Effects of Diet on Insulin and Gastric Inhibitory Polypeptide Levels in Obese Children

Abstract

SummaryTo improve understanding of the relationships between gastric inhibitory polypeptide (GIP) and insulin secretion and food intake in obesity, immunoreactive insulin and immunoreactive GIP were measured in 5 obese children during PO glucose tolerance test carried out before and after diet.Before diet, mean insulin levels were normal at fasting and rose after glucose ingestion. The mean fasting immunoreactive GIP level was very high (1235 * U)9 pg/ml) compared to that of 8 healthy adult controls (411 f 44 pg/ml) and remained at this level throughout the test. There was only a short postabsorptive rise to 1515 * 158 pg/ml at 30 min, which was not significantly different either from the patients' basal values or from the 30-min control values (1356 f 67 pg/ml).After dieting for 3 to 7 months, immunoreactive insulia r e sponses returned to normal ranges. Concomitantly, both basal and total GIP release diminished significantly (basal GIP, 343 f 92 pg/ml, area under the GIP curve, 3820 and 1694 pg/ml/hr before and after diet, respectively). The postabsorptive GIP increment, however, rose significantly from 180 pg/ml,hr, before diet, to 665 pg/ml/hr afterwards. These results might be compatible with the hypothesis that in obesity, hyperinsulinemia, and overactivity of the GIP cells are associated phenomena caused by overeating and reversed by r e duced food intake. However, several contradictory fmdinps remain unexplained. The d i~c r e~a n &~ between insignificant postabsorptive GIP increments and elevated insulin resmnses before diet casts doubts on the causal relationship betwee;] GIP and insulin secretion. The small GIP rise might be due to a limited secretory capacity of the GIP cells or to a diminished stimulatory capacity of glucose. The constantly high level of GIP might reflect chronic hypersecretion and/or some defect in basal regulation and feedback control of GIP release.The change caused by dietary measures in the GIP secretion pattern provides evidence that in obese children, basal GIP secretion is influenced by nutritional factors. SpeculationIn spite of the small number of observations, the present Andings illustrate the complexity of the mechanisms governing the regulation of gastric inhibitory polypeptide and insulin release in obesity. It seems likely that basal gastric inhibitory polypeptide secretion is influenced by food intake, but further studies will be necessary to confirm that gastric inhibitory polypeptide plays a causal role in the hyperinsulinemia of obesity in children.

Species‐specific action of (Pro3)GIP – a full agonist at human GIP receptors, but a partial agonist and competitive antagonist at rat and mouse GIP receptors

“…In humans, although less clear, there is likewise evidence for a role of GIP in fat metabolism with the demonstration of GIP receptor expression in adipose tissue (Ahlqvist et al ., ), an association between high body mass index and increased GIP levels (Ahlqvist et al ., ; Calanna et al ., ), and increased adipose tissue blood flow and triacylglycerol deposition following GIP administration in a state of high insulin and high glucose (Asmar et al ., ). Furthermore, obese children decrease their basal and postprandial GIP levels, when put on a low‐calorie diet (Deschamps et al ., ), and healthy young men increase their fasting GIP levels, when put on a high‐fat diet (Brøns et al ., ).…”

Fasting gut hormone levels change with modest weight loss in obese adolescents

“…Deschamps et al . reported a decrease in fasting GIP levels after a dietary intervention in five obese children. In contrast, Reinehr and colleagues have shown that PP levels increase with significant diet‐induced weight loss (BMI z ‐score decrease ≥0.5) but are unchanged in weight stable obese adolescents .…”

Obesity and Diabetes

“…A direct relationship between increased GIP and overeating was demonstrated long ago. Eating less for a few months can reduce both basal and postprandial levels of GIP (Deschamps et al 1980).…”

“…Indeed, in obese and diabetic patients present high GIP (Vilsboll et al 2003) (mainly a proximal gut product). If they loose weight on a diet, GIP falls (Deschamps et al 1980). GIP is obesogenic and insulinotropic (contributing to hyperinsulinemia) (Miyawaki et al 2002), and the therapeutic blockage of GIP has been shown to be beneficial in MS patients (Irwin and Flatt 2009;Montgomery et al 2010).…”