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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Beneficial effects of kinin B1 receptor antagonism on plasma fatty acid alterations and obesity in Zucker diabetic fatty rats
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Beneficial effects of kinin B1 receptor antagonism on plasma fatty acid alterations and obesity in Zucker diabetic fatty rats

机译:激肽B1受体拮抗作用对Zucker糖尿病脂肪大鼠血浆脂肪酸改变和肥胖的有益作用

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摘要

Kinins are the endogenous ligands of the constitutive B2 receptor (B2R) and the inducible B1 receptor (B1R). Whereas B2R prevents insulin resistance, B1R is involved in insulin resistance and metabolic syndrome. However, the contribution of B1R in type 2 diabetes associated with obesity remains uncertain. The aim of the present study was to examine the impact of 1-week treatment with a selective B1R antagonist (SSR240612, 10 mg/kg per day, by gavage) on hyperglycemia, hyperinsulinemia, leptinemia, body mass gain, and abnormal plasma fatty acids in obese Zucker diabetic fatty (ZDF) rats. Treatment with SSR240612 abolished the body mass gain and reduced polyphagia, polydipsia, and plasma fatty acid alterations in ZDF rats without affecting hyperglycemia, hyperinsulinemia, and hyperleptinemia. The present study suggests that the upregulated B1R plays a role in body mass gain and circulating fatty acid alterations in ZDF rats. However, mechanisms other than B1R induction would be implicated in glucose metabolism disorder in ZDF rats, based on the finding that SSR240612 did not reverse hyperglycemia and hyperinsulinemia.
机译:激肽是组成型B2受体(B2R)和诱导型B1受体(B1R)的内源性配体。 B2R预防胰岛素抵抗,而B1R参与胰岛素抵抗和代谢综合征。但是,B1R在与肥胖相关的2型糖尿病中的作用仍不确定。本研究的目的是研究用选择性B1R拮抗剂(SSR240612,每天10 mg / kg,每天通过管饲法)治疗1周对高血糖,高胰岛素血症,瘦素血症,体重增加和血浆脂肪酸异常的影响在肥胖的Zucker糖尿病脂肪(ZDF)大鼠中。 SSR240612的治疗消除了ZDF大鼠的体重增加,并减少了多食,多饮和血浆脂肪酸的变化,而不会影响高血糖,高胰岛素血症和高瘦素血症。本研究表明,上调的B1R在ZDF大鼠体内的体重增加和循环脂肪酸改变中起作用。然而,基于SSR240612不能逆转高血糖和高胰岛素血症的发现,Z1R大鼠的葡萄糖代谢异常可能与B1R诱导不同。

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