# White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin

> **NIH NIH R01** · UT SOUTHWESTERN MEDICAL CENTER · 2020 · $497,340

## Abstract

White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin
Much attention has been dedicated over recent years towards a better understanding of brown and beige
adipocytes, which are classically characterized by high mitochondrial content. However, the role of
mitochondria in white adipocytes, beyond basic physiology and “housekeeping”, remains vastly
uncharacterized. We have developed systems in which we can address adipocyte-specific manipulation of
mitochondrial function, in an inducible fashion. This allows for induction of key mitochondrial components in the
adult mouse, excluding undesirable developmental effects. Over the previous funding period, we have
examined a number of models in which adipocyte mitochondrial function was selectively enhanced or
compromised. One of our new models allows us to specifically enhance mitochondrial reactive oxygen species
(ROS) levels within the adipocyte. This has profound local and systemic effects that led us to the following
hypothesis: THE LOWERING OF ADIPOCYTE MITOCHONDRIAL ROS LEVELS IS A PREREQUISITE FOR
THE REMODELING AND ADAPTATION OF ADIPOSE TISSUE TO ALTERED SYSTEMIC METABOLIC
CONDITIONS. By carefully timing and titrating mitochondrial activity and ROS levels, we will examine this
hypothesis in the following areas: A) at the cellular level in the mature adipocyte; B) in the microenvironment
at the level of whole adipose tissue remodeling; C) at the organismal level assessing systemic effects of
adipocyte-derived ROS, with a specific focus on pancreatic beta cells. Specifically, we propose to address the
underlying mechanisms with the following hierarchical approaches: In Aim 1, we will examine the effects of
adipocyte-specific mitochondrial dysfunction and mitochondria-generated ROS on the LOCAL cellular
homeostasis of the adipocyte. In Aim 2, we will define the effects of adipocyte-specific mitochondrial
dysfunction and mitochondria-generated ROS on the local ADIPOSE TISSUE microenvironment, function and
remodeling. In Aim 3, we will address the effects of adipocyte-specific mitochondrial dysfunction and
mitochondria-derived ROS on SYSTEMIC metabolic homeostasis. Combined, these studies enable us to
carefully dissect the effects of altered mitochondrial function on adiponectin production, cellular physiology of
the white adipocyte and adaptive remodeling of adipose tissue. While the established role of mitochondrial
function in brown adipocytes is widely appreciated, our data argues that the relevance of mitochondrial function
in the white adipocyte has been mistakenly undervalued. We have generated a unique toolset that allows us to
systematically approach the question of “mitochondrial dysfunction” and, in fact, this toolset helps us to
methodically define the term “dysfunction”. We also want to better understand the mechanisms governing
adiponectin production and release. Based upon our preliminary data, we strongly believe that mitochondrial
activity plays an essential role in...

## Key facts

- **NIH application ID:** 9920126
- **Project number:** 5R01DK099110-08
- **Recipient organization:** UT SOUTHWESTERN MEDICAL CENTER
- **Principal Investigator:** PHILIPP E SCHERER
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $497,340
- **Award type:** 5
- **Project period:** 2013-07-05 → 2023-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9920126

## Citation

> US National Institutes of Health, RePORTER application 9920126, White Adipose Tissue Physiology, Mitochondrial Function and Adiponectin (5R01DK099110-08). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9920126. Licensed CC0.

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