Related Experiment Video
Updated: Mar 20, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Transcriptional Dysregulation of Adipose Tissue Autophagy in Obesity
Nitzan Maixner1, Sapir Bechor2, Zlata Vershinin3
1Department of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva, Israel;
Abstract:
There is growing interest in understanding how dysregulated autophagy may contribute to pathogenesis of disease. Most frequently, disease states are associated with diminished autophagy, mostly attributed to genetic variation in autophagy genes and/or to dysfunctional posttranscriptional mechanisms. In human adipose tissue (AT), in obesity, expression of autophagy genes is upregulated and autophagy is likely activated, associating with adipose dysfunction. This review explores the emerging role of transcriptional mechanisms regulating AT autophagy in obesity.
More Related Videos
06:08Author Spotlight: Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator
Published on: May 19, 2023
09:20An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
Related Concept Videos
Obesity
Overview of Lipid Metabolism
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...
Master Transcription Regulators
Delivery Pathways to the Lysosome
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
Autophagy
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Epigenetic Regulation
X-chromosome...