]
Schultes, B., Ernst, B., Schmid, F., Thurnheer, M.
(2009). Distal gastric bypass surgery for the treatment of hypothalamic obesity after childhood craniopharyngioma. Eur J Endocrinol
161: 201-206
[Abstract][Full Text]
Yang, N., Liu, X., Ding, E. L., Xu, M., Wu, S., Liu, L., Sun, X., Hu, F. B.
(2009). Impaired Ghrelin Response after High-Fat Meals Is Associated with Decreased Satiety in Obese and Lean Chinese Young Adults. J. Nutr.
139: 1286-1291
[Abstract][Full Text]
Thaler, J. P., Cummings, D. E.
(2009). Hormonal and Metabolic Mechanisms of Diabetes Remission after Gastrointestinal Surgery. Endocrinology
150: 2518-2525
[Abstract][Full Text]
Tham, E., Liu, J., Innis, S., Thompson, D., Gaylinn, B. D., Bogarin, R., Haim, A., Thorner, M. O., Chanoine, J.-P.
(2009). Acylated ghrelin concentrations are markedly decreased during pregnancy in mothers with and without gestational diabetes: relationship with cholinesterase. Am. J. Physiol. Endocrinol. Metab.
296: E1093-E1100
[Abstract][Full Text]
Lu, S.-C., Xu, J., Chinookoswong, N., Liu, S., Steavenson, S., Gegg, C., Brankow, D., Lindberg, R., Veniant, M., Gu, W.
(2009). An Acyl-Ghrelin-Specific Neutralizing Antibody Inhibits the Acute Ghrelin-Mediated Orexigenic Effects in Mice. Mol. Pharmacol.
75: 901-907
[Abstract][Full Text]
Vetter, M. L., Cardillo, S., Rickels, M. R., Iqbal, N.
(2009). Narrative Review: Effect of Bariatric Surgery on Type 2 Diabetes Mellitus. ANN INTERN MED
150: 94-103
[Abstract][Full Text]
Bray, G. A, Flatt, J.-P., Volaufova, J., DeLany, J. P, Champagne, C. M
(2008). Corrective responses in human food intake identified from an analysis of 7-d food-intake records. Am. J. Clin. Nutr.
88: 1504-1510
[Abstract][Full Text]
Melanson, K. J, Angelopoulos, T. J, Nguyen, V., Zukley, L., Lowndes, J., Rippe, J. M
(2008). High-fructose corn syrup, energy intake, and appetite regulation. Am. J. Clin. Nutr.
88: 1738S-1744S
[Abstract][Full Text]
Mayorov, A. V., Amara, N., Chang, J. Y., Moss, J. A., Hixon, M. S., Ruiz, D. I., Meijler, M. M., Zorrilla, E. P., Janda, K. D.
(2008). Catalytic antibody degradation of ghrelin increases whole-body metabolic rate and reduces refeeding in fasting mice. Proc. Natl. Acad. Sci. USA
105: 17487-17492
[Abstract][Full Text]
Arepally, A., Barnett, B. P., Patel, T. T., Howland, V., Boston, R. C., Kraitchman, D. L., Malayeri, A. A.
(2008). Catheter-directed Gastric Artery Chemical Embolization Suppresses Systemic Ghrelin Levels in Porcine Model. Radiology
249: 127-133
[Abstract][Full Text]
Geliebter, A., Ochner, C. N., Aviram-Friedman, R.
(2008). Appetite-Related Gut Peptides in Obesity and Binge Eating Disorder. AMERICAN JOURNAL OF LIFESTYLE MEDICINE
2: 305-314
[Abstract]
Mark, A. L.
(2008). Dietary Therapy for Obesity: An Emperor With No Clothes. Hypertension
51: 1426-1434
[Full Text]
Chearskul, S., Delbridge, E., Shulkes, A., Proietto, J., Kriketos, A.
(2008). Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations. Am. J. Clin. Nutr.
