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脂肪储存部分依赖于下丘脑肥胖大鼠的迷走神经活动和胰岛素分泌。

Fat storage is partially dependent on vagal activity and insulin secretion of hypothalamic obese rat.

作者信息

Balbo Sandra Lucinei, Grassiolli Sabrina, Ribeiro Rosane Aparecida, Bonfleur Maria Lúcia, Gravena Clarice, Brito Marcia do Nascimento, Andreazzi Ana Eliza, Mathias Paulo Cezar de Freitas, Torrezan Rosana

机构信息

Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Avenida Colombo 5790, Maringa, PR, 87020-900, Brazil.

出版信息

Endocrine. 2007 Apr;31(2):142-8. doi: 10.1007/s12020-007-0021-z.

Abstract

Hypothalamic MSG-obese rats show hyperinsulinemia and tissue insulin resistance, and they display intense parasympathetic activity. Current analysis investigates whether early subdiaphragmatic vagotomy prevents tissue insulin sensitivity impairment in adult obese MSG-rats. Hypothalamic obesity was induced by MSG (4 mg/g BW), daily, from birth up to 5 days. Control animals receiving saline solution. On the 30th day rats underwent bilateral subdiaphragmatic vagotomy or sham surgery. An intravenous glucose tolerance test (i.v.GTT) was performed when rats turned 90 days old. Total white fat tissue (WAT) from rat carcass was extracted and isolated; the interscapular brown fat tissue (IBAT) was weighed. Rather than blocking obesity, vagotomy reduced WAT and IBAT in MSG-obese rats when the latter were compared to sham MSG-rats. High blood fasting insulin and normal glucose levels were also observed in MSG-obese rats. Although glucose intolerance, high insulin secretion, and significant insulin resistance were recorded, vagotomy improved fasting insulinemia, glucose tolerance and insulin tissue sensitivity in MSG-obese rats. Results suggest that increased fat accumulation is caused, at least in part, by high blood insulin concentration, and enhanced parasympathetic activity on MSG-obese rats.

摘要

下丘脑味精致肥胖大鼠表现出高胰岛素血症和组织胰岛素抵抗,且呈现强烈的副交感神经活动。当前分析研究早期膈下迷走神经切断术是否能预防成年肥胖味精大鼠的组织胰岛素敏感性受损。从出生到5天,每天用味精(4毫克/克体重)诱导下丘脑肥胖。对照动物注射生理盐水。在第30天,大鼠接受双侧膈下迷走神经切断术或假手术。当大鼠90日龄时进行静脉葡萄糖耐量试验(i.v.GTT)。提取并分离大鼠尸体的总白色脂肪组织(WAT);称量肩胛间棕色脂肪组织(IBAT)。与假手术味精大鼠相比,迷走神经切断术并没有阻止味精肥胖大鼠肥胖,反而使其白色脂肪组织和肩胛间棕色脂肪组织减少。味精肥胖大鼠还出现空腹血胰岛素水平高和血糖正常的情况。尽管记录到葡萄糖不耐受、高胰岛素分泌和显著的胰岛素抵抗,但迷走神经切断术改善了味精肥胖大鼠的空腹胰岛素血症、葡萄糖耐量和胰岛素组织敏感性。结果表明,脂肪堆积增加至少部分是由高血胰岛素浓度以及味精肥胖大鼠副交感神经活动增强所致。

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