Our lab studies the role of mitochondrial dynamics and stress response pathways in cardiometabolic health. The prevalence of obesity and associated comorbidities, such as diabetes and cardiovascular disease, have increased dramatically over the last several decades. Activation of thermogenic adipocytes has emerged as a therapeutic strategy to increase energy expenditure and counteract weight gain. Recent evidence in mice and humans suggest a role for brown adipose tissue (BAT) in regulating the secretion of endocrine factors or batokines, such as fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15), that may promote cardiometabolic health by regulating energy homeostasis, glucose metabolism and cardiovascular function.

BAT diagram

Our recent work in mice lacking the mitochondrial fusion protein optic atrophy 1 (OPA1) in BAT and in skeletal muscle demonstrated that mitochondrial stress induces the integrated stress response (ISR), which is required to improve metabolic fitness, partially via FGF21 secretion as a batokine. We also demonstrated that the ISR is induced in BAT in response to physiological stress, such as cold stress. Our research program aims to understand the role of mitochondrial dynamics and the ISR in the regulation of systemic metabolic adaptations in response to cold, diet-induced obesity, cardiac stress and mitochondrial dysfunction.

Our primary research projects focus on: 1. Investigating the role of PKR-like ER kinase (PERK) as an upstream regulator of ISR activation in BAT; 2. The role of the activating transcription factor 4 (ATF4), the main effector of the ISR, in BAT thermogenesis and metabolic homeostasis. 3. The role of GDF15 in the regulation of BAT-mediated metabolic protection. Additional projects in the lab are focused on investigating the role of mitochondrial dynamics and ATF4 in skeletal muscle in the pathophysiology of obesity and insulin resistance. We believe these studies have the potential of identifying new pathways that can be targeted to counteract obesity and its comorbidities.

Renata Pereira portrait

Renata Pereira Alambert, PhD
Assistant Professor
Endocrinology and Metabolism

Dept. of Internal Medicine
FOE Diabetes Research Center
Molecular Medicine Program



  • University of Iowa Carver College of Medicine
  • University of Iowa Fraternal Order of Eagles Diabetes Research Center
  • National Institutes of Health (NIDDK)

Lab Members

Lab Members

Weatherford headshot

Eric Weatherford, PhD

Research Assistant Professor, Endocrinology and Metabolism

Jena headshot

Jayashree Jena, PhD

Postdoctoral Fellow
Endocrinology and Metabolism

Streeter headshot

Jennifer Streeter, MD, PhD

Cardiovascular Medicine

Garcia-Pena headshot

Luis Miguel García-Peña

Research Intern
Endocrinology and Metabolism

Correia headshot

Marcelo Correia, MD MSc PhD

Clinical Assistant Professor, Endocrinology and Metabolism

Ayushi Sood

Rotation student

Jason Chen

Undergraduate Research Assistant

Cally Tucker

Undergraduate Research Assistant

Jason Gao

Undergraduate Research Assistant

Joshua Peterson

Undergraduate Research Assistant

Sanmati Thangavel

Undergraduate Research Assistant

Deeraj Manika

Undergraduate Research Assistant

Former Lab Members

Alex Marti, Research Intern
Kevin Kato, Research Intern
Sarah H. Bjorkman, MD, Fellow
Jivan Koneru, Undergraduate Research Assistant
Angela Nyunt, Undergraduate Research Assistant

lab photo 2022-1

lab group 2022


lab photo 2022-2

lab group 2022


lab photo 2021

lab group 2021


lab photo 2020

lab group 2020




Recent Publications

Pereira RO, Olvera AC, Marti A, Fang S, White JR, Westphal M, Hewezi R, AshShareef ST, García-Peña LM, Koneru J, Potthoff MJ, Abel ED. OPA1 Regulates Lipid Metabolism and Cold-Induced Browning of White Adipose Tissue in Mice. Diabetes. 2022 Dec 1;71(12):2572-2583. doi: 10.2337/db22-0450. PubMed PMID: 36170659.

Pereira RO, Marti A, Olvera AC, Tadinada SM, Bjorkman SH, Weatherford ET, Morgan DA, Westphal M, Patel PH, Kirby AK, Hewezi R, Bùi Trân W, García-Peña LM, Souvenir RA, Mittal M, Adams CM, Rahmouni K, Potthoff MJ, Abel ED. OPA1 deletion in brown adipose tissue improves thermoregulation and systemic metabolism via FGF21. Elife. 2021 May 4;10. doi: 10.7554/eLife.66519. PubMed PMID: 33944779; PubMed Central PMCID: PMC8128440.

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. OPA1 deficiency promotes secretion of FGF21 from muscle that prevents obesity and insulin resistance. EMBO J. 2017 Jul 14;36(14):2126-2145. doi: 10.15252/embj.201696179. Epub 2017 Jun 12. PubMed PMID: 28607005; PubMed Central PMCID: PMC5510002.

Pereira RO, Wende AR, Crum A, Hunter D, Olsen CD, Rawlings T, Riehle C, Ward WF, Abel ED. Maintaining PGC-1α expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function. FASEB J. 2014 Aug;28(8):3691-702. doi: 10.1096/fj.14-253823. Epub 2014 Apr 28. PubMed PMID: 24776744; PubMed Central PMCID: PMC4101649.

Pereira RO, Wende AR, Olsen C, Soto J, Rawlings T, Zhu Y, Riehle C, Abel ED. GLUT1 deficiency in cardiomyocytes does not accelerate the transition from compensated hypertrophy to heart failure. J Mol Cell Cardiol. 2014 Jul;72:95-103. doi: 10.1016/j.yjmcc.2014.02.011. Epub 2014 Feb 25. PubMed PMID: 24583251; PubMed Central PMCID: PMC4037364.

Pereira RO, Wende AR, Olsen C, Soto J, Rawlings T, Zhu Y, Anderson SM, Abel ED. Inducible overexpression of GLUT1 prevents mitochondrial dysfunction and attenuates structural remodeling in pressure overload but does not prevent left ventricular dysfunction. J Am Heart Assoc. 2013 Sep 19;2(5):e000301. doi: 10.1161/JAHA.113.000301. PubMed PMID: 24052497; PubMed Central PMCID: PMC3835233.

All Publications

See Dr. Pereira's complete list of publications.



Pappajohn Biomedical Discovery Building

Papajohn Biomedical Discovery Building

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Office Location:

4322 PBDB
169 Newton Rd
Iowa City, IA 52242
Tel: 319-335-7962