Objective

To investigate the effects of GH signaling on Kupffer cells and the resulting changes in lipid homeostasis and their underlying mechanism(s) in the livers of diet-induced obese (DIO) mice.

Design

Male macrophage specific-growth hormone receptor knockout mice (MacGHR KO) and their litter mate controls were fed a high fat diet containing 60% calories from fat for 26 weeks. Lipid content and lipid profiles in the liver and circulation were analyzed. Expression levels of CD36 in the liver were quantified by RT-PCR and Western Blot.

Results

Increased hepatic lipid content and abundance of long-chain unsaturated fatty acids were observed in the liver of MacGHR KO mice. These findings were associated with increased steady state levels of CD36 mRNA and protein in MacGHR KO mice when compared with their litter mate controls.

Conclusion

GH action in Kupffer cells is required for maintaining hepatic lipid homeostasis, in part via regulation of hepatic CD36 expression.

中文翻译：

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枯否细胞中GH作用的丧失导致肝CD36表达增加和夸张的非酒精性脂肪肝疾病。

目的

研究GH信号对Kupffer细胞的影响以及由此引起的饮食诱导型肥胖（DIO）小鼠肝脏脂质稳态的变化及其潜在机制。

设计

雄性巨噬细胞特异性生长激素受体敲除小鼠（MacGHR KO）及其同窝伴侣对照组接受了高脂肪饮食，其中包含60％的卡路里来自脂肪的食物，持续26周。分析肝脏和循环中的脂质含量和脂质谱。通过RT-PCR和Western Blot对肝脏中CD36的表达水平进行定量。

结果

在MacGHR KO小鼠肝脏中观察到肝脂质含量增加和长链不饱和脂肪酸丰富。这些发现与MacGHR KO小鼠与其同伴对照相比，CD36 mRNA和蛋白的稳态水平升高有关。

结论

库普弗细胞中的GH作用对于维持肝脂质稳态是必需的，部分是通过调节肝CD36的表达来实现的。