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Published on: May 19, 2023
The GDF3-ALK7 signaling axis in adipose tissue: a possible therapeutic target for obesity and associated diabetes?
1Laboratory of Molecular Endocrinology and Metabolism, Department of Molecular Medicine, Institute for Molecular and Cellular Regulation, Gunma University, Gunma 371-8512, Japan.
Abstract:
ALK7, a type I receptor for the transforming growth factor-β superfamily, is known to be predominantly expressed in adipocytes in both mice and humans. The present review describes recent findings suggesting that ALK7 plays a major role in regulating lipid metabolism and fat mass. Furthermore, the ligands and upstream regulators that activate ALK7 signaling are discussed. The focus is on findings in mice and their derivative tissues and cells that harbor the mutations of ALK7 and related molecules. Particular attention is paid to the contradictory nature of the current literature about the loss-of-function phenotypes and the relationship with insulin secretion and sensitivity. Additional attention is paid to the ALK7 gene variants found in humans and their associated traits. The goal is to seek a parsimonious, and preferably singular and unified, description of the underlying mechanism. This review also introduces recent promising findings about ALK7 neutralizing treatment to obese mice.
Insights
Activin receptor type 7 (ALK7) significantly impacts lipid metabolism and fat mass regulation, primarily in adipocytes. Research explores its complex role, including contradictory findings and potential therapeutic applications for obesity.
Area of Science:
- Endocrinology and Metabolism
- Molecular Biology
- Obesity Research
Background:
- Activin receptor type 7 (ALK7), a TGF-β superfamily member, is primarily expressed in adipocytes.
- Emerging evidence highlights ALK7's crucial role in regulating lipid metabolism and overall fat mass.
- Understanding ALK7 signaling is key to addressing metabolic disorders.
Approach:
- Review of recent findings on ALK7 function, focusing on mouse models and derivative tissues.
- Analysis of ligands and upstream regulators activating ALK7 signaling pathways.
- Examination of ALK7 gene variants in humans and their associated metabolic traits.
Key Points:
- ALK7 signaling is central to lipid metabolism and fat mass regulation.
- Contradictory findings exist regarding ALK7 loss-of-function phenotypes and their link to insulin sensitivity.
- Human ALK7 gene variants offer insights into metabolic health and disease.
Conclusions:
- The precise mechanism of ALK7 in metabolic regulation requires further elucidation.
- ALK7 neutralizing treatments show promise for managing obesity in preclinical models.
- Further research is warranted to translate ALK7 findings into clinical applications for metabolic diseases.
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