It has been postulated that the protective effects of lower body subcutaneous adipose tissue (LBSAT) occur via its ability to sequester surplus
lipid and thus serve as a "metabolic sink." However, the mechanisms that mediate this protective function are unknown thus this study addresses this postulate. Ad libitum, chow-fed mice underwent
Sham-surgery or LBSAT removal (IngX, inguinal depot removal) and were subsequently provided chow (Chow; typical adipocyte expansion) or high fat diet (HFD; enhanced adipocyte expansion) for 5 weeks. Primary outcome measures included
glucose tolerance and subsequent
insulin response, muscle
insulin sensitivity, liver and muscle
triglycerides, adipose tissue gene expression, and circulating
lipids and
adipokines. In a follow up study the consequences of extended experiment length post-surgery (13 wks) or pre-existing
glucose intolerance were examined. At 5 wks post-surgery IngX in HFD-fed mice reduced
glucose tolerance and muscle
insulin sensitivity and increased circulating
insulin compared with HFD
Sham. In Chow-fed mice, muscle
insulin sensitivity was the only measurement reduced following IngX. At 13 wks circulating
insulin concentration of HFD IngX mice continued to be higher than HFD
Sham. Surgery did not induce changes in mice with pre-existing
glucose intolerance. IngX also increased muscle, but not liver,
triglyceride concentration in Chow- and HFD-fed mice 5 wks post-surgery, but chow group only at 13 wks. These data suggest that the presence of LBSAT protects against
triglyceride accumulation in the muscle and HFD-induced
glucose intolerance and muscle
insulin resistance. These data suggest that lower body subcutaneous adipose tissue can function as a "metabolic sink."