Reduction in MCP-1 production in preadipocytes is mediated by PPARγ activation and JNK/SIRT1 signaling

• Published in: Biochimica et biophysica acta. General subjects Vol. 1869; no. 2; p. 130737
• Main Authors: Sawamoto, Atsushi, Itagaki, Ibuki, Okuyama, Satoshi, Nakajima, Mitsunari
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.02.2025
• Subjects: 3T3-L1 Cells; Adipocytes - drug effects; Adipocytes - metabolism; Animals; C-Jun N-terminal kinase (JNK); Chemokine CCL2 - biosynthesis; Chemokine CCL2 - metabolism; Insulin resistance; JNK Mitogen-Activated Protein Kinases - metabolism; Lipopolysaccharides - pharmacology; MAP Kinase Signaling System - drug effects; Mice; Mice, Inbred C57BL; Monocyte chemoattractant protein 1 (MCP-1); Peroxisome proliferator-activated receptor gamma (PPARγ); PPAR gamma - agonists; PPAR gamma - genetics; PPAR gamma - metabolism; Preadipocytes; Rosiglitazone; Signal Transduction - drug effects; Silent information regulator 2 homolog 1 (SIRT1); Sirtuin 1 - metabolism; Thiazolidinediones - pharmacology; PBS; MCP-1; SVF; JNK; RSG; Preadipocytes; Monocyte chemoattractant protein 1 (MCP-1); WAT; C-Jun N-terminal kinase (JNK); LPS; BSA; DMEM; LDH; FBS; Silent information regulator 2 homolog 1 (SIRT1); Insulin resistance; Peroxisome proliferator-activated receptor gamma (PPARγ); SEM; ELISA

Obesity-induced monocyte chemoattractant protein 1 (MCP-1) production leads to the infiltration of monocytes/macrophages into white adipose tissue (WAT), which contributes to systemic insulin resistance. Peroxisome proliferator-activated receptor gamma (PPARγ) agonists are known to reduce MCP-1 prod...