title: Sodium butyrate alleviates adipocyte inflammation by inhibiting NLRP3 pathway.
abstract: Insulin resistance (IR) is a common feature of Type II diabetes, metabolic disorders, hypertension and other vascular diseases. Recent studies showed that obesity-induced inflammation may be critical for IR. To investigate the anti-inflammatory effect of sodium butyrate (NaB) on obesity-induced inflammation, the db/db mice were intraperitoneally injected with NaB for 6 weeks. Glucose control was evaluated by glucose tolerance test (GTT) and insulin tolerance test (ITT). Adipose tissue was harvested for gene expression analysis. 3T3-L1 adipocytes were treated with Tnf-α to mimic the inflammatory state and gene expression was detected by realtime PCR and Western blotting. Our results showed that NaB treatment improved glucose control in db/db mice as determined by GTT and ITT tests. Gene expression analysis showed that NaB inhibited cytokines and immunological markers including CD68, Interferon-γ and Mcp in adipose tissues in db/db mice. Moreover, NaB inhibited cytokine releasing in 3T3-L1 adipocytes treated with TNF-α. Further analysis of inflammation pathway showed that NLRP3 was activated in db/db mice, which was efficiently inhibited by NaB treatment. Our data suggest that inhibition of obesity-induced inflammation alleviates IR, and NaB might be a potential anti-inflammatory agent for obesity.
authors.affiliation: Department of Cardiovascular Internal Medicine, Institute of Field Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.
authors.forename: Xukai
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Medical Genetics, College of Basic Medicine, Third Military Medical University, Chongqing, China.
authors.forename: Gang
authors.initials: G
authors.lastname: He
authors.affiliation: Department of Cardiovascular Internal Medicine, Institute of Field Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Peng
authors.affiliation: Department of Cardiovascular Internal Medicine, Institute of Field Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.
authors.forename: Weitian
authors.initials: W
authors.lastname: Zhong
authors.affiliation: Department of Medical Genetics, College of Basic Medicine, Third Military Medical University, Chongqing, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Medical Genetics, College of Basic Medicine, Third Military Medical University, Chongqing, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
mesh_terms: D017667:Adipocytes / Q000187:drug effects*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D020148:Butyric Acid / Q000494:pharmacology* / Q000627:therapeutic use; D002352:Carrier Proteins / Q000037:antagonists & inhibitors*; D004195:Disease Models, Animal; D007249:Inflammation / Q000188:drug therapy*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D002352:Carrier Proteins; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C492716:Nlrp3 protein, mouse; D020148:Butyric Acid