Absence of short-term effects of glucagon-like peptide-1 and of hyperglycemia on plasma leptin levels in man

Shalev, Anath; Vosmeer, S.; Keller, Ulrich

doi:10.1016/s0026-0495(97)90112-8

Cited by 12 publications

(7 citation statements)

References 22 publications

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“…No effect of leptin on short term satiety has been shown in humans as yet, but it has been proposed that the postprandial increase in GLP-1 stimulates adipose tissue to secrete leptin and suppress food intake. In our study, plasma leptin concentrations did not change even during a pharmacological GLP-1 infusion (fig 5), confirming the results of Shalev et al 38. The latter finding indicates that food intake suppression induced by GLP-1 is not mediated by leptin.…”

Section: Discussionsupporting

confidence: 92%

Glucagon-like peptide-1: a potent regulator of food intake in humans

Gutzwiller

Göke

Drewe

et al. 1999

Gut

508

294

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Background/Aims-Studies in animals suggest a physiological role for glucagonlike peptide-1-(7-36)-amide (GLP-1) in regulating satiety. The role of GLP-1 in regulating food intake in man has, however, not been investigated. Subjects-Sixteen healthy male subjects were examined in a double blind placebo controlled fashion. Methods-The eVect of graded intravenous doses (0, 0.375, 0.75, and 1.5 pmol/ kg/min) of synthetic human GLP-1 on food intake and feelings of hunger and satiety was tested in healthy volunteers. Results-Graded GLP-1 infusions resulted in a dose dependent reduction in food intake (maximal inhibition 35%, p<0.001 v control) and a similar reduction in calorie intake (32%; p<0.001). Fluid ingestion was also reduced by GLP-1 (18% reduction, p<0.01). No overt side eVects were produced by GLP-1, but subjects experienced less hunger and early fullness in the period before a meal during GLP-1 infusion at the highest dose (p<0.05). Conclusions-Intravenous infusions of GLP-1 decrease spontaneous food intake even at physiological plasma concentrations, implying an important role for GLP-1 in the regulation of the early satiety response in humans. (Gut 1999;44:81-86)

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Section: Discussionsupporting

confidence: 92%

Glucagon-like peptide-1: a potent regulator of food intake in humans

Gutzwiller

Göke

Drewe

et al. 1999

Gut

508

294

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“…In mammalian and non-mammalian species, glucagon can regulate the production and/or secretion of other hormones, e.g., ghrelin in rats 30, somatostatin in rainbow trout 31 and fibroblast growth factor in rats 32. However, as reported in sheep, glucagon has no effects on blood leptin levels 33, 34. To our knowledge, the effect of glucagon on leptin regulation in fish has not yet been examined previously.…”

Section: Introductionmentioning

confidence: 91%

Signal transduction mechanism for glucagon-induced leptin gene expression in goldfish liver

Yan¹,

Chen²,

Chen³

et al. 2016

Int. J. Biol. Sci.

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Leptin is a peripheral satiety hormone that also plays important roles in energy homeostasis in vertebrates ranging from fish to mammals. In teleost fish, however, the regulatory mechanism for leptin gene expression still remains unclear. In this study, we found that glucagon, a key hormone in glucose homeostasis, was effective at elevating the leptin-AI and leptin-AII transcript levels in goldfish liver via both in vivo intraperitoneal injection and in vitro cells incubation approaches. The responses of leptin-AI and leptin-AII mRNA to glucagon treatment were highly comparable. In contrast, blockade of local glucagon action could reduce the basal and induced leptin-AI and leptin-AII mRNA expression. The stimulation of leptin levels by glucagon was caused by the activation of adenylate cyclase (AC)/cyclic-AMP (cAMP)/ protein kinase A (PKA), and probably cAMP response element-binding protein (CREB) cascades. Our study described the effect and signal transduction mechanism of glucagon on leptin gene expression in goldfish liver, and may also provide new insight into leptin as a mediator in the regulatory network of energy metabolism in the fish model.

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“…Exactly the same time was spent on the two test days for each individual subject. Postprandial resting metabolic rate was measured for 4 h, and blood samples were taken 15,30,45,60,90,120,150,180,210,240 and 270 min after the start of the breakfast and again after the ad libitum lunch, served at 2:15 pm (300 min). Ratings of subjective sensations were made on 100 mm visual analogue scales (VAS) with the text expressing the most positive and the most negative rating anchored at each end.…”

Section: Experimental Protocolmentioning

confidence: 99%

The effect of physiological levels of glucagon-like peptide-1 on appetite, gastric emptying, energy and substrate metabolism in obesity

Flint¹,

Raben²,

Ersbøll³

et al. 2001

Int J Obes

319

228

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OBJECTIVE: Peripheral infusions of glucagon-like peptide-1 (GLP-1) in humans have been shown to inhibit gastrointestinal motility and decrease hunger and energy intake. However, these investigations used supraphysiological doses. The objective of this study was to investigate the effects of a GLP-1 infusion in a physiological dose on appetite sensations, energy intake, gastric emptying, energy and substrate metabolism. METHODS: Eighteen obese men participated in the placebo-controlled, randomized, single-blinded, cross-over study with infusion of GLP-1 or saline. Resting metabolic rate (RMR) and substrate oxidations were measured by ventilated hood before and after an energy-®xed breakfast. Gastric emptying was measured using paracetamol as a marker. Visual analogue scales were used to assess appetite sensations, thirst and comfort throughout the experiment and palatability of the test meals. Blood was sampled for analysis of hormones (GLP-1, GLP-2, glucose-dependent insulinotropic polypeptide (GIP), insulin, glucagon), and substrates (glucose, lactate, non-esteri®ed fatty acids (NEFA), triacylglycerol (TAG)). Ad libitum energy intake at lunch was registered. RESULTS: Following the breakfast, GLP-1 infusion suppressed ratings of hunger and prospective food consumption (P`0.05), whereas all other subjective ratings and ad libitum energy intake were unaffected. RMR, carbohydrate oxidation and gastric emptying rate were lower during the GLP-1 infusion compared with the saline infusion (P`0.001, P`0.05, P`0.0001, respectively). All plasma hormone and substrate pro®les, except NEFA, were signi®cantly reduced by GLP-1 (P`0.0001). CONCLUSION: It is concluded that GLP-1 in physiological concentrations powerfully reduces the rate of entry of nutrients into the circulation by a reduction of gastric emptying rate in obese subjects. The effect of GLP-1 on appetite and food intake may be bene®cial in weight reduction.

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Absence of short-term effects of glucagon-like peptide-1 and of hyperglycemia on plasma leptin levels in man

Cited by 12 publications

References 22 publications

Glucagon-like peptide-1: a potent regulator of food intake in humans

Glucagon-like peptide-1: a potent regulator of food intake in humans

Signal transduction mechanism for glucagon-induced leptin gene expression in goldfish liver

The effect of physiological levels of glucagon-like peptide-1 on appetite, gastric emptying, energy and substrate metabolism in obesity

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