Hollstein Tim, Piaggi Paolo
Obesity and Diabetes Clinical Research Section, Phoenix Epidemiology and Clinical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Phoenix, AZ, USA.
Department of Information Engineering, University of Pisa, Pisa, Italy.
Curr Obes Rep. 2020 Jun;9(2):121-135. doi: 10.1007/s13679-020-00371-4.
There is substantial inter-individual variability in body weight change, which is not fully accounted by differences in daily energy intake and physical activity levels. The metabolic responses to short-term perturbations in energy intake can explain part of this variability by quantifying the degree of metabolic "thriftiness" that confers more susceptibility to weight gain and more resistance to weight loss. It is unclear which metabolic factors and pathways determine this human "thrifty" phenotype. This review will investigate and summarize emerging research in the field of energy metabolism and highlight important metabolic mechanisms implicated in body weight regulation in humans.
Dysfunctional adipose tissue lipolysis, reduced brown adipose tissue activity, blunted fibroblast growth factor 21 secretion in response to low-protein hypercaloric diets, and impaired sympathetic nervous system activity might constitute important metabolic factors characterizing "thriftiness" and favoring weight gain in humans. The individual propensity to weight gain in the current obesogenic environment could be ascertained by measuring specific metabolic factors which might open up new pathways to prevent and treat human obesity.
个体间体重变化存在显著差异,每日能量摄入和身体活动水平的差异并不能完全解释这一现象。对能量摄入短期扰动的代谢反应可通过量化代谢“节俭”程度来解释部分差异,这种“节俭”会使人更易体重增加且更难减重。目前尚不清楚哪些代谢因素和途径决定了这种人类“节俭”表型。本综述将研究并总结能量代谢领域的最新研究,突出与人类体重调节相关的重要代谢机制。
脂肪组织脂解功能障碍、棕色脂肪组织活性降低、对低蛋白高热量饮食的成纤维细胞生长因子21分泌减弱以及交感神经系统活性受损,可能构成表征人类“节俭”并促进体重增加的重要代谢因素。通过测量特定代谢因素,可确定个体在当前致胖环境中体重增加的倾向,这可能为预防和治疗人类肥胖开辟新途径。