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首页> 外文期刊>American Journal of Physiology >Microvascular insulin resistance in skeletal muscle and brain occurs early in the development of juvenile obesity in pigs
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Microvascular insulin resistance in skeletal muscle and brain occurs early in the development of juvenile obesity in pigs

机译：骨骼肌和脑中的微血管胰岛素抵抗力在猪的少年肥胖的发展早期发生

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Impaired microvascular insulin signaling may develop before overt indices of microvascular endothelial dysfunction and represent an early pathological feature of adolescent obesity. Using a translalional porcine model of juvenile obesity, we tested the hypotheses that in the early stages of obesity development, impaired insulin signaling manifests in skeletal muscle (triceps), brain (prefrontal cortex), and corresponding vasculatures, and that depressed insulin-induced vasodilation is reversible with acute inhibition of protein kinase Cβ (PKCP). Juvenile Ossabaw miniature swine (3.5 mo of age) were divided into two groups: lean control (n = 6) and obese (n = 6). Obesity was induced by feeding the animals a high-fat/high-fructose corn syrup/high-cholesterol diet for 10 wk. Juvenile obesity was characterized by excess body mass, hyperglycemia, physical inactivity (accelerometer), and marked lipid accumulation in the skeletal muscle, with no evidence of overt atherosclerotic lesions in athero-prone regions, such as the abdominal aorta. Endothelium-dependent (bradykinin) and -independent (sodium nitroprusside) vasomotor responses in the brachial and carotid arteries (wire myography), as well as in the skeletal muscle resistance and 2A pial arterioles (pressure myography) were unaltered, but insulin-induced microvascular vasodilation was impaired in the obese group. Blunted insulin-stimulated vasodilation, which was reversed with acute PKCp inhibition (LY333-531), occurred alongside decreased tissue perfusion, as well as reduced insulin-stimulated Akt signaling in the prefrontal cortex, but not the triceps. In the early stages of juvenile obesity development, the microvasculature and prefrontal cortex exhibit impaired insulin signaling. Such adaptations may underscore vascular and neurological derangements associated with juvenile obesity.
机译：在微血管内皮功能障碍的公开索引之前，微血管胰岛素信号传导可能发生受损，并且代表青少年肥胖的早期病理特征。使用少年肥胖的透视猪模型，我们测试了在肥胖发展早期阶段的假设，骨骼肌（三头肌），脑（前额叶皮质）和相应的血管内患者患有胰岛素信号传导效果，并且抑郁肠道诱导的血管舒张可逆蛋白激酶Cβ（PKCP）的急性抑制。少年Ossabaw微型猪（3.5月）分为两组：瘦控制（n = 6）和肥胖（n = 6）。通过将动物喂养高脂肪/高果糖玉米糖浆/高胆固醇饮食诱发肥胖诱导10周。少年肥胖的特征在于体重过剩，高血糖，物理不活动（加速度计），并在骨骼肌中标记脂质积累，没有明显动脉粥样硬化病变的证据，例如腹部主动脉。依赖于内皮依赖性（Bradykinin）和 - 依赖性（硝普隆钠）肱动脉（肌瘤动脉（肌动脉肌动脉（Wirceography）以及骨骼肌抗性和2A小粒子动脉杆菌（压力肌图）的血管瘤反应，但胰岛素诱导的微血管肥胖群体受到血管稀释。钝化胰岛素刺激的血管舒张，其与急性PKCP抑制（LY333-531）反转，同时发生了减少的组织灌注，以及预先甲基皮质中的胰岛素刺激的AKT信号传导，但不是TRISTESP。在青少年肥胖发展的早期阶段，微血管结构和前额叶皮质表现出胰岛素信号传导受损。这种适应可能会强调与少年肥胖相关的血管和神经紊乱。

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