Abstract
The aim of the study was to assess the effect of dietary macronutrients on circulating glucagon and insulin levels in obese and normal-weight women. Potentially, the impaired release of glucagon may proceed abnormal glucose metabolism in obese patients ahead of overt diabetes. In 20 insulin-sensitive women (11 obese and 9 normal-weight), plasma concentrations of insulin and glucagon levels were assessed before and after 3 different macronutrient test meals. AUCtotal insulin in the obese group was increased after protein and carbohydrates compared to fatty test meal consumption (3981 ± 2171 and 4869 ± 2784 vs. 2349 ± 1004 μIU∗h/m, p < 0.05, respectively), but without a difference between protein and carbohydrates ingestion. However, in the normal-weight group, AUCtotal insulin was increased after carbohydrates compared to fatty test meal ingestion (3929 ± 1719 vs. 2231 ± 509 μIU∗h/ml, p < 0.05) and similar after carbohydrate and protein as well as after fatty and protein test meals (3929 ± 1719 vs. 2231 ± 509 vs. 3046 ± 1406 μIU∗h/ml, respectively). However, AUCtotal insulin was significantly increased in obese compared to normal-weight women only after carbohydrate test meal ingestion (4869 ± 2784 vs. 3929 ± 1719 μIU∗h/ml, p < 0.05). AUCtotal glucagon was similar after carbohydrate, protein, and fatty test meals ingestion in obese and normal-weight women (921 ± 356 vs. 957 ± 368 vs. 926 ± 262 ng∗h/ml and 1196 ± 14 vs. 1360 ± 662 vs. 1792 ± 1176 ng∗h/ml, respectively). AUCtotal glucagon was significantly lower in obese than normal-weight women after a fatty meal (926 ± 262 vs. 1792 ± 1176 ng∗h/ml, p < 0.01). Postprandial glucagon secretion is not related to the macronutrient composition of the meal in normal-weight women since postprandial glucagon concentrations were stable and did not change after carbohydrate, protein, and fatty test meals. Lower glucagon secretion was observed in obese subjects after fatty meal consumption when compared to normal-weight subjects. Postprandial insulin profile was significantly higher after carbohydrate than fatty test meal intake in the obese group and did not differ between obese and normal-weight groups after carbohydrate, protein, and fatty test meals consumption. Impaired glucagon secretion after fatty meat suggests early pancreatic alpha-cell dysfunction, after a carbohydrate meal is a compensatory mechanism.
Highlights
Postprandial glucagon concentrations did not change after ingestion of carbohydrate and protein test meals when compared to fasting concentrations in the study and control groups. ere were no differences in their concentrations after carbohydrate and protein meals between study and control groups, while postprandial glucagon levels were significantly higher after fatty meal ingestion in normalweight than in the obese group (p < 0.05) (Figure 1)
In our previous study [24]) the protocol of the study was similar as in the present study. ree different solid meals were given to all the subjects, which consisted of 93% energy of carbohydrate, 72% energy of protein, and 84% energy of fat in a sequence parallel with visual scoring of satiety sensation. e results of the study [24] showed that the reduced glucagon-like peptide-1 (GLP-1) release after consumption of a fatty meal in obese women may explain the impaired sensation of satiety, and the impaired postprandial glucose-dependent insulinotropic polypeptide (GIP) release may be the early indicator of incretin axis dysfunction in obese women
Our study shows similar fasting glucagon levels in obese and normal-weight women, but flat glucagon postprandial profile in the obese group, and significantly lower postprandial glucagon levels after fatty test meal intake in obese may represent an adaptive mechanism preventing an increase in postprandial glucose concentration in the early stage of insulin resistance without compensative hyperinsulinemia
Summary
Glucagon is a 29-amino-acid peptide released by the pancreatic α cells with an antagonistic action to insulin, which has a hyperglycemic effect by enhancement of gluconeogenesis and glycogenolysis in the liver [1].Physiologically, the serum concentration of glucagon is the highest in the morning, in a fasting state, and decreases postprandially. e stimulants for glucagon release are amino acids, catecholamines, corticosteroids, and intestinal hormones including cholecystokinin, gastrin, and GIP, as well as adrenergic activation in hypoglycemia, whereas glucose and free fatty acids inhibit its release [1].Insulin, an opponent pancreatic hormone, participating in the regulation of glucose homeostasis, is mainly secreted by the beta cells stimulated by incretin hormones (GLP1—glucagon-like peptide-1 and GIP—glucose-dependent insulinotropic polypeptide) released by enteroendocrine cells of the gut in response to nutrient absorption [2, 3]. e phenomenon of greater stimulation of insulin release after an oral glucose load than intravenous glucose infusion is called the incretin effect [2].Meal volume and its composition, including the composition of amino acids, determine glucagon release postprandially. e main place of glucagon action is the liver. Glucagon is a 29-amino-acid peptide released by the pancreatic α cells with an antagonistic action to insulin, which has a hyperglycemic effect by enhancement of gluconeogenesis and glycogenolysis in the liver [1]. E phenomenon of greater stimulation of insulin release after an oral glucose load than intravenous glucose infusion is called the incretin effect [2]. GLP-1 suppresses its secretion, especially in a hyperglycemic state [5], whereas GIP was found to stimulate glucagon secretion [6] to more extent with lower glucose concentration. Intravenous glucose infusion suppresses glucagon secretion more than oral glucose load at least in healthy subjects [7, 8]
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