87: 1238-1246
[Abstract][Full Text]
Vincent, R P, le Roux, C W
(2008). The satiety hormone peptide YY as a regulator of appetite. J. Clin. Pathol.
61: 548-552
[Abstract][Full Text]
Vergnano, A. M., Ferrini, F., Salio, C., Lossi, L., Baratta, M., Merighi, A.
(2008). The Gastrointestinal Hormone Ghrelin Modulates Inhibitory Neurotransmission in Deep Laminae of Mouse Spinal Cord Dorsal Horn. Endocrinology
149: 2306-2312
[Abstract][Full Text]
Mager, U., Kolehmainen, M., de Mello, V. D F, Schwab, U., Laaksonen, D. E, Rauramaa, R., Gylling, H., Atalay, M., Pulkkinen, L., Uusitupa, M.
(2008). Expression of ghrelin gene in peripheral blood mononuclear cells and plasma ghrelin concentrations in patients with metabolic syndrome.. Eur J Endocrinol
158: 499-510
[Abstract][Full Text]
Bloom, S. R., Kuhajda, F. P., Laher, I., Pi-Sunyer, X., Ronnett, G. V., Tan, T. M.M., Weigle, D. S.
(2008). The Obesity Epidemic: Pharmacological Challenges. Mol. Interv.
8: 82-98
[Abstract][Full Text]
Frecka, J. M., Mattes, R. D.
(2008). Possible entrainment of ghrelin to habitual meal patterns in humans. Am. J. Physiol. Gastrointest. Liver Physiol.
294: G699-G707
[Abstract][Full Text]
Schwartz, A. R., Patil, S. P., Laffan, A. M., Polotsky, V., Schneider, H., Smith, P. L.
(2008). Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches. Proc Am Thorac Soc
5: 185-192
[Abstract][Full Text]
Bult, M. J F, van Dalen, T., Muller, A. F
(2008). Surgical treatment of obesity. Eur J Endocrinol
158: 135-145
[Abstract][Full Text]
Sun, Y., Butte, N. F., Garcia, J. M., Smith, R. G.
(2008). Characterization of Adult Ghrelin and Ghrelin Receptor Knockout Mice under Positive and Negative Energy Balance. Endocrinology
149: 843-850
[Abstract][Full Text]
Cummings, D. E., Flum, D. R.
(2008). Gastrointestinal Surgery as a Treatment for Diabetes. JAMA
299: 341-343
[Full Text]
Taub, L.-F. M., Redeker, N. S.
(2008). Sleep Disorders, Glucose Regulation, and Type 2 Diabetes. Biol Res Nurs
9: 231-243
[Abstract]
O'Neil, C. E., Nicklas, T. A.
(2007). State of the Art Reviews: Relationship Between Diet/ Physical Activity and Health. AMERICAN JOURNAL OF LIFESTYLE MEDICINE
1: 457-481
[Abstract]
Barazzoni, R., Zanetti, M., Ferreira, C., Vinci, P., Pirulli, A., Mucci, M., Dore, F., Fonda, M., Ciocchi, B., Cattin, L., Guarnieri, G.
(2007). Relationships between Desacylated and Acylated Ghrelin and Insulin Sensitivity in the Metabolic Syndrome. J. Clin. Endocrinol. Metab.
92: 3935-3940
[Abstract][Full Text]
Vicennati, V., Genghini, S., De Iasio, R., Pasqui, F., Pagotto, U., Pasquali, R.
(2007). Circulating obestatin levels and the ghrelin/obestatin ratio in obese women. Eur J Endocrinol
157: 295-301
[Abstract][Full Text]
Kasa-Vubu, J. Z., Rosenthal, A., Murdock, E. G., Welch, K. B.
(2007). Impact of Fatness, Fitness, and Ethnicity on the Relationship of Nocturnal Ghrelin to 24-Hour Luteinizing Hormone Concentrations in Adolescent Girls. J. Clin. Endocrinol. Metab.
92: 3246-3252
[Abstract][Full Text]
Seoane, L. M., Al-Massadi, O., Caminos, J. E., Tovar, S. A., Dieguez, C., Casanueva, F. F.
