# Illuminating genetic interactions that affect lipid content in adipocytes

> **NIH NIH F32** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2020 · $65,310

## Abstract

Project Abstract
Obesity and associated metabolic disorders are a major health care crisis that affect millions of people worldwide
and have no long-term treatment. Most of our current knowledge on how cells regulate their metabolism has
been obtained using single gene-driven hypothesis. However, obesity like many other diseases is a polygenic
disorder, in which multiple genes interact, contributing to phenotype, which makes it impossible to establish the
causative allele. If we are to make any headway towards curing obesity and metabolic diseases during this
century, we need bold, creative ideas to tackle cellular pathways as oppose to individual genes that take
advantage of cutting-edge high-throughput approaches.
As of 2016, over 1.9 billion adults worldwide were estimated to be overweight and 650 million adults to be obese.
Obesity is classically characterized by pathological development and differentiation of adipose tissue, which is a
key energy storage organ in the body. Adipose tissue stores energy in lipid droplets- until recently unappreciated
cellular organelles with complex and dynamic functions. Lipid droplets can drastically change in size as a
response to changed calorie intake or metabolism. Since currently FDA-approved anti-obesity drugs act on
appetite or metabolism regulation and not on adipose tissue lipids directly, we need to identify pathways
responsible for lipid droplet biogenesis and breakdown to improve current therapeutics. Surprisingly, very little
is known about the pathways that affect lipid droplets in humans.
I will use a CRISPR system to establish a novel high-throughput high-content screening platform in differentiated
adipocytes. Since most lipid modifying genes have been discovered in non-mammalian model systems such as
C. elegans, Drosophila and S. cerevisiae using siRNA approaches, I aim to develop a novel superior CRISPR
screening platform in mammalian system. I will take advantage of inducible CRISPRi mouse our lab has
developed to perform a single and dual genetic perturbation screen in primary adipocytes. Thus, my proposed
research strategy will illuminate not only new genes but importantly genetic interactions and pathways
responsible for formation and breakdown of lipid droplets and provide new targets for anti-obesity therapy.

## Key facts

- **NIH application ID:** 10066969
- **Project number:** 1F32DK126313-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Olga Gulyaeva
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $65,310
- **Award type:** 1
- **Project period:** 2020-07-01 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10066969

## Citation

> US National Institutes of Health, RePORTER application 10066969, Illuminating genetic interactions that affect lipid content in adipocytes (1F32DK126313-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10066969. Licensed CC0.

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