Year: 2024
Type: dissertation
Abstract: Nrac, a protein expressed in adipose tissue and heart, plays a crucial role in lipid regulation. Deletion of Nrac in mice results in increased lipid uptake, leading to increased fat mass and hypertrophic white adipose tissue. Functionally, Nrac interacts with the fatty acid transporter CD36, influencing its localization in adipocytes. Nrac-deficient adipocytes exhibit elevated CD36 internalization through clathrin-mediated endocytosis, causing increased fatty acid uptake. The response to fatty acid stimulation in Nrac-deficient adipocytes aligns with CD36 internalization, abolishing genotype-specific lipid uptake differences in mice on a high-fat diet.
Authors: Singh, Inderjeet, Pfluger, Paul Thomas 1973-, Technische Universität München
Institution: Technical University of Munich
Language: English
Subfield: Biochemistry
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7011688421