(2007). Sensory Stimuli Directly Acting at the Central Nervous System Regulate Gastric Ghrelin Secretion. An ex Vivo Organ Culture Study. Endocrinology
148: 3998-4006
[Abstract][Full Text]
Hayes, M. R., Miller, C. K., Ulbrecht, J. S., Mauger, J. L., Parker-Klees, L., Gutschall, M. D., Mitchell, D. C., Smiciklas-Wright, H., Covasa, M.
(2007). A Carbohydrate-Restricted Diet Alters Gut Peptides and Adiposity Signals in Men and Women with Metabolic Syndrome. J. Nutr.
137: 1944-1950
[Abstract][Full Text]
Ma, J.-N., Schiffer, H. H., Knapp, A. E., Wang, J., Wong, K. K., Currier, E. A., Owens, M., Nash, N. R., Gardell, L. R., Brann, M. R., Olsson, R., Burstein, E. S.
(2007). Identification of the Atypical L-Type Ca2+ Channel Blocker Diltiazem and Its Metabolites As Ghrelin Receptor Agonists. Mol. Pharmacol.
72: 380-386
[Abstract][Full Text]
Bloomgarden, Z. T.
(2007). Gut Hormones, Obesity, Polycystic Ovarian Syndrome, Malignancy, and Lipodystrophy Syndromes. Diabetes Care
30: 1934-1939
[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]
Arepally, A., Barnett, B. P., Montgomery, E., Patel, T. H.
(2007). Catheter-directed Gastric Artery Chemical Embolization for Modulation of Systemic Ghrelin Levels in a Porcine Model: Initial Experience. Radiology
244: 138-143
[Abstract][Full Text]
Broom, D. R., Stensel, D. J., Bishop, N. C., Burns, S. F., Miyashita, M.
(2007). Exercise-induced suppression of acylated ghrelin in humans. J. Appl. Physiol.
102: 2165-2171
[Abstract][Full Text]
DeBoer, M. D., Zhu, X. X., Levasseur, P., Meguid, M. M., Suzuki, S., Inui, A., Taylor, J. E., Halem, H. A., Dong, J. Z., Datta, R., Culler, M. D., Marks, D. L.
(2007). Ghrelin Treatment Causes Increased Food Intake and Retention of Lean Body Mass in a Rat Model of Cancer Cachexia. Endocrinology
148: 3004-3012
[Abstract][Full Text]
Piccoli, F., Degen, L., MacLean, C., Peter, S., Baselgia, L., Larsen, F., Beglinger, C., Drewe, J.
(2007). Pharmacokinetics and Pharmacodynamic Effects of an Oral Ghrelin Agonist in Healthy Subjects. J. Clin. Endocrinol. Metab.
92: 1814-1820
[Abstract][Full Text]
Guo, Z.-F., Zheng, X., Qin, Y.-W., Hu, J.-Q., Chen, S.-P., Zhang, Z.
(2007). Circulating Preprandial Ghrelin to Obestatin Ratio Is Increased in Human Obesity. J. Clin. Endocrinol. Metab.
92: 1875-1880
[Abstract][Full Text]
Page, A. J., Slattery, J. A., Milte, C., Laker, R., O'Donnell, T., Dorian, C., Brierley, S. M., Blackshaw, L. A.
(2007). Ghrelin selectively reduces mechanosensitivity of upper gastrointestinal vagal afferents. Am. J. Physiol. Gastrointest. Liver Physiol.
292: G1376-G1384
[Abstract][Full Text]
Baessler, A., Fischer, M., Mayer, B., Koehler, M., Wiedmann, S., Stark, K., Doering, A., Erdmann, J., Riegger, G., Schunkert, H., Kwitek, A. E., Hengstenberg, C.
