Peroxisome proliferator-activated receptors as regulators of lipid metabolism; tissue differential expression in adipose tissues during cold acclimatization and hibernation of jerboa (Jaculus orientalis)

Biochimie. 2004 Nov;86(11):763-70. doi: 10.1016/j.biochi.2004.10.003.

Abstract

Brown (BAT) and white (WAT) adipose tissues play a key role in the body energy balance orchestrated by the central nervous system. Hibernators have developed a seasonal obesity to respond to inhospitable environment. Jerboa is one of the deep hibernator originated from sub-desert highlands. Thus, this animal represents an excellent model to study cold adaptation mechanism. We report that the adipogenic factor PPARgamma exhibits a differential expression between BAT and WAT at mRNA level. A specific induction was only seen in WAT of pre-hibernating jerboa. Interestingly, PPAR beta/delta is specifically induced in BAT and brain of pre-hibernating jerboa, highlighting for the first time the possible key role of this ubiquitous isoform in the cold adaptation of this true hibernator. Inductions of PPARgamma(2) in WAT and PPAR beta/delta in BAT are blunted by a hypolipemic drug, the ciprofibrate. These changes may be correlated with hibernation arrest and death of treated jerboa. Mitochondrial acyl-CoA dehydrogenase and peroxisomal acyl-CoA oxidase activities in brown and white adipose tissues are decreased up to 85% during cold acclimatization (without food privation). These enzyme activities are subject to a strong induction in BAT and in WAT (3.4-7.5 fold) during the hibernation period. The BAT thermogenesis marker is also largely induced (approximately 4 fold of UCP1 mRNA level) during pre-hibernation period. Unexpectedly, treatment with ciprofibrate deeply affects lipolysis in BAT by increasing acyl-CoA dehydrogenase activity (3.4 fold) and acyl-CoA oxidase at both activity and mRNA levels (2.8 and 3.8 fold, respectively) and enhances strongly UCP1 mRNA level (9.5 fold) during pre-hibernation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acclimatization / physiology*
  • Acyl-CoA Dehydrogenase / metabolism
  • Acyl-CoA Oxidase
  • Adipose Tissue / metabolism*
  • Animals
  • Carrier Proteins / drug effects
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism
  • Clofibric Acid / analogs & derivatives*
  • Clofibric Acid / pharmacology
  • Cold Temperature
  • Energy Metabolism
  • Fibric Acids
  • Gene Expression Regulation / genetics
  • Gene Expression Regulation / physiology*
  • Hibernation / drug effects
  • Hibernation / physiology*
  • Ion Channels
  • Lipid Metabolism*
  • Lipids / genetics
  • Membrane Proteins / drug effects
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Mitochondria / metabolism
  • Mitochondrial Proteins
  • Oxidoreductases / metabolism
  • Peroxisome Proliferator-Activated Receptors / genetics*
  • Peroxisome Proliferator-Activated Receptors / metabolism
  • Phospholipases / drug effects
  • Phospholipases / genetics
  • Phospholipases / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Rodentia
  • Uncoupling Protein 1

Substances

  • Carrier Proteins
  • Fibric Acids
  • Ion Channels
  • Lipids
  • Membrane Proteins
  • Mitochondrial Proteins
  • Peroxisome Proliferator-Activated Receptors
  • RNA, Messenger
  • Uncoupling Protein 1
  • Clofibric Acid
  • Oxidoreductases
  • peroxisomal acyl-CoA oxidase
  • Acyl-CoA Oxidase
  • Acyl-CoA Dehydrogenase
  • Phospholipases
  • ciprofibrate