Key result
Acute immobilization stress in rats caused a rapid decrease in retroperitoneal white adipose tissue LPL activity and an increase in plasma LPL activity within 5 minutes.
Hypothesis-generating in rodents; leaves open whether acute stress modulates LPL activity in humans.
Tissue-specific regulation of LPL has been widely studied in rats. Previous studies reported that in vivo administration of adrenaline and acute stress cause an increase in plasma LPL activity coinciding with a decrease in white adipose tissue (WAT) LPL activity. We studied the speed of LPL activity changes during 30 min of stress by immobilization (IMMO) in rats. A first experimental approach in permanently cannulated rats permitted sequential blood sampling in the same animal during IMMO and the obtaining of hemodynamic parameters. In a second experimental approach, animals were euthanized at different times after the start of IMMO to determine LPL activity in tissues. Stress was characterized by rises in blood pressure, heart rate, plasma corticosterone, and available circulating energy substrates. Five min after the start of IMMO, LPL activity fell in retroperitoneal WAT and increased in plasma. These data show the quickest LPL activity change ever described in response to a physiological situation. The speed and simultaneity of these changes suggest that the release from endothelium to the bloodstream may constitute a fast nonexplored mechanism of tissue LPL activity regulation, involved in the lipid energy-substrate redistribution between tissues needed to prepare the "fight-or-flight" response.
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Casanovas et al. (2007) studied Acute stress. Immobilization (IMMO) stress was evaluated on LPL activity in retroperitoneal white adipose tissue and plasma. Acute immobilization stress in rats caused a rapid decrease in retroperitoneal white adipose tissue LPL activity and an increase in plasma LPL activity within 5 minutes.
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