(2007). Epistatic interaction between haplotypes of the ghrelin ligand and receptor genes influence susceptibility to myocardial infarction and coronary artery disease. Hum Mol Genet
16: 887-899
[Abstract][Full Text]
Germain, N., Galusca, B., Le Roux, C. W, Bossu, C., Ghatei, M. A, Lang, F., Bloom, S. R, Estour, B.
(2007). Constitutional thinness and lean anorexia nervosa display opposite concentrations of peptide YY, glucagon-like peptide 1, ghrelin, and leptin. Am. J. Clin. Nutr.
85: 967-971
[Abstract][Full Text]
Mottershead, M., Karteris, E., Barclay, J. Y, Suortamo, S., Newbold, M., Randeva, H., Nwokolo, C. U
(2007). Immunohistochemical and quantitative mRNA assessment of ghrelin expression in gastric and oesophageal adenocarcinoma. J. Clin. Pathol.
60: 405-409
[Abstract][Full Text]
Haider, D. G., Schindler, K., Prager, G., Bohdjalian, A., Luger, A., Wolzt, M., Ludvik, B.
(2007). Serum Retinol-Binding Protein 4 Is Reduced after Weight Loss in Morbidly Obese Subjects. J. Clin. Endocrinol. Metab.
92: 1168-1171
[Abstract][Full Text]
Sun, Y., Garcia, J. M., Smith, R. G.
(2007). Ghrelin and Growth Hormone Secretagogue Receptor Expression in Mice during Aging. Endocrinology
148: 1323-1329
[Abstract][Full Text]
Iantorno, M., Chen, H., Kim, J.-a, Tesauro, M., Lauro, D., Cardillo, C., Quon, M. J.
(2007). Ghrelin has novel vascular actions that mimic PI 3-kinase-dependent actions of insulin to stimulate production of NO from endothelial cells. Am. J. Physiol. Endocrinol. Metab.
292: E756-E764
[Abstract][Full Text]
Kraemer, R. R., Castracane, V. D.
(2007). Exercise and Humoral Mediators of Peripheral Energy Balance: Ghrelin and Adiponectin. Exp. Biol. Med.
232: 184-194
[Abstract][Full Text]
Mackelvie, K. J., Meneilly, G. S., Elahi, D., Wong, A. C. K., Barr, S. I., Chanoine, J.-P.
(2007). Regulation of Appetite in Lean and Obese Adolescents after Exercise: Role of Acylated and Desacyl Ghrelin. J. Clin. Endocrinol. Metab.
92: 648-654
[Abstract][Full Text]
Perez-Tilve, D., Gonzalez-Matias, L., Alvarez-Crespo, M., Leiras, R., Tovar, S., Dieguez, C., Mallo, F.
(2007). Exendin-4 Potently Decreases Ghrelin Levels in Fasting Rats. Diabetes
56: 143-151
[Abstract][Full Text]
Murphy, K. G., Dhillo, W. S., Bloom, S. R.
(2006). Gut Peptides in the Regulation of Food Intake and Energy Homeostasis. Endocr. Rev.
27: 719-727
[Abstract][Full Text]
Naslund, E., Kral, J. G.
(2006). Impact of Gastric Bypass Surgery on Gut Hormones and Glucose Homeostasis in Type 2 Diabetes. Diabetes
55: S92-S97
[Abstract][Full Text]
Shah, M., Simha, V., Garg, A.
(2006). Long-Term Impact of Bariatric Surgery on Body Weight, Comorbidities, and Nutritional Status. J. Clin. Endocrinol. Metab.
91: 4223-4231
[Abstract][Full Text]
Marzullo, P., Caumo, A., Savia, G., Verti, B., Walker, G. E., Maestrini, S., Tagliaferri, A., Di Blasio, A. M., Liuzzi, A.
(2006). Predictors of Postabsorptive Ghrelin Secretion after Intake of Different Macronutrients. J. Clin. Endocrinol. Metab.
91: 4124-4130
[Abstract][Full Text]
Arafat, A. M., Perschel, F. H., Otto, B., Weickert, M. O., Rochlitz, H., Schofl, C., Spranger, J., Mohlig, M., Pfeiffer, A. F. H.
