Abstract
Insulin resistance is strongly associated with the metabolic syndrome, and chronic inflammation is known to be a major mechanism of insulin resistance and is a therapeutic target. This study was designed to evaluate the effect of Scutellaria baicalensis (SB) in high-fat diet (HFD)-induced insulin-resistant mice and to investigate its mechanism based on inflammatory responses. Mice were fed a HFD to induce insulin resistance and then administered SB for nine weeks. Body weight, glucose, lipid, insulin, epididymal fat pad and liver weights, and histologic characteristics were evaluated to determine the effect on insulin resistance. In order to evaluate the effects on the inflammatory process, we analyzed the proportions of macrophages in liver and epididymal fat and measured inflammatory gene expression. Fasting and postprandial glucose, fasting insulin, HOMA-IR, triglycerides, and low density lipoprotein cholesterol levels were significantly decreased by SB administration. The epididymal fat and liver showed significant weight decreases and histological improvements. Total adipose tissue macrophages (ATMs) decreased (27.71 ± 3.47% vs. 45.26 ± 7.26%, p < 0.05), M2 ATMs increased (47.02 ± 6.63% vs. 24.28 ± 8.00%, p < 0.05), and CD11b+ Kupffer cells decreased. The expression levels of tumor necrosis factor alpha and F4/80 in the liver were significantly decreased (12.03 ± 1.47% vs. 25.88 ± 4.57%, p < 0.05) compared to HFD group. These results suggest that SB improved insulin resistance through inhibition of macrophage-mediated inflammation.
Highlights
Metabolic syndrome represents a clustering of metabolic risk factors including central obesity, hyperinsulinemia, hypertension, and dyslipidemia; insulin resistance (IR) is considered a common mechanism underlying derangements associated with metabolic syndrome [1]
Body weight gain was higher in the high-fat diet (HFD) and Scutellaria baicalensis (SB) groups than in the normal chow (NC)2g.1r.oEuffpec,tasnofdStBhoenSBBWgarnoduEpphidaiddyamalol Fwaet ranbdoLdivyerwWeiegighhtt cCohmanpgeasred to the HFD group, not significanBtolydy(3w9e.1ig4ht±ga4i.n24wags vhsig.h4er4.i9n8th±e h3ig.1h5-fagt)d(iFeitg(HurFeD1)Aan)d
If we can modulate the systemic inflammation and insulin resistance as well as reduce lipid accumulation, it can be expected to lower the risk of metabolic syndrome
Summary
Metabolic syndrome represents a clustering of metabolic risk factors including central obesity, hyperinsulinemia, hypertension, and dyslipidemia; insulin resistance (IR) is considered a common mechanism underlying derangements associated with metabolic syndrome [1]. Inflammation in adipose tissue promotes the accumulation of macrophages and inflammatory cytokines produced by both adipocytes and macrophages, which causes systemic as well as local inflammation [2,3,4]. Lipid accumulation in the liver is often accompanied by insulin resistance, which causes subacute hepatocellular inflammation and increases the release of pro-inflammatory cytokines [5]. These local pro-inflammatory substances, in addition to systemic inflammatory agents entering through the portal vein, activate Kupffer cells and other immune cells, which in turn release inflammatory cytokines and affect insulin resistance [4]. Stcoi.f20S1c9,u2t0e,lxlaria baicalensis Georgi (SB) has been used for the treatment of fever,2voof m10iting, dysenpoterrtayl, vjaeuinn,daiccteiv, arteespKiurpaftfoerryceinllsfeacntidonost,hearnidmsmkuinnedcieslelas,sewsh[ic6h]. inIntusrenvererlaelassetuidnfileasm, mSBatosrhyowed favorcaybtolekiannestia-nindflaafmfecmt iantsourlyinerfefseiscttasn[c7e,8[4]];. most studies investigated drug-induced acute inflammaTthioenr.ootInof tSecrumtesllaorifa binaiscualleinnsisreGseisotragni c(SeB)anhads breleanteudseddifsoerathsest,retahtme eenffteocftfsevoefr,SvBomointinogb, esity, hypedrtyrsiegnltyecreyr, idjaeumndiiace[,9r]e, sapnirdatohreypiantfoecmtieognsa,lyan[d10s]kihnadviesebaseeesn[6r]e.pIonrtseedve, rbalusttuthdeierse, ShBavsehobweeedn few relatefadvosrtaubdleieasn. ti-Tinhfulasm, minatothryisesffteucdtsy,[7w,8]e; hinowveesvteirg,amteodst tshteudeieffseicntvseostfigSaBtedondruings-iunldinucreedsiasctuatnece in high-ifnafltadmimetat(iHonF.DIn)-fteedrmCs5o7fBiLn/su6limn ircees,isatanndceinavndestrieglaatteedd dtihseeamsese,chthaeniesfmfecstsofofacStBioonnwoibtehsitay,focus on mhsatycuprdoeipretshr.iagTglhyeuc-esmr, ieidndemitahitiased[s9t]cu,hdaryno,dnwhiceepiinantflvoeamsmteigmgaaatleytdi[o1tn0h].eheafvfeecbtseeonf reported, but there have been few related SB on insulin resistance in high-fat diet
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