限制碳水化合物摄入可抑制小鼠的心脏肥大及心衰
创作:药农 审核:szx 2020年10月25日
  • 主动脉狭窄小鼠模型随机分为3组,分别摄入:高脂肪LC饮食、高蛋白LC饮食、高碳水化合物对照饮食,干预4周;
  • 与对照组相比,LC饮食抑制小鼠心脏病理性肥大及收缩功能障碍的发展;
  • 高蛋白(而非高脂肪)LC饮食通过激活丝氨酸/苏氨酸激酶GSK-3β以抑制心脏肥大;
  • 高脂肪(而非高蛋白)LC饮食对心脏GSK-3β特异性敲除小鼠的心脏也具有保护作用,通过增加小鼠心脏中的β-羟基丁酸,以抑制mTOR信号,从而抑制心肌细胞肥大。
主编推荐语
szx
Cardiovascular Research上发表的一项最新研究,发现严格限制饮食中的碳水化合物摄入可缓解小鼠的心脏肥大及心衰进展。其中,高蛋白低碳水化合物(LC)饮食通过激活丝氨酸/苏氨酸激酶GSK-3β,以抑制心脏肥大;而高脂肪LC饮食通过增加小鼠心脏中的酮体(β-羟基丁酸)以抑制mTOR信号,从而起到心脏保护作用。
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Dietary Carbohydrates Restriction Inhibits The Development Of Cardiac Hypertrophy And Heart Failure

限制膳食碳水化合物可抑制心脏肥大和心力衰竭的发展

10.1093/cvr/cvaa298

2020-10-18, Article

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Aims: A diet with modified components, such as a ketogenic low-carbohydrate (LC) diet, potentially extends longevity and healthspan. However, how a LC diet impacts on cardiac pathology during hemodynamic stress remains elusive. This study evaluated the effects of a LC diet high in either fat (Fat-LC) or protein (Pro-LC) in a mouse model of chronic hypertensive cardiac remodeling.
Methods and Results: Wild-type mice were subjected to transverse aortic constriction, followed by feeding with the Fat-LC, the Pro-LC, or a high-carbohydrate control diet. After 4 weeks, echocardiographic, hemodynamic, histological and biochemical analyses were performed. LC diet consumption after pressure overload inhibited the development of pathological hypertrophy and systolic dysfunction compared to the control diet. An anti-hypertrophic serine/threonine kinase, GSK-3β, was re-activated by both LC diets; however, the Fat-LC, but not the Pro-LC, diet exerted cardioprotection in GSK-3β cardiac-specific knockout mice. β-hydroxybutyrate, a major ketone body in mammals, was increased in the hearts of mice fed the Fat-LC, but not the Pro-LC, diet. In cardiomyocytes, ketone body supplementation inhibited phenylephrine-induced hypertrophy, in part by suppressing mTOR signaling.
Conclusions: Strict carbohydrate restriction suppresses pathological cardiac growth and heart failure after pressure overload through distinct anti-hypertrophic mechanisms elicited by supplemented macronutrients.
Translational Perspective: Hemodynamic stress, such as hypertension, induces pathological cardiac hypertrophy, leading to heart failure. There is growing evidence that modulating components of diet affects cardiac function in humans, although the causality and underlying mechanisms are poorly understood. Our study demonstrates that strict restriction of dietary carbohydrates supplemented with either fat or proteins during acute hemodynamic stress attenuates the development and progression of cardiac hypertrophy and heart failure by activating distinct anti-hypertrophic and cardioprotective signaling mechanisms. The study suggests that it would be useful to investigate the therapeutic benefit of carbohydrate restriction in patients with hypertension and cardiac hypertrophy in clinical studies.

First Authors:
Michinari Nakamura

Correspondence Authors:
Junichi Sadoshima

All Authors:
Michinari Nakamura,Natalija Odanovic,Yasuki Nakada,Satomi Dohi,Peiyong Zhai,Andreas Ivessa,Zhi Yang,Maha Abdellatif,Junichi Sadoshima

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