title: ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes.
abstract: BACKGROUND
  Free fatty acids released from adipose tissue affect the synthesis of apolipoprotein B-containing lipoproteins and glucose metabolism in the liver. Whether there also exists a reciprocal metabolic arm affecting energy metabolism in white adipose tissue is unknown.
  
  
  RESULTS
  We investigated the effects of apoB-containing lipoproteins on catecholamine-induced lipolysis in adipocytes from subcutaneous fat cells of obese but otherwise healthy men, fat pads from mice with plasma lipoproteins containing high or intermediate levels of apoB100 or no apoB100, primary cultured adipocytes, and 3T3-L1 cells. In subcutaneous fat cells, the rate of lipolysis was inversely related to plasma apoB levels. In human primary adipocytes, LDL inhibited lipolysis in a concentration-dependent fashion. In contrast, VLDL had no effect. Lipolysis was increased in fat pads from mice lacking plasma apoB100, reduced in apoB100-only mice, and intermediate in wild-type mice. Mice lacking apoB100 also had higher oxygen consumption and lipid oxidation. In 3T3-L1 cells, apoB100-containing lipoproteins inhibited lipolysis in a dose-dependent fashion, but lipoproteins containing apoB48 had no effect. ApoB100-LDL mediated inhibition of lipolysis was abolished in fat pads of mice deficient in the LDL receptor (Ldlr(-/-)Apob(100/100)).
  
  
  CONCLUSIONS
  Our results show that the binding of apoB100-LDL to adipocytes via the LDL receptor inhibits intracellular noradrenaline-induced lipolysis in adipocytes. Thus, apoB100-LDL is a novel signaling molecule from the liver to peripheral fat deposits that may be an important link between atherogenic dyslipidemias and facets of the metabolic syndrome.
authors.affiliation: The Computational Medicine Group, Karolinska Institutet, Karolinska University Hospital, Solna, Stockholm, Sweden. josefin.skogsberg@ki.se
authors.forename: Josefin
authors.initials: J
authors.lastname: Skogsberg
authors.forename: Andrea
authors.initials: A
authors.lastname: Dicker
authors.forename: Mikael
authors.initials: M
authors.lastname: Rydén
authors.forename: Gaby
authors.initials: G
authors.lastname: Aström
authors.forename: Roland
authors.initials: R
authors.lastname: Nilsson
authors.forename: Hasanuzzaman
authors.initials: H
authors.lastname: Bhuiyan
authors.forename: Sigurd
authors.initials: S
authors.lastname: Vitols
authors.forename: Aline
authors.initials: A
authors.lastname: Mairal
authors.forename: Dominique
authors.initials: D
authors.lastname: Langin
authors.forename: Peteris
authors.initials: P
authors.lastname: Alberts
authors.forename: Erik
authors.initials: E
authors.lastname: Walum
authors.forename: Jesper
authors.initials: J
authors.lastname: Tegnér
authors.forename: Anders
authors.initials: A
authors.lastname: Hamsten
authors.forename: Peter
authors.initials: P
authors.lastname: Arner
authors.forename: Johan
authors.initials: J
authors.lastname: Björkegren
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000378:metabolism*; D052436:Adipose Tissue, White / Q000378:metabolism; D000328:Adult; D000368:Aged; D000818:Animals; D053299:Apolipoprotein B-100 / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008066:Lipolysis; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008099:Liver / Q000196:embryology / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism; D051379:Mice; D008875:Middle Aged; D050177:Overweight / Q000378:metabolism
chemical_list: D053299:Apolipoprotein B-100; D008077:Lipoproteins, LDL; D005947:Glucose