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Endocrinology and Diabetes Unit (S.S., A.C.K.W., J.-P.C.) and Eating Disorders Program (P.L.), British Columbia’s Children’s Hospital, University of British Columbia, Vancouver V6H 3V4, Canada; Departments of Physiology and Surgery (T.J.K.), University of British Columbia, Vancouver V6T 1Z3, Canada; and Department of Metabolic Medicine (M.A.G., S.R.B.), Imperial College Faculty of Medicine, Hammersmith Campus, London W12 ONN, United Kingdom
Address all correspondence to: Jean-Pierre Chanoine, M.D., Ph.D., Endocrinology and Diabetes Unit, Room K4-212, British Columbia’s Children’s Hospital, 4480 Oak Street, Vancouver, British Columbia V6H 3V4, Canada. E-mail: jchanoine{at}cw.bc.ca.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Batterham et al. (2) recently demonstrated that plasma PYY concentrations are decreased in obese (OB) subjects, compared with lean adult subjects, and that a continuous infusion of PYY in OB adults for 90 min causes a lasting decrease in food intake. These data raised the possibility that decreased PYY concentrations may play a role in the etiology of obesity and that PYY analogs could potentially be useful in the treatment of obesity. Similarly, plasma ghrelin concentrations are decreased in both OB children (19) and adults (20) and increase with weight loss (12, 19). These lower ghrelin concentrations observed in OB subjects have been interpreted as an adaptive response to obesity. Baseline GIP concentrations and the GIP response to a glucose load during hyperglycemic clamping were found to be normal in a group of OB adolescents (21), a finding similar to what was reported in adults after a mixed meal (22).
Anorexia nervosa is more common in girls than boys and has its onset in adolescence or early adulthood (23). PYY concentrations have been measured in the cerebrospinal fluid of adult women who have recovered from anorexia nervosa and were found to be normal (24). Although a decrease in plasma PYY concentrations could conceptually suggest a role for this peptide in the etiology of anorexia nervosa, peripheral PYY metabolism has not been investigated in anorexic (AN) subjects thus far. Fasting ghrelin concentrations are elevated in AN adults (3, 25, 26, 27) and adolescents (19, 28) and decrease after weight gain (19, 29), suggesting that ghrelin is unlikely to play a role in the pathophysiology of anorexia nervosa. Postprandial GIP concentrations have been reported to be normal (30) or decreased (31) in adult AN patients but have not, to our knowledge, been measured in the pediatric age group.
We hypothesized that plasma PYY concentrations would be higher in AN adolescent subjects, suggesting that it could play a role in the etiology of this disorder, and that the response of PYY, ghrelin, GIP, and satiety to a mixed meal may be impaired in AN and OB adolescents, compared with controls. To this end, we compared plasma PYY, ghrelin, GIP, and satiety measures before and after a liquid mixed meal in AN, OB, and normal-weight control (C) female adolescents.
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Subjects and Methods |
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We prospectively investigated 30 AN, OB, and C female adolescents (n = 10/group) aged 12–18 yr. The reason for limiting the study to girls was the rarity of anorexia nervosa in boys. The study protocol was approved by the Ethics Committee of the University of British Columbia, and written informed consent was received from all subjects and parents, as appropriate.
Anorexia nervosa subjects were recruited from the Eating Disorder Program at British Columbia’s Children’s Hospital. All AN subjects met Diagnostic and Statistical Manual of Mental Disorders IV criteria for AN, restrictive subtype, and had a weight less than 85% of ideal body weight. All AN subjects were within 7 d to 3 months of diagnosis and their mean (SE) weight at the time of testing was 1.1 (0.3) kg or 2.5% (0.3) higher than at the time of diagnosis. Medications used by this group included antidepressants [moclobemide (n = 1), trazodone (n = 3), paroxetine (n = 2), fluoxetine (n = 1), and sertraline (n = 1)]; domperidone (n = 4, held on day of testing because it could affect gastric emptying); cyproterone acetate (n = 1); ferrous sulfate (n = 1); and chloral hydrate (n = 1). Psychotropic drugs were not discontinued because no randomized trial has so far shown that drugs known to affect energy balance could affect weight gain in AN subjects (32). Obese subjects were recruited from the Endocrinology Clinic at British Columbia’s Children’s Hospital. All OB subjects had a body mass index (BMI) greater the 85th centile for chronological age, were not attempting to lose weight, and had no identified endocrine cause for their obesity. One OB subject was taking paroxetine and methylphenidate. Normal-weight C adolescents had a BMI between the 25th and 75th centile for chronological age and were recruited by posted advertisement at local secondary schools. All AN, OB, and C subjects were postmenarchal and nonpregnant. No subjects in the OB and C groups had evidence of an overt eating disorder on screening with the Eating Attitudes Test-26 inventory (33).
