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山东大学学报 (医学版) ›› 2020, Vol. 58 ›› Issue (8): 101-106.doi: 10.6040/j.issn.1671-7554.0.2020.673

• • 上一篇    

52例肥胖患者脂肪分布与代谢综合征及糖代谢指标的相关性

扈艳雯1,王志媛1,郁万江2,赵蕙琛1,韩合理2,徐志鹏2,马红3,张玉超1,刘元涛1   

  1. 青岛大学医学院附属青岛市市立医院 1.内分泌科;2. 放射科;3. 保健科, 山东 青岛 266011
  • 发布日期:2020-08-07
  • 通讯作者: 刘元涛. E-mail:sduliuyuantao@163.com
  • 基金资助:
    青岛市创新领军人才项目(16-8-3-24-zhc)

Correlation of fat distribution with metabolic syndrome and glucose metabolism in 52 obese patients

HU Yanwen1, WANG Zhiyuan1, YU Wanjiang2, ZHAO Huichen1, HAN Heli2, XU Zhipeng2, MA Hong3, ZHANG Yuchao1, LIU Yuantao1   

  1. 1. Department of Endocrinology;
    2. Department of Radiology;
    3. Department of Health Care, Qingdao Municipal Hospital Affiliated to Medical School of Qingdao University, Qingdao 266011, Shandong, China
  • Published:2020-08-07

摘要: 目的 探讨定量CT测量的肥胖人群脂肪分布对代谢综合征及糖代谢水平的影响。 方法 选取体质量指数(BMI)≥28的肥胖患者52例,依据是否合并代谢综合征分为合并代谢综合征组(OB-MS组,n=32例)和单纯肥胖组(OB-NMS组,n=20例);根据口服75 g葡萄糖耐量试验(OGTT)结果分为肥胖糖耐量正常组(OB-NGT组,n=17例)、肥胖糖耐量受损组(OB-IGT组,n=15例)及肥胖糖尿病组(OB-DM组,n=20例)。采用螺旋CT定量测定腰2、3、4、5椎体平面脂肪组织总面积及内脏脂肪面积,双侧腰大肌、后背肌肌肉及脂肪面积,肝脏、胰腺脂肪百分比,同时检测各项代谢生化指标并计算胰岛素抵抗指数及胰岛素分泌指数,比较各组不同指标的差异。 结果 OB-MS组内脏脂肪面积(t=3.37)及胰腺脂肪百分比(t=2.05)大于OB-NMS组(P<0.05)。糖耐量不同的肥胖患者,内脏脂肪面积(F=7.63)、肝脏(F=5.93)及胰头脂肪百分比(F=3.70)差异有统计学意义(P均<0.05),OB-IGT组和OB-DM组内脏脂肪面积均大于OB-NGT组,OB-DM组肝脏及胰头脂肪百分比大于OB-NGT组,差异有统计学意义(P<0.05)。多元线性回归结果显示,调整年龄及胰岛素抵抗指数后,内脏脂肪面积(SB=-0.83,P=0.02)和胰头脂肪百分比(SB=-0.51,P=0.02)与胰岛β细胞功能指数(MBCI)对数呈负相关。 结论 肥胖患者的内脏脂肪沉积与代谢综合征的发生具有密切关系;而内脏、肝脏及胰头脂肪沉积与肥胖患者糖代谢紊乱的发生密切相关。本研究为临床肥胖患者代谢综合征及糖尿病的早期识别提供了可靠的指标。

