The anti-inflammatory and insulin sensitizing attributes of high circulating adiponectin concentrations in the mouse were recently suggested to occur as a result of subcutaneous adipose tissue expansion. Although there is a plethora of data describing the affects adiponectin has on metabolism and inflammation, there are limited data on its role in the growth of adipose tissue. Our data in adiponectin null mice indicate, the consumption of a high fat diet does not significantly change body composition from that of diet matched wild type mice. Furthermore, there was no observable difference in the inflammatory profile of our adiponectin null mice fed high fat diet.

In the absence of the expected increase in adipose tissue, we sought to identify the role of adiponectin in the proliferation and differentiation of stromal vascular cells obtained from ob/ob obese mice or wild type controls. Our study identified a significant reduction in the differentiation of cells derived from ob/ob animals when treated with adiponectin. Conversely, there was no observable change in differentiation of the wild type cells with treatment of adiponectin, leptin or the combination of the two. Furthermore, we report a significant decrease in proliferation in adiponectin treated wild type cells and in leptin rescued ob/ob cells treated with adiponectin.

We also pursued the use of different dietary fatty acids as a means for inducing adiponectin production. We fed swine a diet enriched in the bioactive n-3 fatty acid αLA to examine the effects of this fatty acid on adiponectin and to determine if eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA) can be derived from αLA in vivo. We identified a significant increase in the tissue enrichment of αLA, EPA and DPA in a diet dependent manner. However, there was no statistical difference in serum adiponectin concentrations or adiponectin transcript abundance among diets.

Collectively, these studies indicate adiponectin is not instrumental in the regulation of adipose tissue deposition in normal mice. However, adiponectin does retard the pro-differentiation phenotype of leptin-deficient stromal vascular cells. Our data also indicates that, although αLA is readily converted to EPA and DPA in vivo, the concentrations seem insufficient to alter serum adiponectin concentrations in swine.