Basal α-Cell Up-Regulation in Obese Insulin-Resistant Adolescents

Weiss, Ram; D'Adamo, Ebe; Santoro, Nicola; Hershkop, Karen; Caprio, Sonia

doi:10.1210/jc.2010-1275

Cited by 37 publications

(35 citation statements)

References 22 publications

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“…GLP-2 directly stimulates glucagon secretion and counteracts the glucagonostatic action of GLP-1 in healthy subjects (9), and in type 1 and type 2 diabetic subjects (3,16). Glucagon is counter-regulatory to insulin action, increasing glucose output and inhibiting glucose uptake in the liver, and has been linked to IR in obese subjects with normal or impaired glucose tolerance (17,18).…”

Section: Resultsmentioning

confidence: 99%

Association of insulin resistance and GLP-2 secretion in obesity: a pilot study

Geloneze

Lima

Pareja

et al. 2013

Arq Bras Endocrinol Metab

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Objective: The objective of this pilot study was to determine whether glugagon-like peptide 2 (GLP-2) secretion relates to insulin sensitivity (IS) in obese subjects. Subjects and methods: Twenty four obese subjects [body mass index (BMI) 40.0 ± 3.0 kg/m 2 (mean ± standard deviation)] were included, nine of which were male, age 43 ± 8 years. Twelve subjects had type 2 diabetes, all treated with oral anti-diabetic agents only. The subjects were submitted to standard meal tolerance test (MTT) for dosage of the curves: glucose, insulin, and GLP-2. Insulin sensitivity was measured by HOMA-IR, and OGIS was derived from the MTT. Spearman linear correlations and partial correlations were obtained. Results:

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Section: Resultsmentioning

confidence: 99%

Association of insulin resistance and GLP-2 secretion in obesity: a pilot study

Geloneze

Lima

Pareja

et al. 2013

Arq Bras Endocrinol Metab

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“…Plasma glucagon levels are abnormally elevated in both T1D and T2D subjects, indicating that a-cell hypersecretion is a common diabetic feature [196][197][198][199]. Abnormally high fasting glucagon levels, suggestive of a-cell hypersecretion, have been found also in normoglycemic insulin-resistant obese adults and adolescents [200][201][202][203][204]. In the latter group, high fasting glucagon levels were observed in the face of elevated fasting insulin levels, suggesting that a-cells manifested insulin resistance to the suppressive effect of insulin on glucagon secretion.…”

Section: Pancreatic A-cells Dysfunction May Contribute To Hyperglutammentioning

confidence: 99%

The potential role of glutamate in the current diabetes epidemic

2012

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In the present article, we propose the perspective that abnormal glutamate homeostasis might contribute to diabetes pathogenesis. Previous reports and our recent data indicate that chronically high extracellular glutamate levels exert direct and indirect effects that might participate in the progressive loss of β-cells occurring in both T1D and T2D. In addition, abnormal glutamate homeostasis may impact all the three accelerators of the "accelerator hypothesis" and could partially explain the rising frequency of T1D and T2D.

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“…Hypothesis has been advanced that GLP2-increased secretion could be the cause of insulin resistance as GLP2 increases absorption of nutrients, especially fatty acids, a key factor for insulin resistance (Delarue & Magnan 2007) or for its glucagonotrophic action in healthy or diabetic subjects (Christensen et al 2010, Lund et al 2011. Glucagon is counter-regulatory to insulin action, increasing glucose output and inhibiting glucose uptake in the liver, and it has been linked to insulin resistance in obese subjects with normal or impaired glucose tolerance (Ahrén 2006, Weiss et al 2011. However, this appears unlikely because bariatric surgery, particularly Roux-en-Y gastric bypass (RYGB) (Saeidi et al 2013), which is the most effective therapy for obesity and T2D (Carlsson et al 2012, Cummings 2012, increases blood GLP2 (by 200%) at postprandial status (le Roux et al 2010).…”

Section: Glp2 and Glycaemic Controlmentioning

confidence: 99%

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

Amato¹,

Baldassano²,

Mulè³

2016

Journal of Endocrinology

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Glucagon-like peptide 2 (GLP2) is a proglucagon-derived peptide produced by intestinal enteroendocrine L-cells and by a discrete population of neurons in the brainstem, which projects mainly to the hypothalamus. The main biological actions of GLP2 are related to the regulation of energy absorption and maintenance of mucosal morphology, function and integrity of the intestine; however, recent experimental data suggest that GLP2 exerts beneficial effects on glucose metabolism, especially in conditions related to increased uptake of energy, such as obesity, at least in the animal model. Indeed, mice lacking GLP2 receptor selectively in hypothalamic neurons that express proopiomelanocortin show impaired postprandial glucose tolerance and hepatic insulin resistance (by increased gluconeogenesis). Moreover, GLP2 acts as a beneficial factor for glucose metabolism in mice with high-fat diet-induced obesity. Thus, the aim of this review is to update and summarize current knowledge about the role of GLP2 in the control of glucose homeostasis and to discuss how this molecule could exert protective effects against the onset of related obesity type 2 diabetes.

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Basal α-Cell Up-Regulation in Obese Insulin-Resistant Adolescents

Abstract: Islet up-regulation manifesting as basal elevated glucagon and c-peptide secretion that determines the suppressive effects of hyperinsulinemia appears early in the course of deteriorating glucose tolerance.

Cited by 37 publications

References 22 publications

Association of insulin resistance and GLP-2 secretion in obesity: a pilot study

Association of insulin resistance and GLP-2 secretion in obesity: a pilot study

The potential role of glutamate in the current diabetes epidemic

GLP2: an underestimated signal for improving glycaemic control and insulin sensitivity

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