Leclercq-Meyer V, Malaisse W J
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Life Sci. 1996;58(14):1195-9. doi: 10.1016/0024-3205(96)00078-1.
The glucagon-like peptide 1 (7-36) amide (GLP-1, 1.0 nM) was administered to isolated rat pancreases perfused either in the absence of exogenous nutrient or presence of 10 mM succinic acid dimethyl ester (SAD). In the absence of any exogenous nutrient, GLP-1 failed to affect either insulin or glucagon release. The administration of SAD caused a biphasic stimulation of insulin output and inhibited glucagon secretion. In the presence of SAD, GLP-1 still failed to affect glucagon release, but markedly enhanced insulin secretion. These findings indicate that GLP-1 is not truly a glucose-dependent, but rather nutrient-dependent insulin secretagogue. They also suggest that non-glucidic nutrients, such as SAD, could be used to optimalize the B-cell secretory response to GLP-1 in non-insulin-dependent diabetes mellitus.
将胰高血糖素样肽1（7 - 36）酰胺（GLP - 1，1.0纳摩尔）施用于在无外源性营养物或存在10毫摩尔琥珀酸二甲酯（SAD）的情况下灌注的离体大鼠胰腺。在没有任何外源性营养物的情况下，GLP - 1未能影响胰岛素或胰高血糖素的释放。SAD的施用引起胰岛素分泌的双相刺激并抑制胰高血糖素分泌。在存在SAD的情况下，GLP - 1仍然未能影响胰高血糖素的释放，但显著增强了胰岛素分泌。这些发现表明，GLP - 1并非真正的葡萄糖依赖性，而是营养物依赖性胰岛素促分泌剂。它们还表明，非糖类营养物，如SAD，可用于优化非胰岛素依赖型糖尿病中胰岛B细胞对GLP - 1的分泌反应。
