Inhibition of Food Intake in Obese Subjects by Peptide YY3–36
Rachel L. Batterham, M.B., B.S., Mark A. Cohen, M.B., Ch.B., Sandra M. Ellis, B.Sc., Carel W. Le Roux, M.B., Ch.B., Dominic J. Withers, M.B., B.S., Ph.D., Gary S. Frost, Ph.D., Mohammad A. Ghatei, Ph.D., and Stephen R. Bloom, M.D., D.Sc.
Background The gut hormone fragment peptide YY3–36 (PYY)reduces appetite and food intake when infused into subjectsof normal weight. In common with the adipocyte hormone leptin,PYY reduces food intake by modulating appetite circuits in thehypothalamus. However, in obesity there is a marked resistanceto the action of leptin, which greatly limits its therapeuticeffectiveness. We investigated whether obese subjects were alsoresistant to the anorectic effects of PYY.
Methods We compared the effects of PYY infusion on appetiteand food intake in 12 obese and 12 lean subjects in a double-blind,placebo-controlled, crossover study. The plasma levels of PYY,ghrelin, leptin, and insulin were also determined.
Results Caloric intake during a buffet lunch offered two hoursafter the infusion of PYY was decreased by 30 percent in theobese subjects (P<0.001) and 31 percent in the lean subjects(P<0.001). PYY infusion also caused a significant decreasein the cumulative 24-hour caloric intake in both obese and leansubjects. PYY infusion reduced plasma levels of the appetite-stimulatoryhormone ghrelin. Endogenous fasting and postprandial levelsof PYY were significantly lower in obese subjects (the mean[±SE] fasting PYY levels were 10.2±0.7 pmol perliter in the obese group and 16.9±0.8 pmol per literin the lean group, P<0.001). Furthermore, the fasting PYYlevels correlated negatively with the body-mass index (r = –0.84,P<0.001).
Conclusions We found that obese subjects were not resistantto the anorectic effects of PYY. Endogenous PYY levels werelow in the obese subjects, suggesting that PYY deficiency maycontribute to the pathogenesis of obesity.
Obesity and its associated pathologic features are major causesof illness and death worldwide. In the United States, obesityaccounts for 280,000 deaths annually, and at current rates ofincrease it will supplant smoking as the primary cause of preventabledeath.1 However, despite the recognition that even moderateweight loss confers significant health benefits,2 to date therehave been few effective treatments for obesity, although surgeryhas been shown to be of use in selected patients.3
We recently showed that infusions of the gut hormone fragmentpeptide YY3–36(PYY) that produced typical naturally occurringpostprandial levels reduced 24-hour food intake in human subjectsof normal weight.4 Furthermore, long-term administration ofPYY to rodents decreased weight gain. These observations suggestthat PYY may be a treatment for obesity. Given, however, thatthe majority of obese subjects are resistant to the effectsof the adipocyte hormone leptin, limiting its effectivenessas an antiobesity treatment,5,6 we undertook to compare theeffects of PYY infusion on appetite and food intake in obeseand lean subjects.
Methods
Study Subjects
Healthy obese and lean subjects were recruited by advertisingin local newspapers and on the Hammersmith Hospital campus inLondon. The mean (±SE) body-mass index (the weight inkilograms divided by the square of the height in meters) was33.0±0.9 in the obese group and 20.5±0.1 in thelean group. The inclusion criteria were a body-mass index of27 to 40 for the obese group and 17 to 23 for the lean group.All subjects were between the ages of 18 and 50 years (mean,29.0±2.4 for the obese group and 27.3±0.4 forthe lean group) and had had a stable body weight for at leastthree months. The criteria for exclusion were smoking, substanceabuse, pregnancy, use of medications (except for oral contraceptives),medical or psychiatric illness, and any abnormalities detectedon physical examination, electrocardiography, or screening bloodtests (measurement of complete blood count, electrolytes, fastingglucose, and liver function).
Twelve subjects (six men and six women) were recruited for eachgroup. The subjects gave written informed consent for the study,and approval was obtained from the Hammersmith Hospital researchethics committee. The study was carried out in accordance withthe principles of the Declaration of Helsinki. The subjectswere screened by a dietitian who assessed their eating behaviorwith the Dutch Eating Behavior Questionnaire7 and the EatingAttitudes Test questionnaire.8 They also completed a three-daydiet diary to permit us to assess their usual eating habitsbefore acceptance into the study. Food preferences were assessedat screening with a nine-point hedonic scale to ensure thatthe food offered at the buffet lunch was acceptable.
