title: Teasaponin reduces inflammation and central leptin resistance in diet-induced obese male mice.
abstract: Chronic inflammation is involved in the pathogenesis of obesity and type 2 diabetes. Recently teasaponin, an extract from tea, has been shown to have antiinflammatory effects. We examined the effect of teasaponin on obesity, inflammation, glucose metabolism, and central leptin sensitivity in obese mice fed a high-fat (HF) diet for 16 weeks. Intraperitoneal injections of teasaponin (10 mg/kg, daily) for 21 days significantly decreased the food intake and body weight of HF diet-induced obese mice. Teasaponin treatment also reduced the protein levels of proinflammatory cytokines (TNF-α, IL-6, and/or IL-1β) and nuclear factor-κB signaling (phosphorylated inhibitory-κB kinase and phosphorylated inhibitory-κBα) in adipose tissue and the liver. The antiinflammatory effects of teasaponin were associated with improved glycemic status in the treated animals, evidenced by improved glucose tolerance, homeostasis model assessment, and fasting plasma insulin. In the hypothalamus, teasaponin decreased both proinflammatory cytokines and inflammatory signaling in the mediobasal hypothalamus. Teasaponin treatment also enhanced the anorexigenic effect of central leptin administration, restored leptin phosphorylated signal transducer and activator of transcription-3 (p-STAT3) signaling in the arcuate nucleus, and increased hypothalamic expression of the anorexigenic peptide proopiomelanocortin. These results identify a potential novel application for teasaponin as an antiobesity and antiinflammatory agent.
authors.affiliation: Illawarra Health and Medical Research Institute, School of Health Sciences, University of Wollongong, Northfields Avenue, New South Wales 2522, Australia.
authors.forename: Yinghua
authors.initials: Y
authors.lastname: Yu
authors.forename: Yizhen
authors.initials: Y
authors.lastname: Wu
authors.forename: Alexander
authors.initials: A
authors.lastname: Szabo
authors.forename: Zhixiang
authors.initials: Z
authors.lastname: Wu
authors.forename: Hongqin
authors.initials: H
authors.lastname: Wang
authors.forename: Duo
authors.initials: D
authors.lastname: Li
authors.forename: Xu-Feng
authors.initials: XF
authors.lastname: Huang
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use*; D001067:Appetite Depressants / Q000008:administration & dosage / Q000627:therapeutic use; D028241:Camellia sinensis / Q000737:chemistry*; D059305:Diet, High-Fat / Q000009:adverse effects; D007033:Hypothalamus, Middle / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D007274:Injections, Intraperitoneal; D007333:Insulin Resistance; D020738:Leptin / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D009765:Obesity / Q000188:drug therapy* / Q000209:etiology / Q000276:immunology / Q000378:metabolism; D010936:Plant Extracts / Q000008:administration & dosage / Q000627:therapeutic use*; D011333:Pro-Opiomelanocortin / Q000096:biosynthesis / Q000378:metabolism; D011897:Random Allocation; D015398:Signal Transduction / Q000187:drug effects; D013662:Tea / Q000737:chemistry*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001067:Appetite Depressants; D020738:Leptin; D016328:NF-kappa B; D010936:Plant Extracts; D013662:Tea; D011333:Pro-Opiomelanocortin