GLUCAGON-LIKE PEPTIDE-I-(7-37) SUPPRESSES HYPERGLYCEMIA IN RATS

被引:29
|
作者
HENDRICK, GK
GJINOVCI, A
BAXTER, LA
MOJSOV, S
WOLLHEIM, CB
HABENER, JF
WEIR, GC
机构
[1] HARVARD UNIV,JOSLIN DIABET CTR,SCH MED,1 JOSLIN PL,BOSTON,MA 02215
[2] HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,BOSTON,MA 02215
[3] UNIV GENEVA,DEPT MED,DIV CLIN BIOCHEM,CH-1211 GENEVA 4,SWITZERLAND
[4] MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114
[5] HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1993年 / 42卷 / 01期
关键词
D O I
10.1016/0026-0495(93)90163-I
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Glucagon-like peptide-(GLP) I-(7-37) is an endogenous hormone that has recently been demonstrated to be a potent insulin secretagogue. In these studies, GLP was administered during oral and intravenous (IV) glucose tolerance tests (OGTT and IVGTT, respectively) to determine whether this peptide could enhance postprandial insulin levels and thus reduce glycemic excursions. Surprisingly, during OGTT, GLP administration did not augment insulin secretion; however, GLP administration resulted in significantly lower glycemic excursions. In fasted rats, glycemic excursions were significantly reduced 10 and 20 minutes after receiving GLP (P < .001). Fed rats that received GLP had virtually no initial increase in plasma glucose level after administration of oral glucose. During IVGTT, glucose alone increased insulin levels eightfold, while administration of both glucose and GLP resulted in a 15-fold increase (P < .001). These IVGTT data support previous studies that show GLP to be a potent and glucose-dependent insulin secretagogue. Furthermore, all of these studies suggest that GLP reduces postprandial glycemic excursion and thus may be useful in the treatment of non-insulin-dependent diabetes mellitus. © 1993.
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页码:1 / 6
页数:6
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