Meal-Anticipatory Glucagon-Like Peptide-1 Secretion in Rats

Vahl, Torsten; Drazen, Deborah L.; Seeley, Randy J.; D’Alessio, David A.; Woods, Stephen C.

doi:10.1210/en.2009-1002

Cited by 90 publications

(56 citation statements)

References 48 publications

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“…Circulating GLP-1 levels rise after a meal and fall in the fasted state. Recent evidence also suggests that levels rise in anticipation of a meal [96]. GLP-1 reduces food intake, suppresses glucagon secretion and delays gastric emptying [97].…”

Section: Ghrelinmentioning

confidence: 99%

The role of gut hormones and the hypothalamus in appetite regulation

et al. 2010

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Abstract. The World Health Organisation has estimated that by 2015 approximately 2.3 billion adults will be overweight and more than 700 million obese. Obesity is associated with an increased risk of diabetes, cardiovascular events, stroke and cancer. The hypothalamus is a crucial region for integrating signals from central and peripheral pathways and plays a major role in appetite regulation. In addition, there are reciprocal connections with the brainstem and higher cortical centres. In the arcuate nucleus of the hypothalamus, there are two major neuronal populations which stimulate or inhibit food intake and influence energy homeostasis. Within the brainstem, the dorsal vagal complex plays a role in the interpretation and relaying of peripheral signals. Gut hormones act peripherally to modulate digestion and absorption of nutrients. However, they also act as neurotransmitters within the central nervous system to control food intake. Peptide YY, pancreatic polypeptide, glucagon-like peptide-1 and oxyntomodulin suppress appetite, whilst ghrelin increases appetite through afferent vagal fibres to the caudal brainstem or directly to the hypothalamus. A better understanding of the role of these gut hormones may offer the opportunity to develop successful treatments for obesity. Here we review the current understanding of the role of gut hormones and the hypothalamus on food intake and body weight control.

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Section: Ghrelinmentioning

confidence: 99%

The role of gut hormones and the hypothalamus in appetite regulation

et al. 2010

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“…In rodents, a transient increase in GLP-1 levels was observed in anticipation of food being presented [52], suggesting a cephalic response. However, in humans, the balance of evidence suggests that vagal cholinergic innervation does not play a major role in regulating incretin hormone secretion.…”

Section: Neural Regulationmentioning

confidence: 99%

Physiology of Incretins in Health and Disease

Deacon

Åhrén²

2011

Rev Diabet Stud

112

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■ AbstractThe incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are gut peptides which are secreted by endocrine cells in the intestinal mucosa. Their plasma concentrations increase quickly following food ingestion, and carbohydrate, fat, and protein have all been shown to stimulate GLP-1 and GIP secretion. Although neural and hormonal mechanisms have also been proposed to regulate incretin hormone secretion, direct stimulation of the enteroendocrine cells by the presence of nutrients in the intestinal lumen is probably the most important factor in humans. The actions of the incretin hormones are crucial for maintaining normal islet function and glucose homeostasis. Furthermore, it is also now being recognized that incretin hormones may have other actions in addition to their glucoregulatory effects. Studies have shown that GLP-1 and GIP levels and actions may be perturbed in disease states, but interpretation of the precise relationship between disease and incretins is difficult. The balance of evidence seems to suggest that alterations in secretion and/or action of incretin hormones arise secondarily to the development of insulin resistance, glucose intolerance, and/or increases in body weight rather than being causative factors. However, these impairments may contribute to the deterioration of glycemic control in diabetic patients.

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“…It has already been shown that incretin secretion from the bowel can be regulated by mechanisms other than direct nutrient stimulation. Increased GLP-1 secretion has been shown before an anticipated meal, and these phenomena are known as the cephalic phase of secretion [24]. Other nutrients and possibly any bolus that distends the small bowel can induce a GIP and GLP-1 response.…”

Section: Discussionmentioning

confidence: 99%

Increased Incretin But Not Insulin Response after Oral versus Intravenous Branched Chain Amino Acids

Gojda¹,

Straková²,

Plíhalová³

et al. 2017

Ann Nutr Metab

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Background/Aims: Branched chain amino acids (BCAAs) are known to exert an insulinotropic effect. Whether this effect is mediated by incretins (glucagon like peptide 1 [GLP-1] or glucose-dependent insulinotropic peptide [GIP]) is not known. The aim of this study was to show whether an equivalent dose of BCAA elicits a greater insulin and incretin response when administered orally than intravenously (IV). Methods: Eighteen healthy, male subjects participated in 3 tests: IV application of BCAA solution, oral ingestion of BCAA and placebo in an equivalent dose (30.7 ± 1.1 g). Glucose, insulin, C-peptide, glucagon, GLP-1, GIP, valine, leucine and isoleucine concentrations were measured. Results: Rise in serum BCAA was achieved in both BCAA tests, with incremental areas under the curve (iAUC) being 2.1 times greater for IV BCAA compared with those of the oral BCAA test (p < 0.0001). Oral and IV BCAA induced comparable insulin response greater than placebo (240 min insulin iAUC: oral 3,411 ± 577 vs. IV 2,361 ± 384 vs. placebo 961.2 ± 175 pmol/L, p = 0.0006). Oral BCAA induced higher GLP-1 (p < 0.0001) and GIP response (p < 0.0001) compared with the IV or placebo. Glucose levels declined significantly (p < 0.001) in the same pattern during both BCAA tests with no change in the placebo group. Conclusions: An equivalent dose of BCAA elicited a comparable insulin and greater incretin response when administered orally and not when administered through IV. We conclude that insulinotropic effects of BCAA are partially incretin dependent.

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Meal-Anticipatory Glucagon-Like Peptide-1 Secretion in Rats

Cited by 90 publications

References 48 publications

The role of gut hormones and the hypothalamus in appetite regulation

The role of gut hormones and the hypothalamus in appetite regulation

Physiology of Incretins in Health and Disease

Increased Incretin But Not Insulin Response after Oral versus Intravenous Branched Chain Amino Acids

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