Study Protocol
The study was performed in a randomized, double-blind, placebo-controlled,crossover manner, with each subject studied on two occasionsone week apart. The subjects' food intake for the 48 hours beforeeach study day was standardized, and during this period theycompleted food diaries to confirm compliance. In addition, theyconsumed an identical meal between 7 p.m. and 8 p.m. on thenight before each study. The subjects refrained from alcoholand strenuous exercise for the 24 hours before and after eachstudy day. They fasted and drank only water from 8 p.m. thenight before the study. They arrived at 8:30 a.m. on each studyday. Cannulas were inserted into veins in both forearms, onefor the collection of blood and the other for the infusion ofPYY or saline. After venous cannulation, the subjects relaxedfor 30 minutes before the start of the study protocol. All timecues were removed from the study room, so that the subjectswere unaware of the time. Throughout the study, the subjectswere encouraged to relax by reading or watching videos.
Blood was collected every 30 minutes throughout the study intoheparin-coated tubes (LIP) containing 5000 kallikrein inhibitorunits (0.2 ml) of aprotonin (Bayer). Plasma was separated immediatelyby centrifugation at 4°C and then stored at –70°Cuntil it was analyzed. Basal samples were taken 30 minutes beforeand at the beginning of the infusion. The subjects receiveda 90-minute infusion of either saline or PYY (total dose, 2nmol per square meter of body-surface area). Two hours afterthe termination of the infusion, the subjects were offered abuffet lunch with food in such excess that all appetites couldbe satisfied. The amounts of food and water were quantifiedpreprandially and postprandially, and the caloric intake wascalculated. Appetite ratings were made on 100-mm visual-analoguescales (higher values indicate greater appetite), with the textexpressing the most positive and the most negative ratings anchoredat each end.9 Visual-analogue scores were used to assess hunger,nausea, and meal palatability. The subjects remained in thestudy room for six hours after the beginning of the infusion.They completed a food diary until 1 p.m. the following day toallow continued assessment of food intake. The food diarieswere analyzed by a dietitian who was unaware of study assignments,and energy intake was calculated with the aid of Dietplan (ForestfieldSoftware).
PYY
PYY was obtained from Bachem. The limulus amoebocyte lysateassay test for pyrogen was negative, and the peptide was sterileon culture. PYY was dissolved in 0.9 percent saline (Bayer)containing Haemaccel (Beacon) (5 percent by volume) to reduceadsorption to the syringe and tubing.
Hormone Assays
All samples were assayed in duplicate and in one assay to eliminatethe effects of interassay variation. PYY-like immunoreactivitywas measured with a specific and sensitive radioimmunoassay,as previously described.10,11,12 The assay measured both thehormone fragment (peptide hormone YY3–36) and the full-lengthhormone (peptide hormone YY1–36); both are biologicallyactive. The antiserum (Y21) was produced in a rabbit againstsynthetic porcine PYY (Bachem) coupled to bovine serum albuminby glutaraldehyde and used at a final dilution of 1:50,000.This antibody cross-reacts fully with the biologically activecirculating forms of human PYY, but not with pancreatic polypeptide,neuropeptide Y, or other known gastrointestinal hormones.
Iodine-125–labeled PYY was prepared by the iodogen methodand purified by high-pressure liquid chromatography. The specificactivity of the iodine-125–labeled PYY was 54 Bq per femtomole.The assay was performed in a total volume of 700 µl of0.06 M phosphate buffer, pH 7.3, containing 0.3 percent bovineserum albumin. The sample was incubated for three days at 4°Cbefore the separation of free and antibody-bound label by sheepantirabbit antibody. Two hundred microliters of unextractedplasma was assayed. Two hundred microliters of PYY-free, charcoal-strippedplasma was added to standards and other reference tubes to negateany effects of nonspecific assay interference. The assay detectedchanges of 2 pmol per liter, with an intraassay coefficientof variation of 5.8 percent.
Plasma pancreatic polypeptide, insulin, and glucagon-like peptide1 (GLP-1) were measured in duplicate by established in-houseradioimmunoassays. The pancreatic polypeptide assay detectedchanges of 3 pmol per liter, with an intraassay coefficientof variation of 5.4 percent.13 The GLP-1 assay detected changesof 7.5 pmol per liter, with an intraassay coefficient of variationof 6.1 percent.14 The insulin assay detected changes of 6.2pmol per liter, with an intraassay coefficient of variationof 5.4 percent. Plasma ghrelin was measured in duplicate witha Phoenix Pharmaceutical assay kit, and plasma leptin was measuredin duplicate with a commercially available assay (Linco Research).
