GLP-1 AND GLP-17-36 AMIDE - INFLUENCES ON BASAL AND STIMULATED INSULIN AND GLUCAGON-SECRETION IN THE MOUSE

被引:62
作者
FRIDOLF, T [1 ]
BOTTCHER, G [1 ]
SUNDLER, F [1 ]
AHREN, B [1 ]
机构
[1] UNIV LUND,DEPT PHARMACOL,SOLVEGATAN 10,S-22362 LUND,SWEDEN
关键词
GLP-1; GLP-17-36; IMMUNOHISTOCHEMISTRY; INSULIN SECRETION; GLUCAGON SECRETION; PANCREAS; GUT; MOUSE;
D O I
10.1097/00006676-199103000-00013
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
We studied the cellular distribution of glucagon-like peptide-1 (GLP-1) in the pancreas and gut and the effects of GLP-1 and its truncated form, GLP-1(7)-36 amide, on basal and stimulated insulin and glucagon secretion in the mouse. Immunofluorescence staining showed that GLP-1 immunoreactivity occurred within peripheral islet cells and in cells located mainly distally in the small intestine and in the entire large intestine. Double-immunostaining revealed that the GLP-1-immunoreactive cells were identical to the glucagon/glicentin cells. Experiments in vivo revealed that basal insulin secretion was stimulated by GLP-1(7)-36 amide at the dose levels of 8 and 32 nmol/kg, and by GLP-1 at 32 nmol/kg. Furthermore, GLP-1(7)-36 amide showed additive stimulatory influence with glucose (2.8 mmol/kg), the cholinergic agonist carbachol (0.16-mu-mol/kg), and the C-terminal octapeptide of cholecystokinin (CCK-8, 5.3 nmol/kg), when injected at 8 or 32 nmol/kg. In contrast, stimulated insulin secretion was unaffected by GLP-1. Moreover, the glucagon secretory responses to carbachol and CCK-8 were inhibited by GLP-1(7)-36 amide but were unaffected by the entire GLP-1. We conclude that GLP-1(7)-36 has the potential for being a modulator of islet hormone secretion.
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页码:208 / 215
页数:8
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