Study design
Subjects were admitted to the endocrine testing unit after fasting from 2000 h the previous night. Height and weight were recorded. The subjects were asked to consume 7 cc/kg body weight (maximum 360 cc) of a liquid mixed meal (Boost High Protein; Mead Johnson Nutritionals, Ottawa, Ontario, Canada) over 10 min. The meal contained 55% of carbohydrates (corresponding to 0.96 g/kg body weight of carbohydrates, maximum 49.5 g), 25% of protein, and 20% of fat, a composition similar to the published standard for mixed-meal tolerance testing (34). Blood samples were drawn at baseline (mentioned as time 0 in the figures) between 0800 and 0900 h (35) and 15, 60, 90, 120, 180, and 240 min after the end of the meal. At the time of each blood sampling, subjects also completed a questionnaire evaluating their satiety. They were asked the following questions: how hungry are you; how full are you; how much can you eat; and what is your desire to eat? Their perception was rated from 0 (lowest) to 10 (highest) on a 100-mm visual analog scale (36).
PYY, ghrelin, GIP, insulin, and glucose determinations
Glucose determination was performed immediately after each blood sample using the glucose meter Lifescan Surestep Flex (LifeScan Canada, Burnaby, British Columbia, Canada). For hormonal determinations, blood samples were collected in EDTA tubes and kept on ice until centrifugation at 4 C. Aprotinin (Trasylol, 10,000 KI/ml, 50 µl/ml plasma; Bayer Inc., Toronto, Canada) was added to the plasma as described previously (37), and the samples were stored at –80 C until assays were performed.
PYY-like immunoreactivity was determined using a specific and sensitive RIA as previously described (38). The assay recognizes two biologically active forms of PYY (PYY3–36 and PYY1–36). There was no cross-reactivity with pancreatic polypeptide, neuropeptide Y, or other known gastrointestinal hormones. Plasma total (acylated or active and deacylated) ghrelin immunoreactivity was determined in duplicate by RIA (RK-031-30; Phoenix Pharmaceuticals, Belmont, CA). Intraassay and interassay coefficients of variation were less than 5.3% and less than 13%, respectively. Plasma insulin was determined in singlicate by ultrasensitive chemiluminescent immunoassay (Beckman Coulter, Fullerton, CA). According to the manufacturer, combined intraassay and interassay coefficient of variation was less than 5.6%. GIP was measured using a RIA as described by Kuzio et al. (39) and modified by Morgan et al. (40). Human GIP (46-1-60) was obtained from the American Peptide Co. (Sunnyvale, CA) for tracer and standards. Rabbit anti-GIP was generously supplied by Dr. L. M. Morgan (University of Surrey, Surrey, UK). Inter- and intraassay variations for GIP were 10 and 5%, respectively.
Statistical analysis
Data are presented as mean (SE). Insulin concentrations were log transformed. Comparison of baseline concentrations and the magnitude of the changes between baseline and peak or nadir were performed using ANOVA followed by post hoc analysis using Bonferroni. Area under the curve (AUC) was calculated using the trapezoidal method. To account for the subject-to-subject heterogeneity and within-subject correlation of repeated measurements, semiparametric mixed-effects model analysis (S-Plus 2000 Professional Release 3; MathSoft Inc., Seattle, WA) was used to compare responses in each group over time (41). Final models were subjected to, and passed, standard diagnostic tests to confirm that the cluster errors derived from the model used to generate the spline curves were normally distributed with zero mean and nonhomogenous variance. The significance of the differences between two individual groups was assessed using the Wald test. The relationship between the variables under study was assessed using the Pearson’s coefficient of correlation r after controlling for clinically relevant variables as appropriate. P < 0.05 was considered significant.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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. One AN subject had an episode of asymptomatic hypoglycemia [glucose 32 mg/dl (1.8 mmol/liter)] 75 min after the meal. She was treated with juice and allowed to finish the test. Her results were included in the statistical analysis. All subjects consumed the meal within 10 min and none complained of nausea.
