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Introduction Glucagon-like peptide-1 (GLP-1) is a peptide secreted from the gut in response to food. It acts directly on β cells, enhancing the effect of glucose in stimulating insulin secretion from these cells. When administered to
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-cell desensitisation compared with sulphonylureas may occur following prolonged exposure to nateglinide ( Ball et al. 2004 b ). In vivo , insulin secretion can be stimulated by glucagon-like peptide-1 (GLP-1), a hormone of the enteroinsular axis, released
Integrative Fish Biology Program, School of Aquatic and Fishery Sciences, Northwest Fisheries Science Center, National Marine Fisheries Service, 2725 Montlake Boulevard E., Seattle, Washington 98112, USA
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Integrative Fish Biology Program, School of Aquatic and Fishery Sciences, Northwest Fisheries Science Center, National Marine Fisheries Service, 2725 Montlake Boulevard E., Seattle, Washington 98112, USA
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Integrative Fish Biology Program, School of Aquatic and Fishery Sciences, Northwest Fisheries Science Center, National Marine Fisheries Service, 2725 Montlake Boulevard E., Seattle, Washington 98112, USA
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Integrative Fish Biology Program, School of Aquatic and Fishery Sciences, Northwest Fisheries Science Center, National Marine Fisheries Service, 2725 Montlake Boulevard E., Seattle, Washington 98112, USA
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Integrative Fish Biology Program, School of Aquatic and Fishery Sciences, Northwest Fisheries Science Center, National Marine Fisheries Service, 2725 Montlake Boulevard E., Seattle, Washington 98112, USA
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hormones may modulate the effect of Gh on liver Igf2 production in fishes. To test this hypothesis, we examined basal and Gh-dependent effects of insulin, glucagon, dexamethasone (Dex), and triiodothyronine (T 3 ) on igf2 gene expression in primary
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fall into two major categories: drugs that improve insulin sensitivity, and those that increase insulin secretion from β-cells. Agents that enhance insulin secretion in a glucose-dependent manner, such as glucagon-like peptide-1 (GLP-1) mimetics (e
School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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School of Pharmaceutical and Biological Sciences, Aston University, Birmingham, UK
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Introduction The incretin hormone glucagon-like peptide-1 (GLP-1) has potent insulinotropic effects on pancreatic β-cells, and further promotes glucose lowering by enhancing glucose uptake and glyconeogenesis in peripheral tissues
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Introduction Glucagon-like peptide-1(7–36)amide (GLP-1) is an intestinal peptide synthesised in L-cells. It is also produced in the brain ( Jin et al. 1988 , Kreymann et al. 1989 ), where it exerts some effects on
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This study examines the role of glucagon in the pathogenesis of the obese hyperglycaemic (ob/ob) syndrome in mice. Plasma C-terminal immunoreactive glucagon concentrations were measured in fed and fasted ob/ob mice at different ages between 5–40 weeks, and in 20-week-old mice after the administration of established stimulators and inhibitors of glucagon secretion. Plasma glucagon concentrations were inappropriately raised irrespective of age, nutritional status and the accompanying prominent changes in plasma glucose and insulin concentrations. Glucose suppressed plasma glucagon in the fed but not the fasted state, suggesting a dependence on the marked hyperinsulinaemia associated with feeding. Administration of 0·25 units insulin/kg to fasted mice failed to affect plasma glucagon and glucose concentrations. Increasing the dose to 100 units/kg restored the normal suppressive actions of insulin. Fasted mice showed an exaggerated glucagon response to arginine but not to the parasympathomimetic agent pilocarpine. Fed mice displayed normal plasma glucagon responses to the sympathomimetic agents noradrenaline and adrenaline. Administration of insulin antiserum or 2-deoxy-l-glucose raised plasma glucagon concentrations of fed mice. Contrary to the lack of suppression by glucose in the fasted state, heparin-induced increase in free fatty acids reduced plasma glucagon concentrations. This study demonstrates inappropriate hyperglucagonaemia and defective A-cell function in ob/ob mice. The extent of the abnormality is exacerbated by fasting and appears to result from insensitivity of the A-cell to the normal suppressive action of insulin.
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that aim to improve β-cell function and survival. Glucagon-like peptide 1 (GLP-1) is a potent incretin hormone secreted by the intestinal L cells in response to food intake ( Drucker 2001 ). GLP-1 exerts multiple effects on pancreatic β
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Abstract
We have characterized the specific binding of glucagon in hepatocytes isolated from two teleost species, the American eel (Anguilla rostrata) and the brown bullhead (Ictalurus nebulosus). Specific glucagon binding was 9·3 and 10·7% in bullhead and eel hepatocytes respectively, after a 2-h incubation at 12 °C. Curvilinear Scatchard plots suggest the presence of two classes of binding sites with apparent dissociation constants (K d) of 1·97 nm (high affinity) and 17·3 nm (low affinity) for bullhead and 2·68 and 22·9 nm for eel cells. The number of high-affinity binding sites per cell was significantly higher in the eel (10 413) than in the bullhead (3811). The number of high-affinity insulin-binding sites was approximately two times higher than that for glucagon in bullheads and the opposite in the eel hepatocytes. In competition experiments, insulin did not displace 125I-labelled glucagon binding in the hepatocytes of either species, while glucagon-like peptide-1(7–37) (GLP-1) displaced glucagon but only at high concentrations, suggesting separate glucagon- and GLP-1-binding sites. The rate of dissociation of hepatocyte-bound 125I-labelled glucagon was similar for both species. Preincubation of hepatocytes in 100 nm glucagon decreased the number of high-affinity glucagon-binding sites by approximately 55% in both species, while the K d values remained unchanged. Glucagon bound to the cell surface is internalized by fish hepatocytes. These properties indicate that the glucagon binding to hepatocytes of these two teleost species is similar to that reported for mammalian hepatocytes.
Journal of Endocrinology (1994) 140, 217–227
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SUMMARY
The uptake of glucose by isolated rat diaphragm is increased in the presence of glucagon preparations (at concentrations of 20–200 μg/ml.). Evidence is produced which appears to show that this effect is due to the presence of insulin in preparations of glucagon. The insulin content of an amorphous preparation of glucagon, assayed with isolated diaphragm, appeared to be of the order of 1% (w/w). In view of this finding, it is suggested that no conclusions can be drawn about a possible effect of glucagon on carbohydrate metabolism in muscle until preparations are available which are entirely free from insulin.
