# Mitochondrial PE in Brown Adipose Thermogenesis

> **NIH NIH F31** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 2021 · $35,956

## Abstract

PROJECT SUMMARY
Obesity is a comorbidity for diabetes, cardiovascular disease, stroke, and cancer. Obesity is caused by
consuming calories in excess of energy expenditure for prolonged periods, which also often leads to insulin
resistance and eventually type II diabetes. Exploiting brown adipose thermogenesis offers promising potential
for the long-term treatment of obesity and hyperglycemia given its ability to increase caloric expenditure.
Uncoupling protein 1 (UCP1), a protein located in the inner mitochondrial membrane (IMM), is responsible for
thermogenesis in brown adipose tissue (BAT). Mitochondrial energetics are intimately tied to the IMM
phospholipid composition. In addition to affecting cristae structure and function, these phospholipids regulate
inner mitochondrial transmembrane protein activities due to phospholipid binding and interaction sites. My
preliminary findings suggest that phosphatidylethanolamine (PE) plays an important adaptive role in BAT
mitochondria. Mice housed in progressively colder environments displayed an increase in mitochondrial PE
content concomitant with increased thermogenic capacity (as measured by UCP1-dependent respiration).
Mice deficient in BAT mitochondrial PE are less cold tolerant with the isolated mitochondria from these mice
exhibiting reduced respiratory rates. Based on these observations, I propose that mitochondrial PE is
necessary for optimal UCP1 function and for cold- and diet-induced thermogenesis. To that end, I plan to
interrogate this relationship by studying how increases or decreases in mitochondrial PE affect thermogenesis
and if this phospholipid acts directly through UCP1. My extensive team of expert mentors will support my
wholistic research training experience by reviewing my findings, identifying potential loopholes in my logic,
and assisting with my future route of inquiry into BAT mitochondrial bioenergetics. Additionally, the
collaborative and interactive learning environment at the University of Utah will facilitate my training in utilizing
mouse models to generate quality data, conducting mitochondrial bioenergetic assays, interpreting data, and
promoting diversity in biomedical research using my outreach skills. This proposal addresses a critical need
in metabolic research and our hope is that these findings will provide an important steppingstone for future
researchers to better understand and exploit BAT thermogenesis therapeutically.

## Key facts

- **NIH application ID:** 10313609
- **Project number:** 1F31DK130555-01
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **Principal Investigator:** Alek Peterlin
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $35,956
- **Award type:** 1
- **Project period:** 2021-09-01 → 2024-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10313609

## Citation

> US National Institutes of Health, RePORTER application 10313609, Mitochondrial PE in Brown Adipose Thermogenesis (1F31DK130555-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10313609. Licensed CC0.

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