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蔗糖饮食诱导了酶和激素反应,这些反应影响了两种胰岛素可用性不同的物种(多刺小鼠和ob/ob小鼠)的碳水化合物、脂质和能量代谢。

Sucrose diet induced enzymatic and hormonal responses affecting carbohydrate, lipid and energy metabolism in two species differing in insulin availability: spiny and ob/ob mice.

作者信息

Shafrir E, Trostler N

出版信息

Int J Biochem. 1984;16(4):375-82. doi: 10.1016/0020-711x(84)90135-6.

Abstract

The low-insulin responding spiny mice (Acomys cahirinus), maintained on a 50% sucrose diet vs isocaloric regular diet, responded with an impressive increase in the activity of hepatic enzymes of glycolysis and lipogenesis and in hyperlipidemia. There was no hyperinsulinemia or hyperglycemia and spiny mice did not gain weight on sucrose due to loss of adipose tissue. Serum T3 levels rose 1.8 fold and the activity of the hepatic mitochondrial FAD-glycerol-3-phosphate oxidase became induced 2.6 fold representing the enhancement of multiple, T3-dependent, energy-consuming metabolic cycles. An increased TG lipolysis in adipose tissue was also observed. C57BL/6J ob/ob mice were markedly hyperinsulinemic and gained weight on sucrose almost as much as those on regular diet, without changes in serum glucose or insulin. Serum triglyceride level decreased, whereas liver triglycerides accumulated markedly. The extent of the increase in hepatic enzyme activities related to lipogenesis was much lower both in the ob/ob mice and their lean siblings, than in spiny mice, but the basal enzyme activities in ob/ob mice were remarkably elevated. Serum T3 level was also elevated already on the regular diet and rose only slightly on sucrose. Basal glycerol phosphate oxidase activity in ob/ob mice exceeded that in spiny mice and rose only marginally on sucrose. Adipose tissue lipolysis was not increased. Thus, sucrose diet by enhancing the T3 production appeared to activate protective mechanism against weight gain in normoinsulinemic spiny mice, whereas the full expression of these mechanisms appeared to be precluded by the hyperinsulinemia of ob/ob mice.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

与等热量常规饮食相比,喂食50%蔗糖饮食的低胰岛素反应性刺毛鼠(埃及刺毛鼠),其糖酵解和脂肪生成的肝酶活性显著增加,并出现高脂血症。没有高胰岛素血症或高血糖,且刺毛鼠因脂肪组织流失,在蔗糖饮食下并未增重。血清T3水平升高了1.8倍,肝线粒体FAD - 3 - 磷酸甘油氧化酶的活性被诱导增加了2.6倍,这代表多个T3依赖的耗能代谢循环增强。脂肪组织中的甘油三酯脂解也增加。C57BL/6J ob/ob小鼠有明显的高胰岛素血症,在蔗糖饮食下增重几乎与常规饮食时相同,血糖和胰岛素无变化。血清甘油三酯水平降低,而肝脏甘油三酯明显蓄积。与脂肪生成相关的肝酶活性增加程度,在ob/ob小鼠及其瘦型同胞中均远低于刺毛鼠,但ob/ob小鼠的基础酶活性显著升高。在常规饮食时血清T3水平就已升高,在蔗糖饮食下仅略有上升。ob/ob小鼠的基础磷酸甘油氧化酶活性超过刺毛鼠,在蔗糖饮食下仅略有上升。脂肪组织脂解未增加。因此,蔗糖饮食通过增强T3生成,似乎激活了正常胰岛素水平的刺毛鼠防止体重增加的保护机制,而ob/ob小鼠的高胰岛素血症似乎阻碍了这些机制的充分表达。(摘要截短至250字)

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