Renata Pereira Alambert, PhD

Contact Information

Office: 3314 PBDB
Faculty Profile


Brief description of current research:

Diabetes is one of the fastest growing epidemics nationwide, and its complications remain a major public health burden. Insulin resistance is a hallmark of type 2 diabetes and obesity, and elucidating its pathophysiology will be crucial to combat diabetes. Several studies have correlated mitochondrial dysfunction with insulin resistance and diabetes. However, whether impaired mitochondrial function plays a casual role or is secondary to the disease is still incompletely understood. Preliminary studies in Dr. Abel’s laboratory have suggested that insulin signaling might regulate mitochondrial fusion and fission (mitochondrial dynamics) in cultured muscle cells. Therefore, our current research focuses on elucidating the link between mitochondria dynamics in skeletal muscle and the manifestation of insulin resistance. Our hypothesis is that impaired mitochondrial dynamics might contribute to mitochondrial dysfunction in insulin resistant states. We are also interested on understanding the role of mitochondrial dynamics in overall muscle health and its adaptations to different stressor, such as exercise and muscle wasting.

3 most influential diabetes/obesity/metabolism publications:

  • Insulin receptor substrate signaling suppresses neonatal autophagy in the heart. Riehle C, Wende AR, Sena S, Pires KM, Pereira RO, Zhu Y, Bugger H, Frank D, Bevins J, Chen D, Perry CN, Dong XC, Valdez S, Rech M, Sheng X, Weimer BC, Gottlieb RA, White MF, Abel ED. J Clin Invest. 2013 Dec 2;123(12):5319-33. doi: 10.1172/JCI71171. Epub 2013 Nov 1. PMID: 24177427
  • Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunction. Pereira RO, Wende AR, Olsen C, Soto J, Rawlings T, Zhu Y, Anderson SM, Abel ED. J Am Heart Assoc. 2013 Sep 19;2(5):e000301. doi: 10.1161/JAHA.113.000301. PMID: 24052497
  • Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation. Zhu Y, Pereira RO, O'Neill BT, Riehle C, Ilkun O, Wende AR,Rawlings TA, Zhang YC, Zhang Q, Klip A, Shiojima I, Walsh K, Abel ED. Mol Endocrinol. 2013 Jan;27(1):172-84. doi: 10.1210/me.2012-1210. Epub 2012 Nov 30. PMID: 23204326

Quote:

Working on diabetes research is both challenging and exciting! Better understanding of the pathophysiology of diabetes and elucidating some of the pathways underlying its manifestation will have a huge impact on public health issues worldwide. I have always wanted to do something bigger than myself and make a difference in other people’s lives. I believe that investigating the link between mitochondrial dysfunction in skeletal muscle and insulin resistance will give me the opportunity of doing just that.