Abstract
BackgroundThe aim of the present study was to test the hypotheses that 1) a single exercise bout increases UCP1 mRNA in both inguinal (i)WAT and epididymal (e)WAT, 2) UCP1 expression and responsiveness to exercise are different in iWAT and eWAT, 3) PGC-1α determines the basal levels of UCP1 and PRDM16 in WAT and 4) exercise and exercise training regulate UCP1 and PRDM16 expression in WAT in a PGC-1α-dependent manner.MethodsWhole body PGC-1α knockout (KO) and wildtype (WT) littermate mice performed a single treadmill exercise bout at 14 m/min and 10% slope for 1 hour. Mice were sacrificed and iWAT, eWAT and quadriceps muscle were removed immediately after, 2, 6 and 10 hours after running, and from sedentary mice that served as controls. In addition, PGC-1α KO mice and WT littermates were exercise trained for 5 weeks with sedentary mice as untrained controls. Thirty-six-37 hours after the last exercise bout iWAT was removed.ResultsUCP1 mRNA content increased 19-fold in iWAT and 7.5-fold in eWAT peaking at 6 h and 0′ of recovery, respectively, in WT but with no changes in PGC-1α KO mice. UCP1 protein was undetectable in eWAT and very low in iWAT of untrained mice but increased with exercise training to 4.4 (AU) in iWAT from WT mice without significant effects in PGC-1α KO mice.ConclusionThe present observations provide evidence that exercise training increases UCP1 protein in iWAT through PGC-1α, likely as a cumulative effect of transient increases in UCP1 expression after each exercise bout. Moreover, the results suggest that iWAT is more responsive than eWAT in exercise-induced regulation of UCP1. In addition, as PRDM16 mRNA content decreased in recovery from acute exercise, the present findings suggest that acute exercise elicits regulation of several brown adipose tissue genes in mouse WAT.
Highlights
Life style related metabolic diseases are an increasing problem worldwide and is often associated with obesity and adipose tissue malfunction
PGC-1a KO and WT mice were obtained by intercross breeding of heterozygous parents [18] and homozygous offspring were used for experiments
Resting muscle glycogen content was similar in WT and PGC-1a KO and muscle glycogen was reduced (P#0.05) 25 and 65% after the acute exercise bout in WT and PGC-1a KO, respectively, with no significant difference between genotypes (Table 1)
Summary
Life style related metabolic diseases are an increasing problem worldwide and is often associated with obesity and adipose tissue malfunction. Several studies [1,2] indicate that inguinal white adipose tissue (iWAT), opposite of epididymal white adipose tissue (eWAT), has a protective effect on metabolic diseases. Inguinal- and epididymal-derived cell lines have been reported to exhibit different responsiveness to Forskolin/cAMP stimulation [3] and iWAT has recently been shown to contain beige precursor adipocytes [3,4] while eWAT does not. This indicates potential different responses in eWAT and iWAT to certain stimuli. The aim of the present study was to test the hypotheses that 1) a single exercise bout increases UCP1 mRNA in both inguinal (i)WAT and epididymal (e)WAT, 2) UCP1 expression and responsiveness to exercise are different in iWAT and eWAT, 3) PGC-1a determines the basal levels of UCP1 and PRDM16 in WAT and 4) exercise and exercise training regulate UCP1 and PRDM16 expression in WAT in a PGC-1a-dependent manner
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