过氧化物酶体增殖物激活受体α和γ激动剂对OLETF大鼠内脏脂肪中内脂素、脂联素和肿瘤坏死因子α表达的影响。
Effect of PPAR-alpha and -gamma agonist on the expression of visfatin, adiponectin, and TNF-alpha in visceral fat of OLETF rats.
作者信息
Choi K C, Ryu O H, Lee K W, Kim H Y, Seo J A, Kim S G, Kim N H, Choi D S, Baik S H, Choi K M
机构信息
Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Korea University, Seoul 152-050, Republic of Korea.
出版信息
Biochem Biophys Res Commun. 2005 Oct 28;336(3):747-53. doi: 10.1016/j.bbrc.2005.08.203.
A variety of adipocytokines and peptides secreted from adipocytes have been considered to play a crucial role in obesity, insulin resistance, and type 2 diabetes. Recently, visfatin, a new adipocytokine, known as a pre-B cell colony-enhancing factor, has been isolated from visceral fat deposits. It has been shown to activate insulin receptors in a manner different from insulin. To understand the role of adipocytokines in improving insulin sensitivity via activation of the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and -gamma (PPAR-gamma), we examined the expression of visfatin, adiponectin, and TNF-alpha in visceral fat depots of Otsuka Long-Evans Tokushima fatty (OLETF) rats from early to advanced diabetic stage (from 28 to 40 weeks of age). Serum glucose and insulin concentrations significantly (P<0.05) decreased in rosiglitazone or fenofibrate-treated OLETF rats compared to untreated OLETF rats. Rosiglitazone significantly increased serum adiponectin concentration from 20 to 40 weeks of age (P<0.05), whereas fenofibrate reduced TNF-alpha concentration. The expression of visfatin and adiponectin mRNA in visceral fat deposits was elevated by rosiglitazone or fenofibrate treatments when compared to untreated OLETF rats (P<0.05), whereas, TNF-alpha mRNA was down-regulated by these drugs (P<0.05). These results suggest that rosiglitazone and fenofibrate may prevent type 2 diabetes by regulating adipocytokines including visfatin, adiponectin, and TNF-alpha.
脂肪细胞分泌的多种脂肪细胞因子和肽类被认为在肥胖、胰岛素抵抗及2型糖尿病中起关键作用。最近，一种新的脂肪细胞因子内脂素，即前B细胞集落增强因子，已从内脏脂肪沉积物中分离出来。研究表明，它能以不同于胰岛素的方式激活胰岛素受体。为了解脂肪细胞因子通过激活核受体过氧化物酶体增殖物激活受体α（PPAR-α）和γ（PPAR-γ）来改善胰岛素敏感性的作用，我们检测了大冢长-艾维-德岛肥胖（OLETF）大鼠从糖尿病早期到晚期（28至40周龄）内脏脂肪库中内脂素、脂联素和肿瘤坏死因子α（TNF-α）的表达。与未治疗的OLETF大鼠相比，罗格列酮或非诺贝特治疗的OLETF大鼠血清葡萄糖和胰岛素浓度显著降低（P<0.05）。罗格列酮在20至40周龄时显著提高血清脂联素浓度（P<0.05），而非诺贝特降低TNF-α浓度。与未治疗的OLETF大鼠相比，罗格列酮或非诺贝特治疗可提高内脏脂肪沉积物中内脂素和脂联素mRNA的表达（P<0.05），而这些药物可下调TNF-α mRNA的表达（P<0.０5）。这些结果表明，罗格列酮和非诺贝特可能通过调节包括内脂素、脂联素和TNF-α在内的脂肪细胞因子来预防2型糖尿病。
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