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Published on: June 2, 2015
1α,25(OH)2 Vitamin D3 Signaling in Adipose Tissue: Bridging Classical and Non-Classical Pathways in Metabolic
Alice Lima Rosa Mendes1, Paola Miranda Sulis1, Murilo Ferenz1
1Instituto de Bioeletricidade Celular (IBIOCEL): Ciência & Saúde, Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Rua João Pio Duarte Silva 241, Sala G301, Córrego Grande, Florianópolis 88037-000, Brazil.
Calcitriol (1α,25-D3) influences adipocyte function through classical and non-classical pathways. This review explores its signaling mechanisms, highlighting potential therapeutic targets for metabolic diseases.
Area of Science:
- Endocrinology
- Metabolic Biology
- Molecular Signaling
Background:
- Adipose tissue is an endocrine organ regulating metabolism and immunity.
- Adipocytes store and activate vitamin D3 to calcitriol (1α,25-D3).
- Calcitriol modulates adipocyte function via classical and non-classical pathways involving the vitamin D receptor (VDR).
Purpose of the Study:
- To review calcitriol's signal transduction mechanisms in adipocytes.
- To detail classical (VDRn) and non-classical (VDRm, microRNAs, AMPK, SIRT1) pathways.
- To identify potential therapeutic targets for metabolic diseases.
Main Methods:
- Comprehensive literature search of PubMed, ScienceDirect, and MDPI.
- Prioritization of studies published within the last 10 years.
- Synthesis of current knowledge on calcitriol signaling in adipocytes.
Main Results:
- Calcitriol regulates adipocyte inflammation and energy metabolism via VDRn.
- Non-classical pathways involving AMPK/SIRT1 and microRNAs modulate energy production and mitochondrial function.
- Calcitriol influences metabolic homeostasis and secretion processes.
Conclusions:
- Calcitriol integrates signaling pathways regulating adipocyte metabolic and inflammatory responses.
- Calcitriol shows potential as a therapeutic target and biomarker for metabolic diseases.
- MicroRNAs are key regulators and potential targets/biomarkers in adipocyte function.
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