Related Experiment Video
Updated: Mar 3, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Nck2, an unexpected regulator of adipogenesis
N Haider1,2, J Dusseault1,2, A Rudich3,4
1a Department of Medicine , McGill University , Montreal , Quebec , Canada.
Abstract:
The regulation of adipose tissue expansion by adipocyte hypertrophy and/or hyperplasia is the topic of extensive investigations given the potential differential contribution of the 2 processes to the development of numerous chronic diseases associated with obesity. We recently discovered that the loss-of-function of the Src homology domain-containing protein Nck2 in mice promotes adiposity accompanied with adipocyte hypertrophy and impaired function, and enhanced adipocyte differentiation in vitro. Moreover, in severely-obese human's adipose tissue, we found that Nck2 expression is markedly downregulated. In this commentary, our goal is to expand upon additional findings providing further evidence for a unique Nck2-dependent mechanism regulating adipogenesis. We propose that Nck2 should be further investigated as a regulator of the reliance of white adipose tissue on hyperplasia versus hypertrophy during adipose tissue expansion, and hence, as a potential novel molecular target in obesity.
Insights
Loss of Nck2 protein in mice leads to increased obesity, characterized by larger fat cells and impaired function. Nck2 downregulation in obese humans suggests it
Area of Science:
- Molecular Biology
- Cell Biology
- Metabolic Research
Background:
- Adipose tissue expansion is regulated by adipocyte hypertrophy and hyperplasia, processes implicated in obesity-related chronic diseases.
- Understanding the molecular mechanisms governing these processes is crucial for developing effective obesity interventions.
Purpose of the Study:
- To present evidence for a novel Nck2-dependent mechanism regulating adipogenesis.
- To propose Nck2 as a key regulator of white adipose tissue expansion and a potential molecular target for obesity.
Main Methods:
- Investigated the role of Nck2 loss-of-function in mouse models of adiposity.
- Analyzed Nck2 expression levels in adipose tissue from severely obese human subjects.
- Examined adipocyte differentiation in vitro following Nck2 manipulation.
Main Results:
- Loss of Nck2 in mice resulted in increased adiposity with adipocyte hypertrophy and impaired function.
- Nck2 expression was significantly downregulated in the adipose tissue of severely obese individuals.
- Nck2 deficiency enhanced adipocyte differentiation in vitro.
Conclusions:
- Nck2 plays a critical role in regulating the balance between hyperplasia and hypertrophy during adipose tissue expansion.
- Nck2 is a potential molecular target for novel therapeutic strategies against obesity.
More Related Videos
09:20An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
Published on: May 4, 2021
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
Related Concept Videos
Regulation of Nuclear Protein Sorting
Cell Specific Gene Expression
Master Transcription Regulators
Regulation of the Unfolded Protein Response
PI3K/mTOR/AKT Signaling Pathway
Non-Canonical Wnt Signaling Pathways