(2006). Glucagon Suppression of Ghrelin Secretion Is Exerted at Hypothalamus-Pituitary Level. J. Clin. Endocrinol. Metab.
91: 3528-3533
[Abstract][Full Text]
Gosman, G. G., Katcher, H. I., Legro, R. S.
(2006). Obesity and the role of gut and adipose hormones in female reproduction. Hum Reprod Update
12: 585-601
[Abstract][Full Text]
Zigman, J. M., Elmquist, J. K.
(2006). In search of an effective obesity treatment: A shot in the dark or a shot in the arm?. Proc. Natl. Acad. Sci. USA
103: 12961-12962
[Full Text]
Chaudhri, O., Small, C., Bloom, S.
(2006). Gastrointestinal hormones regulating appetite. Phil Trans R Soc B
361: 1187-1209
[Abstract][Full Text]
Asarian, L., Geary, N.
(2006). Modulation of appetite by gonadal steroid hormones. Phil Trans R Soc B
361: 1251-1263
[Abstract][Full Text]
Xue, B., Kahn, B. B.
(2006). AMPK integrates nutrient and hormonal signals to regulate food intake and energy balance through effects in the hypothalamus and peripheral tissues. J. Physiol.
574: 73-83
[Abstract][Full Text]
Kobelt, P, Helmling, S, Stengel, A, Wlotzka, B, Andresen, V, Klapp, B F, Wiedenmann, B, Klussmann, S, Monnikes, H
(2006). Anti-ghrelin Spiegelmer NOX-B11 inhibits neurostimulatory and orexigenic effects of peripheral ghrelin in rats. Gut
55: 788-792
[Abstract][Full Text]
Gelfand, E. V., Cannon, C. P.
(2006). Rimonabant: A Cannabinoid Receptor Type 1 Blocker for Management of Multiple Cardiometabolic Risk Factors. J Am Coll Cardiol
47: 1919-1926
[Abstract][Full Text]
Day, C., Bailey, C. J
(2006). Review: Pharmacological approaches to reduce adiposity. British Journal of Diabetes & Vascular Disease
6: 121-125
[Abstract]
Mingrone, G., Granato, L., Valera-Mora, E., Iaconelli, A., Calvani, M. F, Bracaglia, R., Manco, M., Nanni, G., Castagneto, M.
(2006). Ultradian ghrelin pulsatility is disrupted in morbidly obese subjects after weight loss induced by malabsorptive bariatric surgery. Am. J. Clin. Nutr.
83: 1017-1024
[Abstract][Full Text]
Morinigo, R., Moize, V., Musri, M., Lacy, A. M., Navarro, S., Marin, J. L., Delgado, S., Casamitjana, R., Vidal, J.
(2006). Glucagon-Like Peptide-1, Peptide YY, Hunger, and Satiety after Gastric Bypass Surgery in Morbidly Obese Subjects. J. Clin. Endocrinol. Metab.
91: 1735-1740
[Abstract][Full Text]
Tritos, N. A., Kokkotou, E. G.
(2006). The Physiology and Potential Clinical Applications of Ghrelin, a Novel Peptide Hormone. Mayo Clin Proc.
81: 653-660
[Abstract][Full Text]
Veldhuis, J. D., Roemmich, J. N., Richmond, E. J., Bowers, C. Y.
(2006). Somatotropic and Gonadotropic Axes Linkages in Infancy, Childhood, and the Puberty-Adult Transition. Endocr. Rev.
27: 101-140
[Abstract][Full Text]
Bouros, D., Tzouvelekis, A., Anevlavis, S., Doris, M., Tryfon, S., Froudarakis, M., Zournatzi, V., Kukuvitis, A.
(2006). Smoking acutely increases plasma ghrelin concentrations.. Clin. Chem.
52: 777-778
[Full Text]
Haider, D. G., Schindler, K., Schaller, G., Prager, G., Wolzt, M., Ludvik, B.
