# FFA Metabolism in Different Types of Human Obesity

> **NIH NIH R01** · MAYO CLINIC ROCHESTER · 2021 · $535,222

## Abstract

Project Summary/Abstract
 The long-term objective of our research is to understand the mechanisms by which obesity, and
specifically upper body obesity (UBO), causes insulin resistance and the other health problems such as Type 2
Diabetes. Our focus is on the release of free fatty acids (FFA) from adipose tissue lipolysis in humans and how
those FFA affect the functioning of other tissues (lipotoxicity). The specific aims of this proposal are to: 1)
Determine whether impaired insulin-induced suppression of lipolysis (as measured by IC50) is related to the
above mentioned lipolysis proteins in groups of volunteers known to vary widely with regards to abdominal
adipocyte size and regulation of adipose tissue lipolysis; 2) Determine whether the improved insulin regulation
of lipolysis resulting from treatment with the PPARγ agonist pioglitazone, with or without weight loss, can be
linked to specific changes in sets of PPARγ-responsive adipocyte lipolysis proteins in UBO adults; 3)
Determine whether the adipose inflammatory cell and cytokine content in Class III obesity is related to lipolysis
insulin resistance and, if so, whether sustained, substantial weight loss one year following bariatric surgery
reduces inflammation in parallel with improved insulin regulation of lipolysis. We will measure of insulin-
regulated adipose tissue lipolysis in vivo and assess adipocyte lipolysis proteins, inflammation and insulin
signaling in obese humans with widely varying degrees of insulin resistance. Our hypothesis is that proteins
involved in the final steps of the regulation of lipolysis are altered in humans with large fat cells, and that these
alterations are responsible for adipose insulin resistance. Combined, we believe these studies will offer insights
as to why adipose tissue lipolysis is abnormal in some obesity phenotypes and provide information on what
therapeutic strategies to treat adipose insulin resistance are most compelling.

## Key facts

- **NIH application ID:** 10132301
- **Project number:** 5R01DK040484-33
- **Recipient organization:** MAYO CLINIC ROCHESTER
- **Principal Investigator:** MICHAEL D. JENSEN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $535,222
- **Award type:** 5
- **Project period:** 1988-08-01 → 2023-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10132301

## Citation

> US National Institutes of Health, RePORTER application 10132301, FFA Metabolism in Different Types of Human Obesity (5R01DK040484-33). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10132301. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*