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Fasting glucose and insulin concentrations are shown in Table 1
. Figure 1 shows the changes in plasma glucose (Fig. 1A) and insulin (Fig. 1B) concentrations after consumption of the mixed meal. Overall, semiparametric mixed model analyses comparing glucose responses in each group over time showed that there was a significant difference among the three groups (P < 0.002) and that this difference was not affected by time of sampling. Blood glucose concentrations were significantly lower in AN compared with OB and C subjects at all time points (P 
0.003). There was also a significant difference in insulin response among the three groups over time (P < 0.0001). Group-by-group analysis showed that each group was significantly different from the other (P 0.0002). Taken together, these data showed that AN subjects had low glucose and insulin concentrations and that OB subjects presented with hyperinsulinemia but normal glucose tolerance, compared with C subjects.
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Baseline PYY, ghrelin, and GIP concentrations and baseline ratings of satiety are shown in Table 1.
Baseline PYY concentrations were similar in all three groups (P = 0.8). Semiparametric mixed-model analyses comparing PYY responses in each group over time showed no effect of group but suggested that a group by time interaction was present (P = 0.06) (Fig. 2A). This means that, averaged over all time points, there was no difference among the three groups but that the changes in these groups over time tended to be different. In fact, PYY concentrations increased significantly 15 min after the mixed meal in the C group [+ 41 (6)%, P < 0.05] but not in AN [+ 20 (6)%] or OB [+ 5 (5)%] adolescents. PYY levels then plateaued until 150–180 min in all groups.
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). Ghrelin concentrations fell significantly in all three groups after the meal, reaching a nadir after 60–90 min, followed by a subsequent rise back to baseline, or higher by the end of the study period. The maximal percent drop in ghrelin [25 (2)%, P < 0.01, compared with baseline] was not affected by grouping. In contrast, the maximal absolute decrease in ghrelin was smaller in the obese group [138 (16) pg/ml], compared with the AN [238 (28) pg/ml] or C subjects [236 (76) pg/ml] (P = 0.007). Visual analysis of the figure showed a clear ordering of the three groups, with ghrelin concentrations highest in AN and lowest in OB subjects, compared with C subjects. Ghrelin nadir came earlier in OB subjects.
Baseline GIP concentrations were significantly different among the three groups (P < 0.01), with concentrations in the AN group being lower than concentrations in C groups. Semiparametric mixed-model analyses comparing GIP responses in each group over time showed a significant difference among the three groups (P = 0.05) (Fig. 2C). Visual analysis of the figure suggests that this difference reflects lower GIP concentrations in AN subjects, compared with OB and C subjects, throughout the test meal. Overall, the mixed meal caused a significant two to three times increase in GIP concentrations, from 191 (19) to 496 (44) pg/ml (P < 0.001), that was independent from grouping.
At baseline, AN subjects reported being significantly less hungry, being able to eat less, and having less desire to eat, compared with control subjects (P < 0.025 by ANOVA). After caloric intake, subjective rating increased (how full are you?) or decreased (how hungry are you; how much can you eat; and what is your desire to eat?) significantly within 15 min (P < 0.0001) in a similar way in all three groups. Semiparametric mixed-model analyses comparing markers of satiety showed a significant difference in hunger (Fig. 3A, P < 0.02), the desire to eat (Fig. 3B, P < 0.0002), and the quantity the subjects felt they could eat (Fig. 3C, P < 0.0005) but not in fullness (data not shown) among the three groups. Visual analysis of the figure suggests that these differences are due to AN adolescents reporting greater satiety.
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There was a highly significant correlation between fasting ghrelin and ghrelin nadir (adjusted r2 = 0.85) and AUC (adjusted r2 = 0.89) after consumption of the test meal (P < 0.0001). The significance of this relationship was not affected by grouping. These relationships were much stronger than for PYY [correlation between fasting PYY and PYY at 15 min (adjusted r2 = 0.37) or PYY AUC (adjusted r2 = 0.56) (P < 0.001)] or GIP [correlation between fasting GIP and GIP AUC (adjusted r2 = 0.29) (P = 0.004)].
There was a negative correlation between fasting ghrelin and insulin (r2 = 0.33) (Fig. 4A) and between fasting ghrelin and BMI (r2 = 0.33) (Fig. 4B) (P = 0.001). There was no significant relationship between PYY (or changes in PYY) concentrations and insulin (Fig. 4C), BMI (Fig. 4D), or glucose (data not shown). In keeping with its insulinotropic action, there was a significant correlation between GIP and glucose (r2 = 0.28) and insulin (r2 = 0.27) (P 0.004) 15 min after the test meal. There was no significant correlation between GIP and BMI.
