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燃料稳态和运动行为:瘦素和黑素皮质素途径的作用。

Fuel homeostasis and locomotor behavior: role of leptin and melanocortin pathways.

机构信息

Obesity Center at the Endocrine Unit, University Hospital of Pisa, Pisa, Italy.

National Research Council, Institute of Clinical Physiology, Pisa, Italy.

出版信息

J Endocrinol Invest. 2015 Feb;38(2):125-31. doi: 10.1007/s40618-014-0225-z. Epub 2014 Dec 13.

Abstract

BACKGROUND

While it is now accepted that genes and their products affect food intake, the concept that locomotor behavior or the propensity for physical activity is controlled by neuro hum oral regulators is frequently underappreciated. In mammals, complex interactions have developed to allow the cross-talk between fuel homeostasis and physical activity.

AIM

The aim of this review is to provide a synopsis of the influence of the leptin-melanocortin pathway, a well-studied pivotal player in body weight regulation, on locomotor behaviors.

CONCLUSIONS

In rodents, reductions in leptin levels that physiologically occur following acute food deprivation or a reduction of the fat mass consequent to prolonged caloric restrictions are associated with a decrease in total locomotor activity and simultaneous increase in food-anticipatory activity, a locomotor behavior which reflects a foraging attitude. These actions can be prevented by leptin administration and are at least partially mediated by the neurons of the melanocortin pathway. In humans, twin studies have attributed to genetic factors approximately 50% of the variance of physical activity. An elevated number of the genes or loci which may affect physical activity are involved in body weight homeostasis. Polymorphisms of the melanocortin-4 and leptin receptors have repeatedly been associated with the level of physical activity. Unraveling the complexity of the regulation of locomotor behavior and the interconnections with the pathways involved in energy homeostasis may help explain the substantial individual variability in physical activities in humans and disentangle the harmful effects of sedentary lifestyle, which may be distinct from the detrimental effects of obesity.

摘要

背景

虽然现在人们已经接受了基因及其产物会影响食物摄入,但运动行为或身体活动倾向受神经激素调节控制的概念常常被低估。在哺乳动物中,已经发展出了复杂的相互作用,以允许燃料平衡和身体活动之间的交流。

目的

本综述的目的是概述瘦素-黑皮质素途径对运动行为的影响,该途径是体重调节中研究得很好的关键参与者。

结论

在啮齿动物中,急性禁食或长期热量限制导致脂肪量减少后,生理上瘦素水平的降低与总运动活动的减少和同时的食物预期活动的增加有关,这种运动行为反映了觅食态度。瘦素的给予可以预防这些作用,并且至少部分是由黑皮质素途径的神经元介导的。在人类中,双胞胎研究将身体活动的 50%左右归因于遗传因素。涉及体重稳态的基因或基因座的数量增加可能会影响身体活动。黑皮质素 4 和瘦素受体的多态性与身体活动水平反复相关。阐明运动行为的调节复杂性以及与能量稳态相关途径的相互联系,可能有助于解释人类身体活动的个体差异,并阐明久坐生活方式的有害影响,这可能与肥胖的有害影响不同。

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