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PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes

Given that obesity and diabetes have been major public health concerns and that disease morbidities have been rising continuously, effective treatment for these diseases is urgently needed. Because adipose tissue metabolism is involved in the progression of obesity and diabetes, it might be efficien...

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Autores principales: Jiang, Na, Yang, Ming, Han, Yachun, Zhao, Hao, Sun, Lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9024053/
https://www.ncbi.nlm.nih.gov/pubmed/35462933
http://dx.doi.org/10.3389/fphar.2022.870250
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author Jiang, Na
Yang, Ming
Han, Yachun
Zhao, Hao
Sun, Lin
author_facet Jiang, Na
Yang, Ming
Han, Yachun
Zhao, Hao
Sun, Lin
author_sort Jiang, Na
collection PubMed
description Given that obesity and diabetes have been major public health concerns and that disease morbidities have been rising continuously, effective treatment for these diseases is urgently needed. Because adipose tissue metabolism is involved in the progression of obesity and diabetes, it might be efficient to target adipocyte metabolic pathways. Positive regulatory domain zinc finger region protein 16 (PRDM16), a transcription factor that is highly expressed in adipocytes, plays a key role in adipose tissue metabolism, such as the browning and thermogenesis of adipocytes, the beigeing of adipocytes, the adipogenic differentiation of myoblasts, and the conversion of visceral adipocytes to subcutaneous adipocytes. Furthermore, clinical and basic studies have shown that the expression of PRDM16 is associated with obesity and diabetes and that PRDM16 signaling participates in the treatment of the two diseases. For example, metformin promotes thermogenesis and alleviates obesity by activating the AMPK/αKG/PRDM16 signaling pathway; rosiglitazone alleviates obesity under the synergistic effect of PRDM16; resveratrol plays an antiobesity role by inducing the expression of PRDM16; liraglupeptide improves insulin resistance by inducing the expression of PRDM16; and mulberry leaves play an anti-inflammatory and antidiabetes role by activating the expression of brown fat cell marker genes (including PRDM16). In this review, we summarize the evidence of PRDM16 involvement in the progression of obesity and diabetes and that PRDM16 may be a promising therapy for obesity and diabetes.
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spelling pubmed-90240532022-04-23 PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes Jiang, Na Yang, Ming Han, Yachun Zhao, Hao Sun, Lin Front Pharmacol Pharmacology Given that obesity and diabetes have been major public health concerns and that disease morbidities have been rising continuously, effective treatment for these diseases is urgently needed. Because adipose tissue metabolism is involved in the progression of obesity and diabetes, it might be efficient to target adipocyte metabolic pathways. Positive regulatory domain zinc finger region protein 16 (PRDM16), a transcription factor that is highly expressed in adipocytes, plays a key role in adipose tissue metabolism, such as the browning and thermogenesis of adipocytes, the beigeing of adipocytes, the adipogenic differentiation of myoblasts, and the conversion of visceral adipocytes to subcutaneous adipocytes. Furthermore, clinical and basic studies have shown that the expression of PRDM16 is associated with obesity and diabetes and that PRDM16 signaling participates in the treatment of the two diseases. For example, metformin promotes thermogenesis and alleviates obesity by activating the AMPK/αKG/PRDM16 signaling pathway; rosiglitazone alleviates obesity under the synergistic effect of PRDM16; resveratrol plays an antiobesity role by inducing the expression of PRDM16; liraglupeptide improves insulin resistance by inducing the expression of PRDM16; and mulberry leaves play an anti-inflammatory and antidiabetes role by activating the expression of brown fat cell marker genes (including PRDM16). In this review, we summarize the evidence of PRDM16 involvement in the progression of obesity and diabetes and that PRDM16 may be a promising therapy for obesity and diabetes. Frontiers Media S.A. 2022-04-08 /pmc/articles/PMC9024053/ /pubmed/35462933 http://dx.doi.org/10.3389/fphar.2022.870250 Text en Copyright © 2022 Jiang, Yang, Han, Zhao and Sun. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Jiang, Na
Yang, Ming
Han, Yachun
Zhao, Hao
Sun, Lin
PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes
title PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes
title_full PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes
title_fullStr PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes
title_full_unstemmed PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes
title_short PRDM16 Regulating Adipocyte Transformation and Thermogenesis: A Promising Therapeutic Target for Obesity and Diabetes
title_sort prdm16 regulating adipocyte transformation and thermogenesis: a promising therapeutic target for obesity and diabetes
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9024053/
https://www.ncbi.nlm.nih.gov/pubmed/35462933
http://dx.doi.org/10.3389/fphar.2022.870250
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