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NEW INTERPRETATION OF ORAL GLUCOSE TOLERANCE.口服葡萄糖耐量的新解读
Lancet. 1964 Jul 4;2(7349):20-1. doi: 10.1016/s0140-6736(64)90011-x.
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The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus.葡萄糖脂肪酸循环。其在胰岛素敏感性及糖尿病代谢紊乱中的作用。
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Biological effects and metabolic rates of glucagonlike peptide-1 7-36 amide and glucagonlike peptide-1 7-37 in healthy subjects are indistinguishable.健康受试者中胰高血糖素样肽-1 7-36酰胺和胰高血糖素样肽-1 7-37的生物学效应和代谢率无明显差异。
Diabetes. 1993 May;42(5):658-61. doi: 10.2337/diab.42.5.658.
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Hypersecretion of truncated glucagon-like peptide-1 and gastric inhibitory polypeptide in obese patients.肥胖患者中截短的胰高血糖素样肽-1和胃抑制多肽分泌过多。
Diabet Med. 1993 Jan-Feb;10(1):44-9. doi: 10.1111/j.1464-5491.1993.tb01995.x.
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Glucagon-like peptide-1 (7-36)amide and glucose-dependent insulinotropic polypeptide secretion in response to nutrient ingestion in man: acute post-prandial and 24-h secretion patterns.胰高血糖素样肽-1(7-36)酰胺与人进食后营养物质摄入相关的葡萄糖依赖性促胰岛素多肽分泌:急性餐后及24小时分泌模式
J Endocrinol. 1993 Jul;138(1):159-66. doi: 10.1677/joe.0.1380159.
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Truncated glucagon-like peptide I, an insulin-releasing hormone from the distal gut.截短的胰高血糖素样肽I,一种来自远端肠道的胰岛素释放激素。
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肥胖时胰高血糖素样肽-1分泌减弱:是原因还是结果?

Attenuated GLP-1 secretion in obesity: cause or consequence?

作者信息

Ranganath L R, Beety J M, Morgan L M, Wright J W, Howland R, Marks V

机构信息

School of Biological Sciences, University of Surrey, Guildford.

出版信息

Gut. 1996 Jun;38(6):916-9. doi: 10.1136/gut.38.6.916.

DOI:10.1136/gut.38.6.916
PMID:8984033
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1383202/
Abstract

BACKGROUND

Hypersecretion of insulinotropic factors such as glucose dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1(7-36)amide (GLP-1) have been postulated to account for the hyperinsulinaemia of obesity.

AIMS

To examine the role of GLP-1 and GIP in obese women and matched controls.

SUBJECTS

Six lean and six obese women subjects matched for age.

METHODS

The gut hormone, plasma glucose, and serum triglyceride responses were studied over 180 minutes after oral carbohydrate and fat meals. Heparin (10,000 units) was given intravenously at 120 minutes.

RESULTS

There was pronounced attenuation of plasma GLP-1 secretion to oral carbohydrate in the obese compared with lean subjects but no such difference in response to oral fat load. There were no differences in the plasma GIP responses to carbohydrate or fat feeding. There was an apparent fall in plasma GLP-1 values in all subjects after administration of heparin.

CONCLUSION

Postprandial GLP-1 secretion in response to oral carbohydrate is considerably attenuated in obese subjects. The cause of this attenuation of GLP-1 secretion is not known although we suggest that both this fall and the overall reduction in GLP-1 values in obese subjects may be related to an increase in plasma non-esterified fatty acids.

摘要

背景

胰岛素促分泌因子如葡萄糖依赖性促胰岛素多肽(GIP)和胰高血糖素样肽-1(7-36)酰胺(GLP-1)分泌过多被认为是肥胖者高胰岛素血症的原因。

目的

研究GLP-1和GIP在肥胖女性及匹配的对照者中的作用。

对象

6名年龄匹配的瘦女性和6名肥胖女性。

方法

研究口服碳水化合物和脂肪餐后180分钟内的肠道激素、血糖和血清甘油三酯反应。在120分钟时静脉注射肝素(10,000单位)。

结果

与瘦受试者相比,肥胖者口服碳水化合物后血浆GLP-1分泌明显减弱,但对口服脂肪负荷的反应无此差异。血浆GIP对碳水化合物或脂肪喂养的反应无差异。注射肝素后,所有受试者的血浆GLP-1值均明显下降。

结论

肥胖受试者餐后口服碳水化合物后GLP-1分泌明显减弱。GLP-1分泌减弱的原因尚不清楚,不过我们认为肥胖者GLP-1值的这种下降及总体降低可能与血浆非酯化脂肪酸增加有关。