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. My current research focuses on elucidating the link between the role of mitochondrial fusion and fission (mitochondrial dynamics) on metabolically relevant tissues on the manifestation of insulin resistance. I have recently demonstrated that, by deleting the fusion protein OPA1 from skeletal muscle we induce mitochondrial stress and ER stress, but surprisingly renderer mice resistant to diet-induced obesity and insulin resistance via FGF21 secretion from muscle. My current research projects aim to understand the mechanisms for muscle regulation of FGF21 and the role of OPA1 and mitochondrial dynamics in adipose tissue physiology and in the adaptation to caloric excess.

3 most influential diabetes/obesity/metabolism publications:

  • OPA1 deficiency promotes secretion of FGF21 from muscle that prevents obesity and insulin resistance. Pereira RO, Tadinada SM, Zasadny FM, Oliveira KJ, Pires KMP, Olvera A, Jeffers J, Souvenir R, Mcglauflin R, Seei A, Funari T, Sesaki H, Potthoff MJ, Adams CM, Anderson EJ, Abel ED. EMBO J. 2017 Jul 14;36(14):2126-2145.
  • Mitochondrial Reactive Oxygen Species in Lipotoxic Hearts Induces Post-Translational Modifications of AKAP121, DRP1 and OPA1 That Promote Mitochondrial Fission. Kensuke Tsushima, Heiko Bugger, Adam R Wende, Jamie Soto, Gregory A Jenson, Austin R Tor, Rose McGlauflin, Helena C Kenny, Yuan Zhang, Rhonda Souvenir, Xiao X Hu, Crystal L Black, Renata O Pereira, Vitor A Lira, Kenneth Spitzer, Terry L Sharp, Kooresh I Shoghi, Genevieve C Sparagna, Eva A Rog-Zielinska, Peter Kohl, Oleh Khalimonchuk, Jean E Schaffer, E. Dale Abel.
  • 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.


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 my career to be impactful and to make a difference in other people’s lives. I hope that by investigating the mechanism underlying the development of insulin resistance I will have the opportunity of doing just that.