Abstract
High physical activity is important to optimize the function of adipose tissue. Dysfunctional adipose tissue contributes to the development of metabolic stress, chronic inflammation, and hypertension. To improve our current understanding of the interaction between physical exercise and adipose tissue, we analyzed the effect of 10 months voluntary running wheel activity of rats on uncoupling protein (UCP) 1 negative white adipose tissue (visceral and subcutaneous adipose tissue, VWAT and SWAT). Analysis was performed via RT-PCR and immunoblot from adipose tissues depicted from adult normotensive and spontaneously hypertensive female rats. UCP1 negative VWAT differed from UCP1 positive WAT and brown adipose tissue (BAT) from interscapular fat depots, by lacking the expression of UCP1 and low expression of Cidea, a transcriptional co-activator of UCP1. High physical activity affected the expression of five genes in SWAT (Visfatin (up), RBP5, adiponectin, Cidea, and Nrg4 (all down)) but only one gene (Visfatin, up) in VWAT. Furthermore, the expression of these genes is differentially regulated in VWAT and SWAT of normotensive and spontaneously hypertensive rats (SHR) under sedentary conditions (UCP2) and exercise (Visfatin, Cidea, Nrg4). Keeping the animals after 6 months of voluntary exercise under observation for an additional period of 4 months without running wheels, Visfatin, Cidea, and Nrg4 were stronger expressed in VWAT of SHRs than in sedentary control rats. In summary, our study shows that SWAT is more responsible to exercise than VWAT.
Highlights
Obesity is more than ever a raising world health problem
We confirmed a high expression of UCP1 in interscapular brown adipose tissue (BAT) and in white adipose tissues (WAT) located in the immediate vicinity of BAT (Fig. 2)
The expression of several browning markers was analyzed in these two different types of adipose tissue in normotensive rats that were kept under standard housing conditions
Summary
Obesity is more than ever a raising world health problem. It occurs as the consequence of an imbalance between caloric intake and caloric consumption. An increase in energy expenditure by exercise can induce a phenotypic change of WAT through a transformation from an energy-storing tissue to a thermogenic beige adipose tissue [1]. This process has been termed browning of WAT. The release of myokines, that are cytokines or hormones derived from the skeletal muscle, may trigger effects of exercise in adipose tissue [5]. Release of IL-6 from skeletal muscle may connect exercise to browning of WAT [1]
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