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丙酸盐对链脲佐菌素诱导的糖尿病大鼠体内碳水化合物代谢的影响。

Effect of propionate on in vivo carbohydrate metabolism in streptozocin-induced diabetic rats.

作者信息

Cameron-Smith D, Collier G R, O'Dea K

机构信息

Department of Human Nutrition, Deakin University, Geelong, Australia.

出版信息

Metabolism. 1994 Jun;43(6):728-34. doi: 10.1016/0026-0495(94)90122-8.

Abstract

Undigested carbohydrates and some dietary fibers are fermented in the large intestine to form short-chain fatty acids (SCFA), including acetate, propionate, and butyrate. It has been suggested that some of the beneficial effects of high-carbohydrate, high-fiber diets on carbohydrate and lipid metabolism are mediated by the metabolism of SCFA in the liver. Propionate has been shown in vitro to decrease glucose production in rat hepatocytes. The aim of the present study was to investigate the effects of propionate on carbohydrate metabolism in normal and streptozocin (STZ)-induced diabetic male Sprague-Dawley rats. Rats were fed a high-fat diet with or without sodium propionate supplementation (either 0.5% or 5% wt/wt) for 4 weeks. At the completion of the feeding period, body weight and liver glycogen concentrations were significantly decreased in STZ-diabetic rats and were unaffected by propionate supplementation. Although STZ-diabetic animals had elevated fasting plasma glucose, cholesterol, and triglyceride levels relative to nondiabetic rats, propionate supplementation had no significant effect on these parameters in either group. Basal and insulin-stimulated carbohydrate metabolism were assessed using the euglycemic clamp technique in overnight-fasted animals with 3(H)-6-glucose infusion. As expected, basal hepatic glucose production (HGP) was higher and the metabolic clearance rate of glucose (MCR) was lower in STZ-diabetic rats. High-dose insulin infusion (3 mU.kg-1.min-1) suppressed HGP in nondiabetic and diabetic animals and increased the MCR in nondiabetic animals. However, propionate supplementation did not alter basal or insulin-stimulated HGP or the MCR in either nondiabetic or diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

未消化的碳水化合物和一些膳食纤维在大肠中发酵形成短链脂肪酸(SCFA),包括乙酸盐、丙酸盐和丁酸盐。有人提出,高碳水化合物、高纤维饮食对碳水化合物和脂质代谢的一些有益作用是由肝脏中SCFA的代谢介导的。丙酸盐在体外已被证明可降低大鼠肝细胞中的葡萄糖生成。本研究的目的是研究丙酸盐对正常和链脲佐菌素(STZ)诱导的糖尿病雄性Sprague-Dawley大鼠碳水化合物代谢的影响。大鼠被喂食高脂饮食,添加或不添加丙酸钠(0.5%或5%重量/重量),持续4周。在喂养期结束时,STZ糖尿病大鼠的体重和肝糖原浓度显著降低,且不受丙酸盐补充的影响。尽管STZ糖尿病动物的空腹血糖、胆固醇和甘油三酯水平相对于非糖尿病大鼠有所升高,但丙酸盐补充对两组中的这些参数均无显著影响。使用正常血糖钳夹技术在过夜禁食并输注3(H)-6-葡萄糖的动物中评估基础和胰岛素刺激的碳水化合物代谢。正如预期的那样,STZ糖尿病大鼠的基础肝葡萄糖生成(HGP)较高,葡萄糖代谢清除率(MCR)较低。高剂量胰岛素输注(3 mU.kg-1.min-1)抑制了非糖尿病和糖尿病动物的HGP,并增加了非糖尿病动物的MCR。然而,丙酸盐补充在非糖尿病或糖尿病动物中均未改变基础或胰岛素刺激的HGP或MCR。(摘要截断于250字)

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