Differential regulation of leptin expression and function in A/J vs. C57BL/6J mice during diet-induced obesity.

Differential regulation of leptin expression and function in A/J vs. C57BL/6J mice during diet-induced obesity.
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DOI:
10.1152/ajpendo.2000.279.2.e356
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发表时间:
2000-08
期刊:
American journal of physiology. Endocrinology and metabolism
影响因子:
--
通讯作者:
P. Watson;S. Commins;Rudolph J. Beiler;H. Hatcher;T. Gettys
P. Watson;S. Commins;Rudolph J. Beiler;H. Hatcher;T. Gettys
中科院分区:
其他
文献类型:
--
作者:
P. Watson;S. Commins;Rudolph J. Beiler;H. Hatcher;T. Gettys

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肥胖抵抗(A/J)和肥胖倾向(C57 BL/6 J)小鼠断奶到低脂肪(LF)或高脂肪(HF)的饮食和研究后2,10和16周。尽管消耗了相同量的食物,但在研究过程中,HF饮食的A/J小鼠沉积的胴体脂质较少,体重增加也比C57 BL/6 J小鼠少。在HF饮食的两种品系中,白色脂肪组织(WAT)中的瘦素mRNA均增加,但A/J小鼠中的瘦素mRNA水平显著高于C57 BL/6 J小鼠。解偶联蛋白1(UCP 1)和UCP 2 mRNA在A/J小鼠的棕色脂肪组织(BAT)和WAT中分别被HF饮食诱导,但在C57 BL/6 J小鼠中不被诱导。UCP 1 mRNA在A/J小鼠腹膜后WAT中的表达也显著高于C57 BL/6 J小鼠。A/J小鼠抵抗饮食诱导的肥胖的能力与脂肪组织中瘦素、UCP 1和UCP 2表达的品系特异性增加相关。研究结果表明,HF饮食不损害瘦素依赖性调节A/J小鼠的脂肪细胞基因表达,并表明维持瘦素反应赋予抵抗饮食诱导的肥胖。
Obesity-resistant (A/J) and obesity-prone (C57BL/6J) mice were weaned onto low-fat (LF) or high-fat (HF) diets and studied after 2, 10, and 16 wk. Despite consuming the same amount of food, A/J mice on the HF diet deposited less carcass lipid and gained less weight than C57BL/6J mice over the course of the study. Leptin mRNA was increased in white adipose tissue (WAT) in both strains on the HF diet but to significantly higher levels in A/J compared with C57BL/6J mice. Uncoupling protein 1 (UCP1) and UCP2 mRNA were induced by the HF diet in brown adipose tissue (BAT) and WAT of A/J mice, respectively, but not in C57BL/6J mice. UCP1 mRNA was also significantly higher in retroperitoneal WAT of A/J compared with C57BL/6J mice. The ability of A/J mice to resist diet-induced obesity is associated with a strain-specific increase in leptin, UCP1, and UCP2 expression in adipose tissue. The findings indicate that the HF diet does not compromise leptin-dependent regulation of adipocyte gene expression in A/J mice and suggest that maintenance of leptin responsiveness confers resistance to diet-induced obesity.