(2006). Increased Plasma Visfatin Concentrations in Morbidly Obese Subjects Are Reduced after Gastric Banding. J. Clin. Endocrinol. Metab.
91: 1578-1581
[Abstract][Full Text]
Owusu-Asiedu, A., Patience, J. F., Laarveld, B., Van Kessel, A. G., Simmins, P. H., Zijlstra, R. T.
(2006). Effects of guar gum and cellulose on digesta passage rate, ileal microbial populations, energy and protein digestibility, and performance of grower pigs. J ANIM SCI
84: 843-852
[Abstract][Full Text]
Christ, E. R, Zehnder, M., Boesch, C., Trepp, R., Mullis, P. E, Diem, P., Decombaz, J.
(2006). The effect of increased lipid intake on hormonal responses during aerobic exercise in endurance-trained men.. Eur J Endocrinol
154: 397-403
[Abstract][Full Text]
Romon, M., Gomila, S., Hincker, P., Soudan, B., Dallongeville, J.
(2006). Influence of Weight Loss on Plasma Ghrelin Responses to High-Fat and High-Carbohydrate Test Meals in Obese Women. J. Clin. Endocrinol. Metab.
91: 1034-1041
[Abstract][Full Text]
Shearman, L. P., Wang, S.-P., Helmling, S., Stribling, D. S., Mazur, P., Ge, L., Wang, L., Klussmann, S., Macintyre, D. E., Howard, A. D., Strack, A. M.
(2006). Ghrelin Neutralization by a Ribonucleic Acid-SPM Ameliorates Obesity in Diet-Induced Obese Mice. Endocrinology
147: 1517-1526
[Abstract][Full Text]
Blom, W. A., Lluch, A., Stafleu, A., Vinoy, S., Holst, J. J, Schaafsma, G., Hendriks, H. F.
(2006). Effect of a high-protein breakfast on the postprandial ghrelin response. Am. J. Clin. Nutr.
83: 211-220
[Abstract][Full Text]
Druce, M, Bloom, S R
(2006). The regulation of appetite. Arch. Dis. Child.
91: 183-187
[Abstract][Full Text]
Drazen, D. L., Vahl, T. P., D'Alessio, D. A., Seeley, R. J., Woods, S. C.
(2006). Effects of a Fixed Meal Pattern on Ghrelin Secretion: Evidence for a Learned Response Independent of Nutrient Status. Endocrinology
147: 23-30
[Abstract][Full Text]
Langenberg, C., Bergstrom, J., Laughlin, G. A., Barrett-Connor, E.
(2005). Ghrelin and the Metabolic Syndrome in Older Adults. J. Clin. Endocrinol. Metab.
90: 6448-6453
[Abstract][Full Text]
Tesauro, M., Schinzari, F., Iantorno, M., Rizza, S., Melina, D., Lauro, D., Cardillo, C.
(2005). Ghrelin Improves Endothelial Function in Patients With Metabolic Syndrome. Circulation
112: 2986-2992
[Abstract][Full Text]
Peeters, T L
(2005). Ghrelin: a new player in the control of gastrointestinal functions. Gut
54: 1638-1649
[Full Text]
Allison, K. C., Ahima, R. S., O'Reardon, J. P., Dinges, D. F., Sharma, V., Cummings, D. E., Heo, M., Martino, N. S., Stunkard, A. J.
(2005). Neuroendocrine Profiles Associated with Energy Intake, Sleep, and Stress in the Night Eating Syndrome. J. Clin. Endocrinol. Metab.
90: 6214-6217
[Abstract][Full Text]
Koutkia, P., Schurgin, S., Berry, J., Breu, J., Lee, B. S. H., Klibanski, A., Grinspoon, S.
(2005). Reciprocal changes in endogenous ghrelin and growth hormone during fasting in healthy women. Am. J. Physiol. Endocrinol. Metab.