Statistical Analysis
Caloric intake and plasma hormone levels are expressed as means±SE. The integrated area under the curve was calculatedwith use of the trapezoid rule. Caloric intake and visual-analoguescores within groups were compared by the Wilcoxon signed-rank,matched-pairs test. Areas under the curve and plasma hormonelevels in the lean and obese groups were compared by Wilcoxonrank-sum analysis.
Results
Effect of Infusion of PYY on Appetite and Food Intake
PYY infusion reduced the caloric intake of all subjects at thebuffet lunch, as compared with their intake after the infusionof saline (Figure 1A and Figure 1B). In the obese subjects,PYY caused a 29.9±4.4 percent reduction (P<0.001)(Figure 1C), and a similar decrease of 31.1±4.5 percentwas observed in the lean subjects (P<0.001) (Figure 1D).There was no change in the proportion of calories obtained fromcarbohydrate, protein, or fat. Furthermore, analysis of thefood diaries showed a significant inhibition of food intakein the 12-hour postinfusion period in both the obese and thelean subjects. In the obese group, on the day when the salineinfusion was given, subjects consumed 2456.0±256.1 kcal,and on the day when the PYY infusion was given, they consumed1810.3±142.6 kcal — a reduction of 26.3±6.8percent. In the lean group, on the day when the saline infusionwas given, subjects consumed 2312.2±167.7 kcal, and onthe day when the PYY infusion was given, they consumed 1533.0±140.0kcal — a reduction of 33.7±5.6 percent.
Figure 1. Caloric Intake by Obese and Lean Subjects after Infusion of Peptide YY3–36 (PYY) or Saline.
Panel A shows the caloric intake by individual obese subjects, and Panel B shows the intake by individual lean subjects, during a buffet lunch two hours after the infusion of PYY or saline. Panel C shows the mean (±SE) caloric intake by obese subjects, and Panel D shows the intake by lean subjects, during a buffet lunch two hours after infusion of saline or PYY. Panel E shows the mean (±SE) cumulative 24-hour caloric intake by obese subjects, and Panel F shows the intake by lean subjects, after infusion of saline or PYY. In all panels, the lean and obese groups each consisted of 12 subjects: 6 women and 6 men.
However, food intake during the period from 12 to 24 hours afterinfusion was unaffected by PYY in either group. In the obesegroup, on the day when they received saline, the subjects consumed884.9±170.4 kcal, and on the day when they received PYY,they consumed 723.7±118.6 kcal. In the lean group, onthe day when they received saline, the subjects consumed 706.5±84.9kcal, and on the day when they received PYY, they consumed 712.2±84.9kcal. Overall, PYY significantly reduced 24-hour caloric intake(Figure 1E and Figure 1F) in both the obese and the lean groups.The reduction was 16.5±6.6 percent in the obese group(P=0.02) and 23.5±5.8 percent in the lean group (P=0.001).PYY infusion reduced hunger, as assessed by visual-analoguescores (Figure 2), but there was no effect on the palatabilityof the meal or feelings of nausea (data not shown). The subjectsreported no other side effects during or after the PYY infusion.
Figure 2. Appetite Scores for the Lean Subjects (Panel A) and the Obese Subjects (Panel B).
The scores are based on visual-analogue scales for perceived hunger during and after infusions, with negative values indicating less appetite. Scores were estimated every 30 minutes. The results are presented as the mean (±SE) change from base-line scores for all 12 subjects.
Plasma Levels of PYY
PYY infusion produced similar plasma PYY profiles in the obeseand lean groups. The peak PYY level was 57.1±3.8 pmolper liter in the obese group and 53.7±3.5 pmol per literin the lean group.
Plasma PYY levels were measured in subjects receiving salineto make possible the assessment of fasting and postprandiallevels (Figure 3). The fasting PYY levels were significantlylower in obese than in lean subjects. The base-line PYY levelsat the beginning of the infusion were 10.2±0.7 pmol perliter in the obese group and 16.9±0.8 pmol per literin the lean group (P<0.001). Furthermore, the area underthe curve for PYY during the fasting period (from the beginningof the infusion until 210 minutes later) was significantly lowerin the obese group than in the lean group: 558.6±43.0vs. 929.8±47.6 pmol per hour per liter (P<0.001).The fasting PYY levels were negatively correlated with body-massindex (r = –0.84, P<0.001) (Figure 4).
Figure 4. Correlation between Fasting Plasma Peptide YY (PYY) Levels Measured at Base Line and Body-Mass Index.
