Glucose deprivation accelerates VLDL receptor-mediated TG-rich lipoprotein uptake by AMPK activation in skeletal muscle cells

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• 作者：Yasuo Zenimaru ; Sadao Takahashi ; Masafumi Takahashi ; Kazuya Yamada ; Tadao Iwasaki ; Hiroaki Hattori ; Michiko Imagawa ; Masami Ueno ; Jinya Suzuki ; Isamu Miyamori
• 关键词：Energy switching ; Fatty acid metabolism ; Glucose metabolism ; Lipoprotein metabolism ; Skeletal muscle ; VLDL receptor ; AMP-activated protein kinase (AMPK) ; Metformin
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2008
• 出版时间：11 April 2008
• 年：2008
• 卷：368
• 期：3
• 页码：716-722
• 全文大小：496 K

文摘

Glucose and fatty acids are major energy sources in skeletal muscle. Very low-density lipoprotein receptor (VLDL-R), which is highly expressed in heart, skeletal muscle and adipose tissue, plays a crucial role in metabolism of triglyceride (TG)-rich lipoproteins. To explore energy switching between glucose and fatty acids, we studied expression of VLDL-R and lipoprotein uptake in rat L6 myoblasts. l-Glucose or d-glucose deprivation in the medium noticeably induced the AMPK (AMP-activated protein kinase) activation and VLDL-R expression. Dose-dependent induction of VLDL-R expression was observed when d-glucose was less than 4.2 mM. The same phenomenon was also observed in rat primary skeletal myoblasts and cultured vascular smooth muscle cells. The uptake of β-VLDL but not LDL was accompanied by induction of VLDL-R expression. Our study suggests that the VLDL-R-mediated uptake of TG-rich lipoproteins might compensate for glucose shortfall through AMPK activation in skeletal muscle.