September 1, 2016
A transmission electron micrograph of mitochondria in inguinal fat tissue of mice lacking MnSOD in fat cells is featured on the cover of Diabetes: A Journal of the American Diabetes Association; Volume 65 Issue 9. This image was taken by members of the Boudina Lab during a study on oxidative stress. The corresponding article, Adipocyte-Specific Deletion of Manganese Superoxide Dismutase Protects From Diet-Induced Obesity Through Increased Mitochondrial Uncoupling and Biogenesis, is also featured in the issue.
August 1, 2016
The Boudina Laboratory was awarded the Grant-in-Aid from the American Heart Association thanks to Marcio Buffolo’s work investigating the role of a new subpopulation of epididymal (visceral) progenitor cells (EPCs) in metabolic diseases. Previous studies have described that EPC do not differentiate in vitro. This data has been associated with the decrease of cellular renewal that might be related to the detrimental visceral cell hypertrophy we see in obesity. Marcio has shown that there are two EPCs, instead of only one population as previously described. He has named them according to their CD34 expression as Visceral High (VHp) and Visceral Low (VLp) progenitors. VHp recapitulates the non-differentiative phenotype first described for EPCs. However, VLp shows a very robust in vitro differentiation. Marcio has also shown a significant increase in VHp number in various metabolic diseases, such as genetic and diet-induced obesity. He is focused now on understanding the phenotypic differences and interactions between these two populations.
July 2, 2016
Dr. Karla Pires has been granted an AHA post-doctoral fellowship award for her project, which is focused on autophagy modulation by insulin resistance in the heart. Autophagy is a mechanism by which cells recycle damaged molecules and organelles through lysosomal degradation. Alterations in autophagy have been described in various metabolic diseases such as obesity, type I and type II diabetes. However, there are few reports on cardiac insulin resistance-induced autophagy modulation. She has shown that cardiac autophagy is reduced in an obesity-induced insulin resistance (ob/ob mice). Also, her data clearly points out to a participation of the IGF1R signaling on this phenotype. Her goal is to describe IGF1R signaling influence on cardiac autophagy reduction by studying a heterozygote obob/IGF1R mutant.
July 1, 2016
The Lab was awarded the Funding Incentive Seed Grant from the University of Utah Research Foundation for their evaluation of the role of Oct1 in adipogenesis.