The postprandial PYY levels increased in both lean and obesesubjects. However, even though they consumed more calories atthe buffet lunch, the obese subjects showed a diminished postprandialPYY response as compared with that in the lean subjects. Thepeak PYY value was 14.4±1.2 pmol per liter in the obesegroup and 23.5±0.9 pmol per liter in the lean group.In addition, the postprandial area under the curve for PYY (from210 to 360 minutes after the beginning of the infusion) wassignificantly less in obese subjects than in lean subjects (562.0±44.6vs. 841.4±34.9 pmol per hour per liter, P<0.001).
Plasma Levels of Ghrelin
In the lean group, the levels of the appetite-stimulating hormoneghrelin increased throughout the fasting period on the day thesubjects received saline (from 207.7±12.6 pmol per literat the beginning of the infusion to 247.4±13.8 pmol perliter 210 minutes later) and then fell postprandially to 170.2±13.2pmol per liter 30 minutes after the meal began (Figure 5). PYYinfusion significantly decreased ghrelin levels during the fastingperiod and abolished the preprandial rise: the area under thecurve for ghrelin from the beginning of the infusion to 210minutes later was 13,510.6±813.5 pmol per hour per literon the day they received saline and 11,272.0±724.3 pmolper hour per liter on the day they received PYY (P=0.001).
Figure 5. Mean (±SE) Plasma Ghrelin Levels in 12 Obese and 12 Lean Subjects during and after Infusion of Saline or Peptide YY3–36 (PYY).
A buffet lunch was provided at the time indicated.
The ghrelin levels were markedly lower in obese subjects and,in contrast to the lean subjects, they had no significant preprandialrise in ghrelin levels during the infusion of saline: the ghrelinlevel was 87.7±14.1 pmol per liter at the beginning ofthe infusion and 108.4±18.7 pmol per liter 210 minuteslater. However, as in the lean subjects, the ghrelin levelsdecreased postprandially to 78.2±12.6 pmol per liter30 minutes after the start of the meal, and PYY infusion reducedthe fasting ghrelin levels. The area under the curve for ghrelinin the obese subjects from the beginning of the infusion to210 minutes later was 5973.2±1051.4 pmol per hour perliter on the day they received saline and 4418.5±743.0pmol per hour per liter on the day they received PYY (P=0.02).
Plasma Levels of Leptin, Insulin, Pancreatic Peptide, and GLP-1
The fasting plasma leptin levels were significantly higher inthe obese group (1.98±0.3 and 0.5±0.1 nmol perliter for obese and lean women, respectively; 0.71±0.2and 0.2±0.1 nmol per liter for obese and lean men, respectively)and were unaffected by PYY infusion. Likewise, the fasting insulinlevels were higher in obese subjects (61.3±8.5 pmol perliter in the obese group and 19.2±4.3 pmol per literin the lean group), and there was no effect of PYY infusion.The fasting plasma levels of GLP-1 were similar in obese andlean subjects (14.0±1.1 and 13.9±1.4 pmol perliter, respectively) and were not affected by PYY infusion.The fasting levels of pancreatic peptide were similar in obeseand lean subjects (14.4±1.4 and 15.6±1.8 pmolper liter, respectively) and were unaffected by PYY infusion.
Discussion
We have previously found that PYY is released from the gut inproportion to the calories ingested15 and signals food intaketo the appetite-regulating circuits of the brain.4 Furthermore,PYY infusion reduces food intake in subjects of normal weight,and repeated administration to rodents reduces weight gain.4These findings suggest that PYY may be a useful treatment forobesity. PYY acts on the same hypothalamic neural circuits asleptin to regulate food intake.16,17 However, obesity is associatedwith resistance to the action of leptin, which greatly limitsits therapeutic effectiveness in this condition.5,6 We thereforestudied whether obese subjects responded to the anorectic effectsof PYY.
Infusion of PYY caused an equivalent inhibition of appetiteand food intake in the obese and lean groups, resulting in reducedcumulative 24-hour food intake. These findings indicate thatobesity is not associated with substantial resistance to PYY.We found that fasting PYY levels were lower in the obese groupthan in the lean group and that there was a negative correlationbetween fasting PYY levels and body-mass index. Furthermore,postprandial PYY release was lower in obese than in lean subjects,despite the fact that the obese subjects consumed more caloriesat the buffet lunch. These findings are consistent with thehypothesis that a deficiency in circulating PYY may be involvedin the pathogenesis of obesity. It is unclear whether low PYYlevels initiate the development of obesity or whether PYY levelsare reduced as a result of obesity. PYY appears to be a majorfactor limiting appetite after meals.17,18 If obesity is thecause of low levels of circulating PYY, impaired postprandialsatiety signaling would result, leading to increased appetiteand food intake, which would act to perpetuate the condition.
