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首页> 外文期刊>Cell metabolism >Regulation of gluconeogenesis by Kruppel-like factor 15.
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Regulation of gluconeogenesis by Kruppel-like factor 15.

机译：通过Kruppel样因子15调节糖异生。

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摘要

In the postabsorptive state, certain tissues, including the brain, require glucose as the sole source of energy. After an overnight fast, hepatic glycogen stores are depleted, and gluconeogenesis becomes essential for preventing life-threatening hypoglycemia. Mice with a targeted deletion of KLF15, a member of the Kruppel-like family of transcription factors, display severe hypoglycemia after an overnight (18 hr) fast. We provide evidence that defective amino acid catabolism promotes the development of fasting hypoglycemia in KLF15-/- mice by limiting gluconeogenic substrate availability. KLF15-/- liver and skeletal muscle show markedly reduced mRNA expression of amino acid-degrading enzymes. Furthermore, the enzymatic activity of alanine aminotransferase (ALT), which converts the critical gluconeogenic amino acid alanine into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes. Consistent with this observation, intraperitoneal injection of pyruvate, but not alanine, rescues fasting hypoglycemia in KLF15-/- mice. We conclude that KLF15 plays an important role in the regulation of gluconeogenesis.
机译：在吸收后状态下，包括大脑在内的某些组织需要葡萄糖作为唯一的能量来源。过夜禁食后，肝糖原存储被耗尽，糖原异生对于预防威胁生命的低血糖至关重要。靶向KLF15（一种Kruppel样转录因子家族的成员）的靶点缺失的小鼠在禁食过夜（18小时）后显示严重的低血糖。我们提供的证据表明，有缺陷的氨基酸分解代谢通过限制糖异生底物的可用性促进了KLF15-/-小鼠的空腹低血糖症的发展。 KLF15-/-肝脏和骨骼肌显示出氨基酸降解酶的mRNA表达明显降低。此外，在KLF15-/-肝细胞中，将关键的糖异生氨基酸丙氨酸转化为丙酮酸的丙氨酸氨基转移酶（ALT）的酶活性降低了（约50％）。与该观察结果一致，腹膜内注射丙酮酸而非丙氨酸可挽救KLF15-/-小鼠的空腹低血糖。我们得出结论，KLF15在糖异生的调节中起重要作用。

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