Chronic cold acclimation increases thermogenic capacity, non-shivering thermogenesis and muscle citrate synthase activity in both wild-type and brown adipose tissue deficient mice

Comp Biochem Physiol A Mol Integr Physiol. 2012 Apr;161(4):395-400. doi: 10.1016/j.cbpa.2011.12.012. Epub 2011 Dec 29.

Abstract

The purpose of this study was to determine whether chronic cold exposure would increase the aerobic capacity of skeletal muscle in UCP-dta mice, a transgenic line lacking brown adipose tissue (BAT). Wild type and UCP-dta mice were acclimated to either warm (23 °C), or cold (4 °C) conditions. Cold increased muscle oxidative capacity nearly equivalently in wild-type and UCP-dta mice, but did not affect the respiratory function of isolated mitochondria. Summit metabolism ( ̇V O2summit) and norepinephrine-induced thermogenesis ( ̇V O2NST) were significantly lower in UCP-dta mice relative to wild-type mice regardless of temperature treatment, but both were significantly higher in cold relative to warm acclimated mice. BAT mass was significantly higher in the cold relative to warm acclimated wild-type mice, but not in cold acclimated UCP-dta mice. BAT citrate synthase activity was lower in transgenic animals regardless of acclimation temperature and BAT citrate synthase activity per depot was significantly higher only in the cold acclimated wild-type mice. Muscle citrate synthase activity was increased in both genotypes. As defects in muscle oxidative function have been observed with obesity and type 2 diabetes, these results suggest that chronic cold exposure is a useful intervention to drive skeletal muscle oxidative capacity in mouse models of obesity.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acclimatization*
  • Adipose Tissue, Brown / metabolism*
  • Adipose Tissue, Brown / pathology
  • Animals
  • Body Weight
  • Cell Respiration
  • Citrate (si)-Synthase / metabolism*
  • Cold Temperature*
  • Diphtheria Toxin / genetics
  • Diphtheria Toxin / metabolism
  • Disease Models, Animal
  • Energy Metabolism*
  • Fatty Acids / metabolism
  • Genotype
  • Hypertrophy
  • Hypertrophy, Left Ventricular / metabolism
  • Hypertrophy, Left Ventricular / pathology
  • Ion Channels / genetics
  • Mice
  • Mice, Transgenic
  • Mitochondria, Muscle / enzymology*
  • Mitochondrial Proteins / genetics
  • Muscle, Skeletal / enzymology*
  • Norepinephrine / pharmacology
  • Obesity / genetics
  • Obesity / metabolism*
  • Obesity / pathology
  • Oxidation-Reduction
  • Oxygen Consumption
  • Peptide Fragments / genetics
  • Peptide Fragments / metabolism
  • Phenotype
  • Promoter Regions, Genetic
  • Shivering
  • Thermogenesis* / drug effects
  • Time Factors
  • Uncoupling Protein 1

Substances

  • Diphtheria Toxin
  • Fatty Acids
  • Ion Channels
  • Mitochondrial Proteins
  • Peptide Fragments
  • Uncoupling Protein 1
  • diphtheria toxin fragment A
  • Citrate (si)-Synthase
  • Norepinephrine