c-peptide and Anorexia-Nervosa

Anorexia nervosa (AN) is an eating disorder characterized by self-induced starvation due to fear of adiposity. Ghrelin, gastric peptide with potent orexigenic, adipogenic, GH-releasing and metabolic properties, is elevated in AN. We have previously shown that intervention with exogenous ghrelin is not effective in terms of inducing neuroendocrine and appetite responses in AN. In this arm of the same study protocol we investigated glucose metabolism responses to 5 h i.v. infusion of active ghrelin in a) 9 severely malnourished AN patients, b) 6 AN patients who partially recovered body weight (PRAN), c) 10 constitutionally thin female subjects with regular menstrual cycles. At baseline, no significant differences were observed in blood glucose, insulin, c-peptide, adiponectin, and homeostasis model assessment index values, between the studied groups. During ghrelin infusions, blood glucose levels significantly increased in all groups although significantly less in low-weight AN; insulin levels were not significantly affected, while c-peptide levels were significantly suppressed only in the constitutionally thin and PRAN subjects. In addition to our previous findings of impaired neuroendocrine and appetite responses in patients with AN, we conclude that metabolic responses to ghrelin are attenuated in these patients, which tend to recover with weight gain.

Topics: Adult; Anorexia Nervosa; Blood Glucose; Body Weight; C-Peptide; Eating; Female; Ghrelin; Humans; Infusions, Intravenous; Insulin; Thinness

Postprandial glucose is reduced in malnourished patients with anorexia nervosa (AN), but the mechanisms and duration for this remain unclear. We examined blood glucose, gastric emptying, and glucoregulatory hormone changes in malnourished patients with AN and during 2 wk of acute refeeding compared with healthy controls (HCs). Twenty-two female adolescents with AN and 17 age-matched female HCs were assessed after a 4-h fast. Patients were commenced on a refeeding protocol of 2,400 kcal/day. Gastric emptying (

Topics: 3-O-Methylglucose; Adolescent; Anorexia Nervosa; Blood Glucose; Breath Tests; C-Peptide; Caprylates; Carbon Isotopes; Case-Control Studies; Female; Gastric Emptying; Gastric Inhibitory Polypeptide; Glucagon; Glucagon-Like Peptide 1; Humans; Insulin; Postprandial Period; Starvation; Young Adult

Leptin, which was discovered only a decade ago, is a peptide that informs hypothalamic areas about the energy balance of the body. New research findings, has suggested a possible role of leptin in eating disorders as well. Few data are available about the relationship between leptin, insulin and glucose metabolism in the pathomechanism of eating disorders. The authors were searching for answers to these relationships in their investigations.. The study groups included 56 patients with eating disorders and 22 healthy subjects served as controls. The diagnosis was based on DSM-IV criteria. For measuring leptin, insulin and C-peptide serum concentrations a radioimmunoassay method was applied, and serum glucose concentrations were detected by spectrofluorimetry. Detailed statistical analysis of the results was carried out.. A correlation between BMI and serum leptin concentration could be proved only in anorectic patients. In contrast to former findings, there was no correlation between BMI and leptin concentration in the bulimia group, and the leptin concentrations were significantly higher in bulimic patients than in the control group. During the glucose tolerance test, leptin levels showed a significant decrease in the anorexia group.. The results raise the possibility of a direct effect of central regulatory mechanisms of food intake in the pathomechanism of anorexia nervosa.

Topics: Adult; Anorexia Nervosa; Blood Glucose; Body Mass Index; Bulimia Nervosa; C-Peptide; Case-Control Studies; Feeding and Eating Disorders; Female; Glucose Tolerance Test; Humans; Insulin; Leptin; Male; Middle Aged; Radioimmunoassay; Spectrometry, Fluorescence

The present study was conducted in order to analyze the relationship existing between leptin and insulin levels in massive weight loss and weight recovery. Thirteen patients with severe obesity, 14 patients with anorexia nervosa and 13 healthy control subjects were studied. The patients with severe obesity underwent a vertical banded gastroplasty followed by an 800 kcal/day diet for 12 weeks. They were evaluated prior to (body mass index [BMI] 51.2 +/- 8.8 Kg/m2) and after drastic weight loss (BMI 40.6 +/- 6.7 Kg/m2). Patients with anorexia nervosa were treated exclusively with nutritional therapy during 12 weeks, and they were evaluated at their lowest weight status (BMI 16.2 +/- 2.2 Kg/m2) and after weight recovery (BMI 17.9 +/- 2.3 Kg/m2). The BMI of the normal subjects was in the normal range of 20 to 27 Kg/m2 (average 22.8 +/- 2.6 Kg/m2). BMI, percentage of body fat, waist circumference, and serum levels of leptin, insulin, and C-peptide were determined in each patient and normal subject. In severely obese patients, serum leptin and insulin decreased significantly after drastic weight reduction (leptin: from 51.8 +/- 22.3 to 23.7 +/- 10.2 ng/ml; insulin: from 27.1 +/- 13.3 to 17.2 +/- 7.2 mU/ml). In patients with anorexia nervosa, the mean serum leptin levels were significantly higher after weight recovery (5.5 +/- 3.2 vs 7.6 +/- 6 ng/ml). Serum leptin in the severe obesity group correlated positively with BMI, percentage body fat and waist circumference before and after weight loss. In those patients suffering from anorexia nervosa, serum leptin correlated positively with the BMI, percentage of body fat, and waist circumference in the low weight state and after weight recovery. In addition, their serum insulin correlated with BMI and waist circumference after weight recovery. These data reveal that serum leptin concentration correlates significantly with the BMI and body fat content 1) in subjects with a range of weight and caloric intake, 2) in obese patients after drastic weight loss; 3) in anorexic patients after weight gain; and that hyper- or normoinsulinemia do not seem to have any influence on the leptin changes caused by weight loss or gain.