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). Thus, the greater plasma PYY concentrations 15 min after the end of the mixed meal, the greater the decrease in hunger. No other clinically relevant correlations were found among ghrelin, PYY, or GIP data and markers of satiety.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Anorexia nervosa (restrictive type) is characterized by drastically reduced food intake that leads to pathological weight loss and significant morbidity. It typically affects adolescent girls (23, 42). The underlying mechanisms leading to the voluntary caloric restriction include a complex interplay of individual and family psychological factors and broader social cultural influences. We hypothesized that excessive PYY concentrations may play a role in the pathophysiology of anorexia nervosa by sending an inappropriately strong signal of food intake inhibition to the hypothalamus. In contrast to our hypothesis, we found normal baseline PYY concentrations among AN subjects. In addition, PYY response to the test meal was lower than, or similar to, the PYY response observed in controls. Elevated fasting ghrelin concentrations have been consistently reported in AN compared with normal-weight subjects; however, reports of ghrelin response to caloric intake have been more variable. Several authors did not observe significant changes in total ghrelin concentration after a test meal (25) or an oral glucose load (26) in AN adults. In contrast, Nakai et al. (27) reported a significant decrease in active ghrelin during an oral glucose tolerance test. Consistent with our results, Misra et al. (28) recently reported a similar ghrelin decrease in AN and C adolescent girls. However, in contrast to our study, their group of AN patients had significant BMI overlap with C subjects. The reason for the discrepancies in ghrelin responses among these studies is unclear, but differences in sample collection (43) or the assays [different standards (44), recognition of different ghrelin fragments (45) by different antibodies] are potential explanations. Taken together, our data do not support a role for ghrelin or PYY in the pathophysiology of anorexia nervosa. We observed a 29% decrease in the AUC for GIP over the 4 h of the test in anorexia nervosa, compared with C subjects, together with a 47% decrease in AUC for insulin. The volume of the mixed meal was only slightly (9%) lower in anorexia nervosa, compared with C subjects, and this was associated with a modest 15% decrease in the AUC for glucose. Such a lower insulin response has been reported (46) and suggests greater insulin sensitivity in AN patients, although this hypothesis has not been consistently confirmed (47). Our results suggest that the lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients.
In adult OB subjects, Batterham et al. (2) recently reported lower baseline and postmeal PYY concentrations, compared with controls, raising the possibility that decreased PYY concentrations could play a role in the etiology of obesity. Using the same assay, we found similar baseline PYY concentrations in our young OB and C subjects. Although there seems to be a trend toward even higher baseline PYY concentrations in OB subjects, the SD is large and this assumption is not supported by the statistical analysis (P = 0.8). In contrast, whereas the increase in PYY after the meal is highly significant in C subjects, it is completely blunted in OB subjects. Fasting plasma ghrelin concentrations have been consistently found to be lower in adult (20, 48) and adolescent (19) OB subjects. In contrast, both normal (12, 48) and blunted (49) ghrelin responses to caloric intake have been reported in obese adults. To our knowledge, the ghrelin response to food intake in young OB subjects has not been assessed. Similar to what has been reported in adults, we observed lower baseline ghrelin concentrations in OB adolescents, compared with C subjects. Ghrelin concentrations decreased after the test meal, but, whereas the percent maximum decrease in ghrelin was similar to controls, the absolute decrease in ghrelin was smaller. Interestingly, ghrelin nadir came earlier in OB adolescents, compared with lean controls. The reason for this difference is unclear, but we speculate that it may be due to the faster gastrointestinal transit reported in this condition (50). Taken together, these data suggest that OB adolescents have lower ghrelin concentrations, which may reflect an adaptive response to obesity, as is hypothesized in adults. In contrast, the blunted PYY response to a test meal may favor greater food intake in OB subjects and play a role in the etiology of obesity. As reported previously with the administration of glucose only (21), GIP concentrations were similar in OB and C subjects. A potential explanation for this observation is that both baseline and postmeal concentrations of glucose, a major stimulus of GIP secretion, were similar in OB and C adolescents. Nevertheless, our data do not suggest a causal role for GIP in the development of obesity or the hyperinsulinemia observed in OB subjects.
Our results also provide new insight into the understanding of satiety in AN and OB subjects. The concepts of perceived hunger, desire to eat, and how much can I eat were consistently lower in the AN group than OB and C subjects over time. These results are in agreement with previous studies showing suppressed hunger in this condition, compared with normal-weight controls (51, 52, 53, 54, 55). Baseline hunger in OB was similar to controls, again consistent with previous data (56). Interestingly, higher postprandial PYY concentrations (but not absolute or relative ghrelin or GIP concentrations) were associated with less hunger. This significant but modest temporal relationship (r2 = 0.20) is consistent with but does not prove the concept that PYY is involved in the physiology of appetite (2).