关键词: 肥胖, 脂肪分布, 代谢综合征, 糖代谢异常

Abstract: Objective To investigate the effects of fat distribution measured by quantitative-computed tomography(Q-CT)on metabolic syndrome(MS)and glucose metabolism in obese people. Methods Totally 52 patients with body mass index(BMI)≥28 were collected and divided into two groups: obesity with MS group(OB-MS group, n=32)and obesity without MS group(OB-NMS group, n=20). According to the results of 75g oral glucose tolerance test(OGTT), the subjects were divided into three groups: obesity with normal glucose tolerance group(OB-NGT group, n=17), impaired glucose tolerance group(OB-IGT group, n=15), and obesity with diabetes mellitus group(OB-DM group, n=20). The adipose tissue area and visceral fat area of lumbar vertebras 2, 3, 4 and 5, the muscle and fat area of bilateral psoas major and back muscles, and the percentages of liver fat and pancreatic fat were quantitatively determined with spiral CT. Meanwhile, various metabolic and biochemical indexes were detected and compared. Results OB-MS group had significantly larger visceral fat area(t=3.37)and higher percentage of pancreatic fat(t=2.05)than OB-NMS group. There were statistically significant differences in visceral fat area(F=7.63), percentage of liver fat(F=5.93)and percentage of pancreatic head fat(F=3.70)among the three groups with different glucose tolerance(P<0.05). OB-IGT and OB-DM groups had larger visceral fat area than OB-NGT group, and OB-DM group had greater percentages of liver fat and pancreatic head fat than OB-NGT group(P<0.05). Multiple linear regression results showed that after age and insulin resistance index were adjusted, visceral fat area(SB=-0.83, P=0.02)and percentage of pancreatic head fat(SB=-0.51, P=0.02)were negatively correlated with modified β-cell function index(MBCI). Conclusion The accumulation of visceral fat is an important factor leading to metabolic syndrome, while visceral fat, liver fat and pancreatic head fat are important risk factors leading to abnormal glucose metabolism in obese people. These results provide clinical indicators for the early identification of metabolic syndrome and diabetes in obese patients.

Key words: Obesity, Fat distribution, Metabolic syndrome, Abnormal glucose metabolism

中图分类号: 

