Abstract
LPL is an enzyme involved in the breakdown and uptake of lipoprotein triglycerides. In the present study, we examined how the transgenic (Tg) overexpression of human LPL in mouse skeletal muscle affected tolerance to cold temperatures, cold-induced thermogenesis, and fuel utilization during this response. Tg mice and their nontransgenic controls were placed in an environmental chamber and housed in metabolic chambers that monitored oxygen consumption and carbon dioxide production with calorimetry. When exposed to 4 degrees C, an attenuation in the decline in body temperature in Tg mice was accompanied by an increased metabolic rate (15%; P < 0.001) and a reduction in respiratory quotient (P < 0.05). Activity levels, the expression of uncoupling proteins in brown fat and muscle, and lean mass failed to explain the enhanced cold tolerance and thermogenesis in Tg mice. The more oxidative type IIa fibers were favored over the more glycolytic type IIb fibers (P < 0.001) in the gastrocnemius and quadriceps muscles of Tg mice. These data suggest that Tg overexpression of LPL in skeletal muscle increases cold tolerance by enhancing the capacity for fat oxidation, producing an avian-like phenotype in which skeletal muscle contributes significantly to the thermogenic response to cold temperatures.
Highlights
LPL is an enzyme involved in the breakdown and uptake of lipoprotein triglycerides
Nonshivering thermogenesis (NST) becomes the critical source of internal heat and is thought to occur primarily in brown adipose tissue (BAT), where mitochondrial respiration is uncoupled by uncoupling protein-1 (UCP-1) [3]
We report a novel role of skeletal muscle LPL in the thermoregulation of mice during cold exposure
Summary
LPL is an enzyme involved in the breakdown and uptake of lipoprotein triglycerides. In the present study, we examined how the transgenic (Tg) overexpression of human LPL in mouse skeletal muscle affected tolerance to cold temperatures, cold-induced thermogenesis, and fuel utilization during this response. The more oxidative type IIa fibers were favored over the more glycolytic type IIb fibers (P , 0.001) in the gastrocnemius and quadriceps muscles of Tg mice These data suggest that Tg overexpression of LPL in skeletal muscle increases cold tolerance by enhancing the capacity for fat oxidation, producing an avian-like phenotype in which skeletal muscle contributes significantly to the thermogenic response to cold temperatures.—Jensen, D. Nonshivering thermogenesis (NST) becomes the critical source of internal heat and is thought to occur primarily in brown adipose tissue (BAT), where mitochondrial respiration is uncoupled by uncoupling protein-1 (UCP-1) [3] Both the activity and mass of BAT increase with cold exposure [1], and cold intolerance is exhibited in mice with no BAT [4], no UCP-1 [5], or without the ability to synthesize noradrenaline or adrenaline [6]. Given the importance of skeletal muscle in whole body fuel metabolism and the critical role of LPL in fuel trafficking, we have pursued a better understanding of the function of skeletal muscle LPL in adapting to metabolic stress
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