To test PYY, ghrelin, and GIP responses to caloric intake, we chose a mixed meal containing 55% carbohydrates, 25% protein, and 20% fat. The volume of the mixed meal was based on the subject’s body weight, with a maximum of 360 ml, a quantity reached by most of the adolescents. As a consequence, the energy consumed by the OB subjects was only 14 and 3% greater than the energy consumed by AN and C subjects (Table 1). In addition, the source of carbohydrates in the liquid mixed meal (corn syrup and sucrose) was partially fructose. Although the presence of fructose is likely to have decreased the magnitude of glucose, insulin, and ghrelin responses to the meal, compared with a glucose-rich meal (57), we feel that the composition of our mixed meal better reflects a real-life situation. Because the composition of the meal was the same in all three groups, the conclusions of our study are unlikely to be affected by the composition of the meal.
We measured total ghrelin concentrations but not the active form of ghrelin. This raises the possibility that changes in total ghrelin concentrations may not reflect changes in active ghrelin concentrations. However, recent studies (27, 58) report similar changes in total and active ghrelin concentrations in control and AN adults, suggesting that total ghrelin is a good marker for active ghrelin. We also observed an excellent correlation between fasting total ghrelin concentrations and the ghrelin nadir or integrated concentrations of circulating ghrelin over the duration of the study. This suggests that, at least in AN, OB, and C subjects, fasting ghrelin concentrations are a reliable marker of ghrelin changes during the 4–5 h after a mixed meal and that serial determinations of ghrelin may not be systematically needed in studies looking at the effect of caloric intake on circulating ghrelin. This association was much less significant for PYY.
In summary, we have shown that PYY does not increase after a meal in OB adolescents, suggesting that it may contribute to increasing the caloric intake in these subjects. Similar to adults, ghrelin concentrations are increased in AN and decreased in OB subjects as early as in adolescence. Although this may represent an adaptive response to these underlying conditions, we would like to speculate that ghrelin levels in AN and OB subjects reflect a set point that is specific to the individual and is present early in life. Longitudinal studies investigating whether these changes preexist the development of AN and OB will help further address this question. Finally, we observed a marked decrease in GIP response to a meal in AN subjects despite a similar caloric intake that may appropriately prevent an excessive insulin response in these patients.
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Acknowledgments |
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Footnotes |
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Abbreviations: AN, Anorexic; AUC, area under the curve; BMI, body mass index; C, normal-weight control subjects; GIP, glucose-dependent insulinotropic polypeptide; OB, obese; PYY, peptide YY.
Received August 17, 2004.
Accepted January 10, 2005.
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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M. Misra, K. K. Miller, P. Tsai, K. Gallagher, A. Lin, N. Lee, D. B. Herzog, and A. Klibanski Elevated Peptide YY Levels in Adolescent Girls with Anorexia Nervosa J. Clin. Endocrinol. Metab., March 1, 2006; 91(3): 1027 - 1033. [Abstract] [Full Text] [PDF]
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C. Maffeis, R. C Bonadonna, A. Consolaro, R. Vettor, C. Banzato, D. Silvagni, G. Bogoni, M. Pellegrino, and L. Tato Ghrelin, insulin sensitivity and postprandial glucose disposal in overweight and obese children Eur. J. Endocrinol., January 1, 2006; 154(1): 61 - 68. [Abstract] [Full Text] [PDF]
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C. W. le Roux, R. L. Batterham, S. J. B. Aylwin, M. Patterson, C. M. Borg, K. J. Wynne, A. Kent, R. P. Vincent, J. Gardiner, M. A. Ghatei, et al. Attenuated Peptide YY Release in Obese Subjects Is Associated with Reduced Satiety Endocrinology, January 1, 2006; 147(1): 3 - 8. [Abstract] [Full Text] [PDF]
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C. L. Roth, P. J. Enriori, K. Harz, J. Woelfle, M. A. Cowley, and T. Reinehr Peptide YY Is a Regulator of Energy Homeostasis in Obese Children before and after Weight Loss J. Clin. Endocrinol. Metab., December 1, 2005; 90(12): 6386 - 6391. [Abstract] [Full Text] [PDF]
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 T. Siahanidou, H. Mandyla, M. Vounatsou, D. Anagnostakis, I. Papassotiriou, and G. P. Chrousos Circulating Peptide YY Concentrations Are Higher in Preterm than Full-Term Infants and Correlate Negatively with Body Weight and Positively with Serum Ghrelin Concentrations Clin. Chem., November 1, 2005; 51(11): 2131 - 2137. [Abstract] [Full Text] [PDF]
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