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首页> 外文期刊>Life sciences >Central melanocortin receptor agonist reduces hepatic lipogenic gene expression in streptozotocin-induced diabetic mice.
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Central melanocortin receptor agonist reduces hepatic lipogenic gene expression in streptozotocin-induced diabetic mice.

机译：中央黑皮质素受体激动剂降低链脲佐菌素诱导的糖尿病小鼠肝脂肪基因的表达。

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AIMS: The central melanocortin system regulates a variety of metabolic functions including lipid metabolism and hepatic lipogenic gene expression. The objective of the present study was to determine whether central melanocortin regulates hepatic lipogenic gene expression under insulin insufficient condition. MAIN METHODS: We examined the effect of intracerebroventricular (i.c.v.) injection of MTII, a melanocortin agonist, on hepatic gene expression in a mouse model of the insulin-deficient diabetes. Diabetes was induced in male C57BL/6J mice by intraperitoneal injections of streptozotocin (STZ). Diabetic mice received daily i.c.v. injections of MTII (3 nmol) for 11 days. Hepatic expression levels of lipogenic genes and their transcription factors were measured. KEY FINDINGS: MTII treatment significantly reduced hepatic expression levels of genes encoding lipid biosynthetic enzymes, stearoyl-CoA desaturase 1 (SCD1), glycerol-3-phosphate acyltransferase 1 (GPAT1), acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1), and DGAT2 mRNA without significant changes in serum insulin levels, homeostasis model-assessment of insulin resistance (HOMA-IR) and glucose tolerance in STZ-induced diabetic mice. MTII treatment also reduced fatty acid synthase (FAS) and SCD1 protein levels in the liver of diabetic mice. Expression levels of genes encoding transcription factors of these lipogenic genes, sterol regulatory element-binding protein 1c (SREBP-1c) and peroxisome proliferator-activated receptor gamma2 (PPARgamma2) were also significantly reduced by MTII treatment. SIGNIFICANCE: These data suggest that the insulin-independent mechanism is involved in the regulation of hepatic lipogenic gene expression. Enhanced central melanocortin signaling may be effective in improving abnormal lipid metabolism associated with insulin-deficiency or insulin-insufficiency.
机译：目的：中央黑皮质素系统调节多种代谢功能，包括脂质代谢和肝脂肪形成基因表达。本研究的目的是确定在胰岛素不足的情况下中枢黑皮质素是否调节肝脂肪基因的表达。主要方法：我们检查了脑室内（i.c.v.）注射MTII（一种黑皮质素激动剂）对胰岛素缺乏型糖尿病小鼠模型中肝基因表达的影响。通过腹膜内注射链脲佐菌素（STZ）在雄性C57BL / 6J小鼠中诱发糖尿病。糖尿病小鼠每天接受腹腔注射。注射MTII（3 nmol），持续11天。测量脂肪形成基因的肝表达水平及其转录因子。关键发现：MTII处理显着降低了编码脂质生物合成酶，硬脂酰辅酶A去饱和酶1（SCD1），3-磷酸甘油酰基转移酶1（GPAT1），酰基-CoA：二酰基甘油酰基转移酶1（DGAT1）和DGAT2的基因的肝表达水平。在STZ诱导的糖尿病小鼠中，血清胰岛素水平，稳态模型评估的胰岛素抵抗（HOMA-IR）和葡萄糖耐量没有显着变化的mRNA。 MTII治疗还降低了糖尿病小鼠肝脏中的脂肪酸合酶（FAS）和SCD1蛋白水平。 MTII处理也显着降低了编码这些脂肪形成基因，固醇调节元件结合蛋白1c（SREBP-1c）和过氧化物酶体增殖物激活受体gamma2（PPARgamma2）转录因子的基因的表达水平。意义：这些数据表明胰岛素非依赖性机制参与肝脂肪形成基因表达的调节。增强的中心黑皮质素信号传导可能有效改善与胰岛素缺乏或胰岛素不足有关的异常脂质代谢。

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