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青春期饮食诱导肥胖大鼠心肌去神经适应的机械变化。

Mechanical adaptations of skinned cardiac muscle in response to dietary-induced obesity during adolescence in rats.

机构信息

Faculty of Kinesiology, University of Calgary, Calgary, AB T2N 1N4, Canada.

Human Performance Laboratory, University of Calgary, Calgary, AB T2N 1N4, Canada.

出版信息

Appl Physiol Nutr Metab. 2020 Aug;45(8):893-901. doi: 10.1139/apnm-2019-0726. Epub 2020 Mar 5.

Abstract

Childhood obesity is a major risk factor for heart disease during adulthood, independent of adulthood behaviours. Therefore, it seems that childhood obesity leads to partly irreversible decrements in cardiac function. Little is known about how obesity during maturation affects the mechanical properties of the heart. The purpose of this study was to evaluate contractile properties in developing hearts from animals with dietary-induced obesity (high-fat high-sucrose diet). We hypothesized that obesity induced during adolescence results in decrements in cardiac contractile function. Three-week-old rats ( = 16) were randomized into control (chow) or dietary-induced obesity (high-fat high-sucrose diet) groups. Following 14 weeks on the diet, skinned cardiac trabeculae fibre bundle testing was performed to evaluate active and passive force, maximum shortening velocity, and calcium sensitivity. Rats in the high-fat high-sucrose diet group had significantly larger body mass and total body fat percentage. There were no differences in maximal active or passive properties of hearts between groups. Hearts from the high-fat high-sucrose diet rats had significantly slower maximum shortening velocities and lower calcium sensitivity than controls. Decreased shortening velocity and calcium sensitivity in hearts of obese animals may constitute increased risk of cardiac disease in adulthood. Cardiac muscle from animals exposed to an obesogenic diet during development had lower shortening velocity and calcium sensitivity than those from animals fed a chow diet. These alterations in mechanical function may be a mechanism for the increased risk of cardiac disease observed in adulthood.

摘要

儿童肥胖是成年后患心脏病的一个主要危险因素,与成年后的行为无关。因此,儿童肥胖似乎导致心脏功能部分不可逆转的下降。关于肥胖在成熟过程中如何影响心脏的机械性能知之甚少。本研究旨在评估饮食诱导肥胖(高脂肪高蔗糖饮食)动物发育中心脏的收缩性能。我们假设青春期肥胖会导致心脏收缩功能下降。将 3 周大的大鼠(n=16)随机分为对照组(常规饮食)或饮食诱导肥胖组(高脂肪高蔗糖饮食)。饮食 14 周后,进行去皮心肌横桥纤维束测试,以评估主动和被动力、最大缩短速度和钙敏感性。高脂肪高蔗糖饮食组大鼠的体重和体脂百分比明显更大。两组之间的心脏最大主动或被动性能没有差异。高脂肪高蔗糖饮食组大鼠的最大缩短速度明显较慢,钙敏感性也低于对照组。肥胖动物心脏的缩短速度和钙敏感性降低可能构成成年后患心脏病的风险增加。在发育过程中暴露于致肥胖饮食的动物的心肌比那些喂食常规饮食的动物的心肌缩短速度和钙敏感性更低。这些机械功能的改变可能是成年期观察到的心脏病风险增加的一种机制。

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