289: E814-E822
[Abstract][Full Text]
Vestergaard, E T, Hansen, T K, Nielsen, S, Moller, N, Christiansen, J S, Jorgensen, J O L
(2005). Effects of GH replacement therapy in adults on serum levels of leptin and ghrelin: the role of lipolysis. Eur J Endocrinol
153: 545-549
[Abstract][Full Text]
Stanley, S., Wynne, K., McGowan, B., Bloom, S.
(2005). Hormonal Regulation of Food Intake. Physiol. Rev.
85: 1131-1158
[Abstract][Full Text]
Chang, C.-C., Hung, C.-H., Yen, C.-S., Hwang, K.-L., Lin, C.-Y.
(2005). The relationship of plasma ghrelin level to energy regulation, feeding and left ventricular function in non-diabetic haemodialysis patients. Nephrol Dial Transplant
20: 2172-2177
[Abstract][Full Text]
Arafat, M A, Otto, B, Rochlitz, H, Tschop, M, Bahr, V, Mohlig, M, Diederich, S, Spranger, J, Pfeiffer, A F H
(2005). Glucagon inhibits ghrelin secretion in humans. Eur J Endocrinol
153: 397-402
[Abstract][Full Text]
Suematsu, M., Katsuki, A., Sumida, Y., Gabazza, E. C, Murashima, S., Matsumoto, K., Kitagawa, N., Akatsuka, H., Hori, Y., Nakatani, K., Togashi, K., Yano, Y., Adachi, Y.
(2005). Decreased circulating levels of active ghrelin are associated with increased oxidative stress in obese subjects. Eur J Endocrinol
153: 403-407
[Abstract][Full Text]
Choe, Y. H., Song, S. Y., Paik, K.-H., Oh, Y. J., Chu, S.-H., Yeo, S. H., Kwon, E. K., Kim, E. M., Rha, M. Y., Jin, D.-K.
(2005). Increased Density of Ghrelin-Expressing Cells in the Gastric Fundus and Body in Prader-Willi Syndrome. J. Clin. Endocrinol. Metab.
90: 5441-5445
[Abstract][Full Text]
Daousi, C., MacFarlane, I. A., English, P. J., Wilding, J. P. H., Patterson, M., Dovey, T. M., Halford, J. C. G., Ghatei, M. A., Pinkney, J. H.
(2005). Is There a Role for Ghrelin and Peptide-YY in the Pathogenesis of Obesity in Adults with Acquired Structural Hypothalamic Damage?. J. Clin. Endocrinol. Metab.
90: 5025-5030
[Abstract][Full Text]
Moran, L. J., Luscombe-Marsh, N. D., Noakes, M., Wittert, G. A., Keogh, J. B., Clifton, P. M.
(2005). The Satiating Effect of Dietary Protein Is Unrelated to Postprandial Ghrelin Secretion. J. Clin. Endocrinol. Metab.
90: 5205-5211
[Abstract][Full Text]
Layman, D. K., Evans, E., Baum, J. I., Seyler, J., Erickson, D. J., Boileau, R. A.
(2005). Dietary Protein and Exercise Have Additive Effects on Body Composition during Weight Loss in Adult Women. J. Nutr.
135: 1903-1910
[Abstract][Full Text]
Cummings, D. E.
(2005). Gastric Bypass and Nesidioblastosis -- Too Much of a Good Thing for Islets?. NEJM
353: 300-302
[Full Text]
Wu, M.-S., Lee, W.-J., Wang, H.-H., Huang, S.-P., Lin, J.-T.
(2005). A Case-Control Study of Association of Helicobacter pylori Infection With Morbid Obesity in Taiwan. Arch Intern Med
165: 1552-1555
[Abstract][Full Text]
Gimenez-Palop, O., Gimenez-Perez, G., Mauricio, D., Berlanga, E., Potau, N., Vilardell, C., Arroyo, J., Gonzalez-Clemente, J.-M., Caixas, A.
(2005). Circulating ghrelin in thyroid dysfunction is related to insulin resistance and not to hunger, food intake or anthropometric changes. Eur J Endocrinol
153: 73-79
[Abstract][Full Text]
Previous
