title: Glucose deprivation accelerates VLDL receptor-mediated TG-rich lipoprotein uptake by AMPK activation in skeletal muscle cells.
abstract: 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 4.2mM. The same phenomenon was also observed in rat primary skeletal myoblasts and cultured vascular smooth muscle cells. The uptake of beta-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.
authors.affiliation: Third Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Eiheiji-cho, Fukui 910-1193, Japan.
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Zenimaru
authors.forename: Sadao
authors.initials: S
authors.lastname: Takahashi
authors.forename: Masafumi
authors.initials: M
authors.lastname: Takahashi
authors.forename: Kazuya
authors.initials: K
authors.lastname: Yamada
authors.forename: Tadao
authors.initials: T
authors.lastname: Iwasaki
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Hattori
authors.forename: Michiko
authors.initials: M
authors.lastname: Imagawa
authors.forename: Masami
authors.initials: M
authors.lastname: Ueno
authors.forename: Jinya
authors.initials: J
authors.lastname: Suzuki
authors.forename: Isamu
authors.initials: I
authors.lastname: Miyamori
mesh_terms: D000091162:AMP-Activated Protein Kinase Kinases; D000818:Animals; D002460:Cell Line; D004789:Enzyme Activation; D005227:Fatty Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D008074:Lipoproteins / Q000378:metabolism*; D018485:Muscle Fibers, Skeletal / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D011494:Protein Kinases / Q000378:metabolism*; D051381:Rats; D011973:Receptors, LDL / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D005227:Fatty Acids; D008074:Lipoproteins; D011973:Receptors, LDL; D014280:Triglycerides; C036053:VLDL receptor; D011494:Protein Kinases; D000091162:AMP-Activated Protein Kinase Kinases; D005947:Glucose