Song S
Department of Medicine, University of Melbourne, Australia.
Med Hypotheses. 2000 May;54(5):739-47. doi: 10.1054/mehy.1999.0943.
Recent studies have shown that increased hepatic gluconeogenesis is the predominant contributor to fasting hyperglycemia - the hallmark of type 2 diabetes. Although it has been known for a long time that over-supply of fat is able to stimulate gluconeogenesis both in-vitro and in-vivo, neither the leading substrate nor the mechanism responsible for this phenomenon have been fully identified. Recent observations that the glyoxylate pathway may exist in animals has shed light on this question. The glyoxylate pathway is able to convert fatty acid into glucose but has been thought to be absent in animals. Although further evidence is needed, current available data does suggest a possible mechanism which, by integrating both glucose and lipid metabolism together rather than interpreting them separately, may explain the role of fatty acids in hepatic insulin resistance. This hypothesis is based on current understanding of insulin resistance and supported by many laboratory observations.
最近的研究表明，肝脏糖异生增加是空腹血糖升高的主要原因，而空腹血糖升高是2型糖尿病的标志。尽管长期以来人们都知道脂肪供应过多能够在体外和体内刺激糖异生，但导致这种现象的主要底物和机制都尚未完全明确。最近关于乙醛酸循环途径可能存在于动物体内的观察结果为这个问题提供了线索。乙醛酸循环途径能够将脂肪酸转化为葡萄糖，但一直被认为在动物体内不存在。尽管还需要进一步的证据，但目前可得的数据确实提示了一种可能的机制，该机制通过将葡萄糖和脂质代谢整合在一起而非分别进行解读，可能解释脂肪酸在肝脏胰岛素抵抗中的作用。这一假说基于对胰岛素抵抗的当前理解，并得到了许多实验室观察结果的支持。
