Diet-induced obese rats exhibit impaired LKB1-AMPK signaling in hypothalamus and adipose tissue

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• 作者：Fei-Wang^a ; ^c ; De-Run Tian^b ; ^{tiandr@tijmu.edu.cn} ; Patrick Tso^c ; Ji-Sheng Han^a
• 关键词：Diet-induced obesity ; AMPK ; LKB1 ; NPY ; POMC
• 刊名：Peptides
• 出版年：2012
• 期刊代码：59_01969781
• 类别：neu
• 出版时间：May, 2012
• 卷：35
• 期：1
• 页码：23-30
• 文件大小：1299 K

摘要

AMPK not only acts as a sensor of cellular energy status but also plays a critical role in the energy balance of the body. In this study, LKB1-AMPK signaling was investigated in diet-induced obese (DIO) and diet resistant (DR) rats. In hypothalamus, DIO rats had lower level of LKB1, AMPK伪 and pAMPK伪 than chow-fed or DR rats. Both orexigenic peptide NPY and anorexigenic peptide POMC expression were reduced in hypothalamus of DIO rats. i.c.v. injection of AICAR, an activator of AMPK, increased NPY expression but did not alter POMC expression in DIO rats. In periphery, LKB1 protein content and pAMPK伪 level were lower in the adipose tissue of DIO rats compared to chow-fed and DR rats. Moreover, pAMPK伪 and LKB1 protein levels obtained from epididymal fat pad were inversely correlated with epididymal fat mass. LKB1 protein content and pAMPK伪 in skeletal muscle of DIO rats were not different from those in the muscles of chow-fed and DR rats. In summary, DIO rats, but not DR rats, have impaired LKB1-AMPK signaling in hypothalamus and adipose tissue, suggesting the disturbed energy balance observed in DIO rats is related with abnormalities of AMPK signaling in a tissue specific manner.