Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA.
Trends Endocrinol Metab. 2013 Jan;24(1):4-12. doi: 10.1016/j.tem.2012.09.005. Epub 2012 Oct 5.
Fatty liver disease is epidemiologically associated with type 2 diabetes (T2D), leading to a speculation of a reciprocal cause-effect relationship and a vicious cycle of pathology. Here, we summarize recent literature reporting dissociation of hepatosteatosis from insulin resistance in genetic mouse models and clinical studies. We highlight rhythmic flows of metabolic intermediates between hepatic lipid synthesis and glucose production in normal circadian physiology. Blocking triglyceride (TG) secretion, subcellular lipid sequestration, lipolysis deficiency, enhanced lipogenesis, gluconeogenesis defects, or inhibition of fatty acid oxidation all result in hepatosteatosis without causing hyperglycemia or insulin resistance, suggesting that the cause-effect relationship between hepatosteatosis and diabetes does not exist in all situations.
脂肪肝疾病在流行病学上与 2 型糖尿病（T2D）相关，导致人们推测存在一种相互的因果关系和病理的恶性循环。在这里，我们总结了最近的文献报道，这些报道表明在遗传小鼠模型和临床研究中，肝脂肪变性与胰岛素抵抗分离。我们强调了正常昼夜生理中肝内脂质合成和葡萄糖生成之间代谢中间产物的节律性流动。阻断甘油三酯（TG）分泌、亚细胞脂质隔离、脂肪分解缺陷、增强的脂肪生成、糖异生缺陷或抑制脂肪酸氧化都会导致肝脂肪变性而不会引起高血糖或胰岛素抵抗，这表明肝脂肪变性和糖尿病之间的因果关系并非在所有情况下都存在。
