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胰高血糖素样肽1受体激动剂exendin-4增加高脂喂养的C57BL/6J小鼠棕色脂肪脂代谢 被引量:3

Exendin-4 improves fat metabolism of brown adipose tissue in high-fat diet-induced obese C57BL/ 6J mice
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摘要 目的观察胰高血糖素样肽1(GLP-1)受体激动剂exendin-4干预对高脂饮食喂养的C57BL/6J小鼠棕色脂肪脂代谢的影响。方法将30只健康雄性6周龄C57BL/6J小鼠采用随机数字法分为正常组、高脂组、exendin-4干预组,每组10只。高脂组给予高脂饲料喂养、exendin-4干预组给予高脂饲料喂养联合exendin-4皮下注射。16周后,测定各组体重、体脂含量、游离脂肪酸、瘦素、甘油三酯水平,同时利用实时定量PCR和Western blotting法检测各组小鼠肩胛棕色脂肪葡萄糖转运体4(GLUT-4)、过氧化物酶体增殖剂激活受体γ2(PPAR-γ2)、脂滴包被蛋白(perilipin)和解偶联蛋白1(UCP-1)mRNA及蛋白表达。多组间数据比较采用单因素方差分析,两组问比较采用t检验。结果与正常组相比,高脂组小鼠体重、体脂成分、游离脂肪酸、瘦素、甘油三酯的水平明显升高(t=7.34、6.11、8.33、10.51、4.19,均P〈0.05);且高脂组肩胛棕色脂肪GLUT-4、PPAR—v2、perilipin和UCP-1的基因和蛋白表达均显著下降(t=7.15~34.79,均P〈0.05)。与高脂组相比,exendin-4干预组小鼠体重、体脂成分、游离脂肪酸、瘦素、甘油三酯均较高脂组显著降低(t=5.63、4.04、8.85、6.06、3.07,均P〈0.05),同时exendin-4干预组小鼠肩胛棕色脂肪GLUT-4、PPAR-γ2、perilipin和UCP—1基因和蛋白表达均较高脂组显著升高(t=5.38—21.69,均P〈0.05)。结论GLP-1受体激动剂可能通过调控棕色脂肪脂代谢而影响体重。 Objective To investigate the role of exendin-4 treatment on fat metabolism of brown adipose tissue in C57BL/6J mice induced with high-fat diet. Methods Thirty six-week-old C57BL/6J mice were randomly divided into 3 groups(10 mice in each group): control group, high-fat diet (HFD) group, and HFD group treated with exendin-4. After 16 weeks, the body weight, body fat composition, free fatty acids, leptin, triglyeerides level of each group were measured. The mRNA and protein expression of glucose transporter type 4 (GLUT-4), peroxisome proliferative activated receptor γ2(PPAR-γ2), perilipin and uncoupling protein I(UCP-1) in the scapular brown adipose tissue were detected with real-time quantitative polymerase chain reaction(PCR) and Western blotting methods. One-way ANOVA was used when data were compared among multiple groups and t analysis was applied for comparison between two groups. Results Compared with those in control group, the body weight, body fat composition, free fatty acids, leptin and triglyceride levels increased significantly in the HFD group (t=7.34, 6.11, 8.33, 10.51, 4.19, all P〈0.05); the mRNA and protein expression of GLUT-4, PPAR-γ2, perilipin and UCP- 1 in the scapular brown adipose tissue in HFD group decreased significantly when compared with those in control group (t=7.15-34.79, all P〈0.05). Compared with those in the HFD group, the body weight, body fat composition, free fatty acids, leptin and triglyceride leve|s decreased significantly in the exendin-4-treating group(t=5.63, 4.04, 8.85, 6.06, 3.07, all P〈0.05), while the mRNA and protein expression of GLUT-4, PPAR-y2, perilipin and UCP-1 increased significantly in the scapular brown adipose tissue in the exendin-4-treating group(t=5.38-21.69, all P〈0.05). Conclusion GLP-1 receptor agonist may reduce body weight via regulating lipid metabolism in brown fat.
出处 《中华糖尿病杂志》 CAS CSCD 2015年第9期571-575,共5页 CHINESE JOURNAL OF DIABETES MELLITUS
基金 国家自然科学青年基金(81401157)
关键词 肥胖 棕色脂肪 胰高血糖素样肽1受体激动剂 Obesity Brown fat Glucagon-like peptide-1 receptor agonist
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  • 1Gutzwiller JP, Drewe J, G:ke B, S,et al. Glucagon-likepeptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2[J]. Am J Physiol, 1999, 276 (5 Pt 2):R1541-1544. 被引量:1
  • 2Polakof S, Miguez JM, Soengas JL. Evidence for a gut-brain axis used by glucagon-like peptide-1 to elicit hyperglycaemia in fish[J]. J Neuroendocrinol, 2011, 23 (6):508-518. 被引量:1
  • 3Ding X, Saxena NK, Lin S, et al.Exendin-4, a glucagon-like protein-1 (GLP-1) receptor agonist, reverses hepatic steatosis in ob/ob mice[J]. Hepatology, 2006, 43(1): 173-181. 被引量:1
  • 4Lockie SH, Stefanidis A, Oldfield BJ, et al. Brown adipose tissue thermogenesis in the resistance to and reversal of obesity: a potential new mechanism contributing to the metabolic benefits of proglucagon-derived peptides[J]. Adipocyte, 2013, 2(4): 196-200. 被引量:1
  • 5Giorgino F, Laviola L, Leonardini A, et al.GLP-1: a new approach for type 2 diabetes therapy[J]. Diabetes Res Clin Pract, 2006, 74(2):S152-S155. 被引量:1
  • 6Thorens B, Porret A, Biihler L,et al. Cloning and functional expression of the human islet GLP- 1 receptor: demonstration that exendin-4 is an agonist and exendin-(9 - 39) an antagonist of the receptor[J]. Diabete, 1993(11), 42:1678-1682. 被引量:1
  • 7Lee J, Hong SW, Chae SW, et al.Exendin-4 improves steatohepatitis by increasing Sirt 1 expression in high-fat diet- induced obese C57BL/6J mice[J]. PLoS One, 2012, 7(2): 17. 被引量:1
  • 8Cannon B, Nedergaard J. Brown adipose tissue: function and physiological significance[J]. Physiol Rev, 2004, 84(1 ):277-359. 被引量:1
  • 9Ren D, Collingwood TN, Rebar E J, et al.PPARgamma knockdown by engineered transcription factors: exogenous PPARgamma2 but not PPARgammal reactivates adipogenesis[J]. Genes Dev, 2002, 16(1):27-32. 被引量:1
  • 10Chert W, Yang CC, Sheu HM,et al. Expression of peroxiSome proliferator-activated receptor and CCAAT/enhancer binding protein transcription factors in cultured human sebocytes[J]. J Invest Dermatol,2003, 121(3):441-447. 被引量:1

