[1]张珊 于雪梅.3-羧-4-甲-5-丙基呋喃戊酮酸与糖尿病[J].国际内分泌代谢杂志,2018,38(02):99-101.[doi:10.3760/cma.j.issn.1673-4157.2018.02.007]
 Zhang Shan,Yu Xuemei.3-Carboxy-4-methyl-5-propyl-2-furanpropanoic acid and diabetes mellitus[J].International Journal of Endocrinology and Metabolism,2018,38(02):99-101.[doi:10.3760/cma.j.issn.1673-4157.2018.02.007]
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3-羧-4-甲-5-丙基呋喃戊酮酸与糖尿病()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
38
期数:
2018年02期
页码:
99-101
栏目:
综述
出版日期:
2018-03-20

文章信息/Info

Title:
3-Carboxy-4-methyl-5-propyl-2-furanpropanoic acid and diabetes mellitus
作者:
张珊 于雪梅
201499 上海市奉贤区中心医院内分泌代谢科
Author(s):
Zhang Shan Yu Xuemei
Department of Endocrinology and Metabolism, Fengxian District Central Hospital of Shanghai, Shanghai 201499,China
关键词:
3-羧-4-甲-5-丙基呋喃戊酮酸 妊娠期糖尿病 2型糖尿病 2型糖尿病一级亲属 胰岛β细胞功能障碍
Keywords:
3-Carboxy-4-methyl-5-propyl-2-furanpropanoic acid Gestational diabetes mellitus Type 2 diabetes mellitus First-degree relatives of type 2 diabetes patients Islet β cell dysfunction
DOI:
10.3760/cma.j.issn.1673-4157.2018.02.007
摘要:
3-羧-4-甲-5-丙基呋喃戊酮酸(CMPF)是一种内源性的呋喃脂肪酸代谢产物,代谢组学研究发现,妊娠期糖尿病、糖耐量减低以及2型糖尿病患者,血清CMPF水平明显升高。血清高浓度的CMPF造成糖耐量减低,抑制葡萄糖刺激的胰岛素分泌,并且降低葡萄糖的利用率。研究发现,CMPF可以导致线粒体功能异常,减少葡萄糖诱导的三磷酸腺苷积累,诱导氧化应激反应,造成转录因子的调节异常,并且增加了晚期糖基化终末产物及胰岛素前体的合成,最终导致胰岛素生物合成减少。因此,进一步探索CMPF与糖代谢的关联,可为探索糖尿病的发生及发展提供新的方向。
Abstract:
3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid(CMPF)is an endogenous metabolites of furan fatty acids. Metabolomics research found that patients with gestational diabetes, impaired glucose tolerance or type 2 diabetes mellitus had significantly higher serum CMPF levels. Elevated serum concentration of CMPF causes impaired glucose tolerance, inhibites glucose stimulated insulin secretion and decreases glucose utilization. Further research found that CMPF can lead to mitochondrial dysfunction, reduce glucose-induced accumulation of adenosine triphosphate, induce oxidative stress response, resulting in dysregulation of transcription factors and increasing formation of advanced glycation end-product and immature proinsulin, finally leading to reduced insulin biosynthesis. Therefore, further exploration of the relationship between CMPF and glycolipid metabolism can give new direction for studies of the occurrence and development of diabetes.

参考文献/References:


[1] Spiteller G.Furan fatty acids: occurrence, synthesis, and reactions. Are furan fatty acids responsible for the cardioprotective effects of a fish diet?[J].Lipids,2005,40(8):755-771.
[2] Pirondini M,Colombini S,Mele M,et al.Effect of dietary starch concentration and fish oil supplementation on milk yield and composition, diet digestibility, and methane emissions in lactating dairy cows[J].J Dairy Sci,2015,98(1):357-372.DOI:10.3168/jds.2014-8092.
[3] Hanhineva K,Lankinen MA,Pedret A,et al.Nontargeted metabolite profiling discriminates diet-specific biomarkers for consumption of whole grains, fatty fish, and bilberries in a randomized controlled trial[J].J Nutr,2015,145(1):7-17.DOI:10.3945/jn.114.196840.
[4] Lankinen MA,Hanhineva K,Kolehmainen M,et al.CMPF does not associate with impaired glucose metabolism in individuals with features of metabolic syndrome[J]. PLoS One,2015,10(4):e0124379.DOI:10.1371/journal.pone.0124379.
[5] Prentice KJ,Luu L,Allister EM,et al.The furan fatty acid metabolite CMPF is elevated in diabetes and induces β cell dysfunction[J].Cell Metab,2014,19(4):653-666.DOI:10.1016/j.cmet.2014.03.008.
[6] Retnakaran R,Ye C,Kramer CK,et al.Evaluation of circulating determinants of Beta-cell function in women with and without gestational diabetes[J].J Clin Endocrinol Metab,2016,101(7):2683-2691.DOI:10.1210/jc.2016-1402.
[7] Liu Y,Prentice KJ,Eversley JA,et al.Rapid elevation in CMPF may act as a tipping point in diabetes development[J].Cell Rep,2016,14(12):2889-2900.DOI:10.1016/j.celrep.2016.02.079.
[8] Meert N, Schepers E, De Smet R,et al. Inconsistency of reported uremic toxin concentrations[J].Artif Organs,2007,31(8):600-611. DOI:10.1111/j.1525-1594.2007.00434.x.
[9] Zheng JS,Lin M,Imamura F,et al.Serum metabolomics profiles in response to n-3 fatty acids in Chinese patients with type 2 diabetes: a double-blind randomised controlled trial[J].Sci Rep,2016,6:29522. DOI:10.1038/srep29522.
[10] Retnakaran R,Ye C,Kramer CK,et al.Maternal serum prolactin and prediction of postpartum β-cell function and risk of prediabetes/diabetes[J].Diabetes Care,2016,39(7):1250-1258.DOI:10.2337/dc16-0043.
[11] Zhang S,Chen P,Jin H,et al.Circulating 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid(CMPF)levels are associated with hyperglycemia and β cell dysfunction in a Chinese population[J].Sci Rep,2017,7(1):3114.DOI:10.1038/s41598-017-03271-1.
[12] Boucher MJ,Selander L,Carlsson L,et al.Phosphorylation marks IPF1/PDX1 protein for degradation by glycogen synthase kinase 3-dependent mechanisms[J].J Biol Chem,2006,281(10):6395-6403.
[13] Robson-Doucette CA,Sultan S,Allister EM,et al.Beta-cell uncoupling protein 2 regulates reactive oxygen species production, which influences both insulin and glucagon secretion[J].Diabetes,2011,60(11):2710-2719.DOI:10.2337/db11-0132.
[14] Masini M,Marselli L,Bugliani M,et al.Ultrastructural morphometric analysis of insulin secretory granules in human type 2 diabetes[J].Acta Diabetol,2012,49(Suppl 1):S247-S252.DOI:10.1007/s00592-012-0446-6.
[15] Deguchi T,Kusuhara H,Takadate A,et al.Characterization of uremic toxin transport by organic anion transporters in the kidney[J].Kidney Int,2004,65(1):162-174.DOI:10.1111/j.1523-1755.2004.00354.x.

备注/Memo

备注/Memo:
基金项目:上海市科学技术委员会医学引导项目(134119b2500); 上海申康医院发展中心(SHDC12012302)
通信作者:于雪梅,Email: xuemeiyu12@163.com
更新日期/Last Update: 1900-01-01