PYY is synthesized and released from specialized endocrine cells(L cells) that are found primarily in the distal gastrointestinaltract. In response to the ingestion of nutrients, plasma PYYlevels increase within 15 minutes, peak at around 60 minutes,and remain elevated for up to 6 hours.15 The initial increaseoccurs before nutrients have reached the L cells, implicatinga neural or endocrine mechanism. The sustained release is thoughtto be due to the direct effects of the intraluminal gut contentson the L cells.19 The reduced PYY levels in obesity may resultfrom abnormalities in its synthesis, release, or clearance.Increased clearance is unlikely to have a major role, sinceafter exogenous administration the rate of elimination was similarin the lean and the obese groups. However, the precise factorscontrolling PYY synthesis and release and the effect of obesityon these remain to be determined.
Our current studies give further insights into the potentialmechanisms by which PYY inhibits food intake. Plasma levelsof the gut hormone ghrelin rise preprandially,20 and administrationof ghrelin increases food intake in rodents and humans.21,22,23These findings suggest that ghrelin has a role in the regulationof meal initiation.20 In our current study of both lean andobese subjects, PYY infusion significantly decreases plasmaghrelin levels. This suppression may add to the effects of PYYon appetite reduction.
Currently, surgery is the only effective treatment for morbidobesity (body-mass index, >40).3,24 Recently, gastric-bypasssurgery has been shown to be associated with low ghrelin levels,which may be responsible for the reduced appetite associatedwith this procedure.25 Interestingly, PYY levels have been shownto be elevated in patients after jejunoileal-bypass surgery,suggesting that increased PYY levels may also contribute tothe reduced appetite and food intake observed in these patients.26
In summary, we have demonstrated that PYY levels are low inobesity, suggesting that PYY may be involved in the pathogenesisof this condition. Furthermore, the administration of PYY reducesappetite and food intake in normal and obese subjects. Thus,the administration of exogenous PYY or stimulation of the releaseof endogenous PYY may be an attractive therapeutic option forobesity.
Supported in part by the Wellcome Trust and by a grant (G7811974)from the Medical Research Council.
We are indebted to the volunteers who participated in the study.
Source Information
From the Department of Metabolic Medicine, Imperial College Faculty of Medicine at Hammersmith Campus, Du Cane Rd., London W12 0NN, United Kingdom.
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Parkinson, J. R. C., Dhillo, W. S., Small, C. J., Chaudhri, O. B., Bewick, G. A., Pritchard, I., Moore, S., Ghatei, M. A., Bloom, S. R.
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Young, A. A.
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le Roux, C. W., Batterham, R. L., Aylwin, S. J. B., Patterson, M., Borg, C. M., Wynne, K. J., Kent, A., Vincent, R. P., Gardiner, J., Ghatei, M. A., Bloom, S. R.
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Sainsbury, A., Bergen, H. T., Boey, D., Bamming, D., Cooney, G. J., Lin, S., Couzens, M., Stroth, N., Lee, N. J., Lindner, D., Singewald, N., Karl, T., Duffy, L., Enriquez, R., Slack, K., Sperk, G., Herzog, H.
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Feinle-Bisset, C., Patterson, M., Ghatei, M. A., Bloom, S. R., Horowitz, M.
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Koegler, F. H., Enriori, P. J., Billes, S. K., Takahashi, D. L., Martin, M. S., Clark, R. L., Evans, A. E., Grove, K. L., Cameron, J. L., Cowley, M. A.
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Wynne, K., Park, A. J., Small, C. J., Patterson, M., Ellis, S. M., Murphy, K. G., Wren, A. M., Frost, G. S., Meeran, K., Ghatei, M. A., Bloom, S. R.
(2005). Subcutaneous Oxyntomodulin Reduces Body Weight in Overweight and Obese Subjects: A Double-Blind, Randomized, Controlled Trial. Diabetes
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Torekov, S. S., Larsen, L. H., Glumer, C., Borch-Johnsen, K., Jorgensen, T., Holst, J. J., Madsen, O. D., Hansen, T., Pedersen, O.
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Goldstone, A. P., Patterson, M., Kalingag, N., Ghatei, M. A., Brynes, A. E., Bloom, S. R., Grossman, A. B., Korbonits, M.
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(2005). Active Ghrelin Levels and Active to Total Ghrelin Ratio in Cancer-Induced Cachexia. J. Clin. Endocrinol. Metab.
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(2005). Variations in Peptide YY and Y2 Receptor Genes Are Associated With Severe Obesity in Pima Indian Men. Diabetes
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