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  • 1Cousin B, Cinti S, Morroni M, et al. Occurrence of brown adipocytes in rat white adipose tissue: molecular and morphological characterization[J]. 'i Cell Sci,1992,103 (Pt 4): 931-942. 被引量:1
  • 2Vosselman MJ, van Marken Lichtenbelt WD, Schrauwen P. Energy dissipation in brown adipose tissue: from mice to men [J]. Mol Cell Endocrinol,2013,379(1-2):43-50. DOI:10.1016/j. mce.2013.04.017. 被引量:1
  • 3van Marken Lichtenbelt WD, Schrauwen P. Implications of nonshivering thermogenesis for energy balance regulation in humans [J]. Am J Physiol Regul Integr Comp Physiol,2011,301 (2):R285-296. 被引量:1
  • 4DOh 10.1152/ajpregu.O0652.2010. Anderson ZL, Clements ,IN. Exenatide extended-release: a once-weekly option for patients with type 2 diabetes[J]. JAAPA, 20"14,27(6):44-46. DOh10.1097/01.JAA.0000443811.42907. a5. 被引量:1
  • 5Flint A, Raben A, Rehfeld ,IF, et al. The effect of glucagon- like peptide-1 on energy expenditure and substrate metabolism in humans[J]. Int J Obes Relat Metab Disord,2000, 24(3):288-298. 被引量:1
  • 6Obesity: preventing and managing the global epidemic. Report of a WHO consultation [J].World Health Organ Tech Rep Ser, 2000,894:i-xii, 1-253. 被引量:1
  • 7Klonoff DC, Buse JB, Nielsen LL, et al. Exenatide effects on diabetes, obesity, cardiovascular risk factors and hepatic biomarkers in patients with type 2 diabetes treated for at least 3 years [J].Curr Med Res Opin,2008,24(1):275-286. 被引量:1
  • 8Jaishy B, Zhang Q, Chung HS, et al. Lipid-induced NOX2 activation inhibits autophagic flux by impairing lysosomal enzyme activity [J].J Lipid Res,2015,56(3):546-561. DOI: 10.1194/jlr.M055152. 被引量:1
  • 9Sciarretta S, olpe M, Sadoshima J. Is reactivation of autophagy a possible therapeutic solution for obesity and metabolic syndrome? [J].Autophagy,2012,8(8):1252-1254. DOI:10.4161/ auto.20670. 被引量:1
  • 10Gonzdez-Rodrfguez A, Mayoral R, Agra N, et al. Impaired autophagic flux is associated with increased endoplasmic reticulum stress during the development of NAFLD [J].Cell Death Dis,2014,5:e1179. DOI:10.1038/cddis.2014.162. 被引量:1

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