Sanford-Burnham Medical Research Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA.
Trends Endocrinol Metab. 2011 Feb;22(2):45-52. doi: 10.1016/j.tem.2010.11.002. Epub 2011 Jan 7.
The global prevalence of obesity has grown to epidemic proportions, and 400 million people are now considered to be obese. Excessive accumulation of dietary lipids (obesity) is a known risk factor for the development of deleterious metabolic conditions and has been strongly linked to the progression of heart disease and type 2 diabetes. Investigating the origin and effects of high-fat diet (HFD)-induced obesity and its genetic mediators is an important step in understanding the mechanisms that contribute to obesity. However, the mechanisms that underlie HFD pathophysiology have yet to be elucidated fully. Here we describe recent work in a Drosophila model to investigate the origin and genetic mechanisms that could underlie HFD-induced obesity, type 2 diabetes and cardiac dysfunction.
全球肥胖症的患病率已上升到流行程度,目前有 4 亿人被认为患有肥胖症。饮食脂质的过度积累(肥胖)是发生有害代谢状况的已知风险因素,并且与心脏病和 2 型糖尿病的进展密切相关。研究高脂肪饮食(HFD)诱导的肥胖及其遗传介质的起源和作用是理解导致肥胖的机制的重要步骤。然而,HFD 病理生理学的机制尚未完全阐明。在这里,我们描述了在果蝇模型中进行的最新研究工作,以研究可能导致 HFD 诱导的肥胖、2 型糖尿病和心脏功能障碍的起源和遗传机制。