Insights by which TUDCA is a potential therapy against adiposity
Israelle Netto Freitas1,2, Joel Alves da Silva2, Kênia Moreno de Oliveira2
1Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, SP, Brazil.
Frontiers in Endocrinology
|March 10, 2023
Summary
Tauroursodeoxycholic acid (TUDCA) can mitigate obesity-related metabolic issues by reducing endoplasmic reticulum stress, inflammation, and cell death in fat cells. TUDCA shows promise as a therapeutic for obesity and related conditions.
Area of Science:
- Metabolic and endocrine functions of adipose tissue.
- Role of endoplasmic reticulum (ER) stress in obesity.
- Therapeutic potential of bile acids.
Background:
- Adipose tissue is a dynamic organ regulating energy balance, undergoing significant changes during obesity.
- Endoplasmic reticulum (ER) stress is a key molecular factor in metabolic disorders like obesity.
- Tauroursodeoxycholic acid (TUDCA), a bile acid, acts as an ER stress inhibitor and chemical chaperone.
Purpose of the Study:
- To review the effects of TUDCA, TGR5, and FXR on adipose tissue in obesity.
- To highlight TUDCA's potential in managing obesity-related metabolic dysfunction.
- To explore TUDCA's impact on perivascular adipose tissue (PVAT) and cardiovascular health.
Main Methods:
- Review of existing literature on TUDCA, TGR5, and FXR in adipose tissue.
- Analysis of TUDCA's mechanisms in inhibiting ER stress, inflammation, and apoptosis in adipocytes.
- Examination of TUDCA's influence on PVAT function and adiponectin secretion.
Main Results:
- TUDCA effectively reduces ER stress, inflammation, and apoptosis in adipocytes, counteracting obesity-related metabolic disturbances.
- TUDCA may offer cardiovascular protection in obesity through beneficial effects on PVAT and adiponectin release.
- TUDCA demonstrates potential as a therapeutic agent for obesity and associated comorbidities.
Conclusions:
- TUDCA emerges as a promising therapeutic strategy for obesity and its comorbidities.
- Inhibition of ER stress by TUDCA is a key mechanism for improving adipose tissue function.
- Further research is needed to fully elucidate TUDCA's cardiovascular protective mechanisms in obesity.
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