Meeting Abstract
P2.100 Wednesday, Jan. 5 Expression of Myostatin and Akirin Isoforms in Mice (Mus Musculus) fed a High Fat Diet CHRISTENSEN, D.J.*; PAKALA, K.P.; BIGA, P.R.; North Dakota State University; North Dakota State University; North Dakota State University Delci.Christensen@ndsu.edu
Myostatin (mstn) is known to negatively regulate muscle growth and to regulate adipogenesis. A novel downstream target of myostatin signaling, akirin, has recently been identified and is related to the regulation of the innate immune system. An interesting link exists between local inflammation and metabolism in exaggerated cases of overnutrition. The aim of this study was to evaluate effects of high-fat dietary intake on the expression of mstn and akirin isoforms in muscle and spleen tissue in order to understand potential regulatory pathways between immunity and metabolism. Myostatin was recently shown to attenuate akirin1 expression, and removing functional mstn results in resistance to high-fat diet induced obesity. Therefore, this study was designed to test the hypothesis that high-fat diet intake will increase mstn expression and, in turn, decrease akirin expression in high-fat diet induced obesity (HFDIO) susceptible mice. To evalaute this relationship, we utilized two strains of mice exhibiting varying propensities to HFDIO. Myostatin mRNA levels were elevated in response to high-fat diet intake in diet-induced obesity susceptible mice. Interestingly, a dramatic decrease in mstn expression was detected in spleen tissue of HFDIO-resistant mice. The two akirin isoforms, akirin1 and akirin2, were differentially regulated between the strains of mice, and HFDIO-susceptible mice exhibit increased expression in both muscle and spleen tissue, suggesting a direct relationship between myostatin and akirin is unlikely in vivo. In addition, a more complex regulatory mechanism for akirin1 and akirin2 may exist. These results demonstrate a clear metabolic role of mstn and support the hypothesis that low levels of mstn expression protect against dietary induced metabolic dysfunction.
