Troglitazone activates TRPV1 and causes deacetylation of PPARγ in 3T3-L1 cells

Autor: Baskaran Thyagarajan, Vivek Krishnan, Padmamalini Baskaran
Rok vydání: 2019
Předmět:
Male
0301 basic medicine
Cellular differentiation
White adipose tissue
Mice
chemistry.chemical_compound
0302 clinical medicine
Sirtuin 1
Thiazolidinedione
Receptor
Uncoupling Protein 1
Epididymis
Adipogenesis
biology
musculoskeletal
neural
and ocular physiology
Acetylation
Thermogenesis
Adipose Tissue
Bone Morphogenetic Proteins
Molecular Medicine
lipids (amino acids
peptides
and proteins)
Capsazepine
Ion Channel Gating
medicine.drug
medicine.medical_specialty
medicine.drug_class
TRPV1
TRPV Cation Channels
030209 endocrinology & metabolism
Diet
High-Fat
Article
Troglitazone
03 medical and health sciences
3T3-L1 Cells
Internal medicine
Weight Loss
medicine
Animals
PPAR alpha
RNA
Messenger
Molecular Biology
Feeding Behavior
Lipid Metabolism
PPAR gamma
030104 developmental biology
Endocrinology
nervous system
chemistry
CCAAT-Enhancer-Binding Proteins
biology.protein
Capsaicin
Zdroj: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1865:445-453
ISSN: 0925-4439
Popis: Published research suggests that activation of transient receptor potential vanilloid subfamily 1 (TRPV1) enhances the expression and deacetylation of peroxisome proliferator-activated receptor gamma (PPARγ) to cause browning of white adipose tissue. Here, we show that TRPV1 activation by capsaicin significantly prevents high fat diet-induced obesity in mice. This is associated with an increase in the expression and deacetylation of PPARγ in the epididymal fat of these mice. Consistent with the TRPV1 activation in vivo, overexpression of TRPV1 enhanced the PPARγ and other thermogenic genes in cultured 3T3-L1 preadipocytes. To determine the interaction between TRPV1 and PPARγ signaling, we analyzed the effect of Troglitazone (Trog; a thiazolidinedione derivative and an agonist of PAARγ) treatment on cultured 3T3-L1 cells. Trog enhanced the expression of TRPV1, PPARγ and thermogenic proteins in undifferentiated 3T3-L1 cells but not in differentiated cells. Acute application of Trog stimulated a robust Ca2+ influx into 3T3-L1 cells and TRPV1 inhibition by capsazepine prevented this. More interestingly, Trog or capsaicin treatment caused the deacetylation of PPARγ in 3T3-L1 cells and inhibition of TRPV1 or Sirtuin 1 - prevented this. Our data suggest a novel effect of Trog to induce PPARγ deacetylation by activating TRPV1. This research has a significant implication on the role of TRPV1 and PPARγ signaling in the browning of white adipose tissue.
Databáze: OpenAIRE
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