Topics: Adipose Tissue; Adolescent; Adult; Anorexia Nervosa; Anthropometry; Body Mass Index; C-Peptide; Combined Modality Therapy; Female; Gastroplasty; Humans; Hyperinsulinism; Insulin; Leptin; Male; Middle Aged; Obesity, Morbid; Postoperative Period; Weight Gain; Weight Loss

From a metabolic point of view, anorexia nervosa may be viewed as a mirror image of obesity. We compared insulin secretion, clearance and action on glucose metabolism during an intravenous glucose tolerance test in nine women with anorexia nervosa and in nine age-matched normal-weight controls. Insulin secretion (ISR) was derived by deconvolution of plasma C-peptide levels, insulin clearance (MCR(I)) was obtained by dividing the area under the curve (AUC(0-180 min)) of ISR by the corresponding AUC of plasma insulin levels, insulin sensitivity (S(I)) and glucose effectiveness index (S(G)) were calculated by Bergman's minimal model. The anorectic women had markedly lower BMI values (13.7+/-0.6 vs 23.2+/-0.8 kg/m2, p<0.0001) and serum basal leptin levels (2.8+/-0.6 vs 8.9+/-1.8 ng/mL, p=0.005) than control women. The anorectic women exhibited clear-cut lower fasting and post-glucose plasma insulin levels but similar corresponding plasma C-peptide concentrations when compared to controls. Consequently, ISR was similar in both groups while MCR(I) was significantly increased in anorexia nervosa (MCR(I): 3320+/-881 vs 822+/-79 mL x min(-1) x m(-2), p<0.02). The index S(I) tended to be higher in anorectic women than in normal-weight subjects, but without reaching the level of statistical significance because of a high between-subject variability (20.2+/-5.7 vs 12.5+/-2.2 10(-5) x min(-1)/pmol x L(-1), NS). The index S(G) was similar in both groups (0.022+/-0.004 vs 0.018+/-0.002 min(-1), NS). In conclusion, low plasma insulin levels observed in women with anorexia nervosa result from high MCR(I) rather than from depressed insulin secretion. Insulin sensitivity is not systematically increased and glucose effectiveness is unchanged in anorectic women when compared to normal-weight controls.

Topics: Adult; Anorexia Nervosa; Body Mass Index; C-Peptide; Female; Glucose; Glucose Tolerance Test; Humans; Insulin; Insulin Secretion; Leptin

To assess the total insulin secretion in children in different nutritional states we have analysed the 24 h urinary C-peptide excretion in 32 obese children (16 boys and 16 girls) 8-15 years of age as well as in 7 girls with anorexia nervosa 11-16 years of age. Obese children had a median urinary C-peptide excretion rate of 0.27 nmol/kg/24 h, which was not different from that of a group of normal-weight children. In the group of anorectic girls, on the other hand, the median value 0.47 nmol/kg/24 h was significantly (p less than 0.05) higher than for normal-weight girls of the same age (median = 0.26 nmol/kg/24 h). These results indicate that in obese children insulin secretion, measured as the 24 h urinary C-peptide excretion per kg body weight, is the same as in normal-weight children. Total insulin secretion is consequently increased. In anorexia nervosa, on the other hand, the higher C-peptide excretion per kg body weight compared with normal-weight children, indicates that insulin secretion is increased in relation to body weight.

Topics: Adolescent; Anorexia Nervosa; Body Weight; C-Peptide; Child; Circadian Rhythm; Female; Humans; Insulin; Insulin Secretion; Islets of Langerhans; Male; Obesity

Decreased food intake and weight loss are seen in eating and depressive disorders. No satisfactory pathophysiological mechanisms have been proposed to explain those findings. While it should be kept in mind that the etiology of those diseases is still unclear, it seems reasonable to propose that the maintenance of anorectic behavior in the eating disorders as well as the decreased food intake of major depression, leading to continued weight loss seen in both conditions, are either caused or mediated by insulin in levels which are elevated but insufficient to cause hypoglycemia. A brief review is made of the role of insulin in satiety and in the control of body weight, and of the newly available techniques to accurately quantify secretion, hepatic extraction, and post-hepatic delivery rates of insulin. Neural, metabolic, and endocrine stimuli affect insulin secretion. The hypothesis is therefore compatible with several etiologic factors leading to hyperinsulinemia in anorexia nervosa and major depression, and resulting in decreased food intake and weight loss.

Topics: Anorexia Nervosa; C-Peptide; Depressive Disorder; Eating; Humans; Hyperinsulinism; Insulin; Liver; Weight Loss