  • R589
[1] 倪国华, 张璟, 郑风田. 中国肥胖流行的现状与趋势[J]. 中国食物与营养, 2013, 19(10): 70-74. NI Guohua, ZHANG Jing, ZHENG Fengtian. Status and trends of Chinese obesity epidemic[J]. Food and Nutrition in China, 2013, 19(10): 70-74.
[2] Rangel H, Pastor V, Gil. Are we close to defining a metabolomic signature of human obesity? A systematic review of metabolomics studies[J]. Metabolomics, 2019, 15(6): 93.
[3] Despres JP, Lemieux. Abdominal obesity and metabolic syndrome[J]. Nature, 2006, 444(7121): 881-887.
[4] Martin KA, Mani MV, Mani A. New targets to treat obesity and the metabolic syndrome[J]. Eur J Pharmacol, 2015, 763: 64-74. doi: 10.1016/j.ejphar.
[5] Wang TG, Lu JL, Shi LX, et al. Association of insulin resistance and β-cell dysfunction with incident diabetes among adults in China: a nationwide, population-based, prospective cohort study[J]. Lancet Diabetes Endocrinol, 2020, 8(2): 115-124.
[6] Yi KH, Hwang JS, Kim EY, et al. Prevalence of insulin resistance and cardiometabolic risk in Korean children and adolescents: A population-based study[J]. Diabetes Res Clin Pract, 2014, 103(1): 106-113.
[7] Sukran P, Firdevs B, Feyaza D. Metabolic syndrome in young people[J]. Curr Opin Endocrinol Diabetes Obes, 2014, 21(1): 56-63.
[8] Yao WJ, Guo Z, Wang L, et al. Pancreas fat quantification with quantitative CT: an MRI correlation analysis[J]. Clin Radiol, 2020, 75(5):397.
[9] 张晨鑫, 张勇, 王玲, 等. 定量CT与MRI测量腹部脂肪面积及分布的比较[J]. 重庆医学, 2016, 45(30): 4179-4181. ZHANG Chenxin, ZHANG Yong, WANG Ling, et al. Comparison of abdominal fat area and distribution assessment with quantitative CT and MRI[J]. Chongqing Medicine, 2016, 45(30): 4179-4181.
[10] 石劢, 朱燕波. 肥胖诊断标准及其临床应用的研究进展[J]. 中国食物与营养, 2014, 20(9): 76-80. SHI Mai, ZHU Yanbo. Research progress on the diagnostic criteria of obesity and its clinical application[J]. Food and Nutrition in China, 2014, 20(9): 76-80.
[11] 中华医学会糖尿病学分会代谢综合征研究协作组. 中华医学会糖尿病学分会关于代谢综合征的建议[J]. 中华糖尿病杂志, 2004, 12(3): 156-161.
[12] 中国肥胖问题工作组. 中国成人超重和肥胖症预防与控制指南(节录)[J]. 营养学报, 2004, 26(1): 1-4.
[13] Han XL, Wu Y, Gao H, et al. Correlation of abdominal adipose distribution, lipid content of liver and obesity using quantitative CT[J]. Chin J Med Imaging Technol, 2017, 33(Suppl 1): 90-92.
[14] Sun J, Du Q, Wang GP, et al. Research on β cell function and insulin resistance in patients with type 2 diabetes mellitus[J]. Chin J Diabetes, 2015, 23(7): 592-594.
[15] Sun Z, Ma L, Qiu YQ, et al. Recent progress of islets beta-cells dysfunction in type 2 diabetes[J]. Medical Recapitulate, 2008, 14(9): 1371-1373.
[16] 杨菊, 王红, 尹维珍, 等. 新β细胞功能指数MBCI在2型糖尿病临床评估探讨[J]. 实用糖尿病杂志, 2005, 1(3): 20-21.
[17] Li GW, Yang WY, Jiang Y, et al. The possibility of(FINS×FPG)/(PG2h+PG1h-2FPG)being taken as an index of pancreatic β cell insulin secretion in a population-based study[J]. Chin J Intern Med, 2000, 39(4): 234-238.
[18] 蒋建家, 孙炳庆, 庄玉君, 等. 内脏脂肪蓄积与血尿酸和代谢综合征的关系[J]. 福建医科大学学报, 2009, 43(4): 327-330. JIANG Jianjia, SUN Bingqing, ZHUANG Yujun. The relation between accumulation of visceral fat and serum uric acid and metabolic syndrome[J]. Journal of Fujian medical university, 2009, 43(4): 327-330.
[19] Neeland IJ, Poirier P, Despres J, et al. Cardiovascular and metabolic heterogeneity of obesity: clinical challenges and implications for management[J]. Circulation, 2018, 137(13): 1391-1406.
[20] Park SK, Seo MH, Shin HC, et al. Clinical availability of nonalcoholic fatty liver disease as an early predictor of type 2 diabetes mellitus in Korean men: 5-year prospective cohort study[J]. Hepatology, 2013, 57(4): 1378-1383.
[21] Wang CY, Ou HY, Chen MF, et al. Enigmatic Ectopic Fat: Prevalence of nonalcoholic fatty pancreas disease and its associated factors in a Chinese population[J]. J Am Heart Assoc, 2014, 3(1): 1-9.
[22] Chai J, Liu P, Jin E, et al. MRI chemical shift imaging of the fat content of the pancreas and liver of patients with type 2 diabetes mellitus[J]. Exp Ther Med, 2016, 11(2): 476-480.
[23] Van der Zijl NJ, Goossens GH, Moors CCM, et al. Ectopic fat storage in the pancreas, liver, and abdominal fat depots: impact on β-cell function in individuals with impaired glucose metabolism[J]. J Clin Endocrinol Metab, 2011, 96(2): 459-467.
[24] 侯海青, 蔡美娟, 王文, 等. 代谢综合征对非酒精性脂肪肝患者肝脏脂肪含量的影响及相关因素[J]. 中国老年学杂志, 2019, 39(1):81-84.
[25] Li H, Zhang GG, Zhao WJ, et al. Effect of visceral fat content on the insulin resistance and islet β cell function in type 2 diabetes mellitus[J]. Progress in Modern Biomedicine, 2019, 19(14): 2740-2742.
[26] Kharroubi I, Ladrière L, Cardozo AK, et al. Free fatty acids and cytokines induce pancreatic β-cell apoptosis by different mechanisms: role of nuclear factor-κB and endoplasmic reticulum stress[J]. Endocrinology, 2004, 145(11): 5087-5096.
[27] Shimabukuro M, Higa M, Zhou YT. Lipoapoptosis in beta-cells of obese prediabetic fa/fa rats[J]. J Biol Chem, 1998, 273(49): 32487-32490.
[28] Zhang X, Cui Y, Fang L, et al. Chronic high-fat diets induce oxide injuries and fibrogenesis of pancreatic cells in rats[J]. Pancreas, 2008, 37(3): 31-38.
[29] Heni M, Machann J, Staiger H, et al. Pancreatic fat is negatively associated with insulin secretion in individuals with impaired fasting glucose and/or impaired glucose tolerance: a nuclear magnetic resonance study[J]. Diabetes Metab Res Rev, 2010, 26(3): 200-205.
[30] Tushuizen ME, Bunck MC, Pouwels PJ, et al. Pancreatic fat content and β-cell function in men with and without type 2 diabetes[J]. Diabetes Care, 2007, 30(11): 2916-2921.
[31] Lingvay I, Esser V, Legendre JL, et al. Noninvasive quantification of pancreatic fat in humans[J]. J Clin Endocrinol Metab, 2009, 94(10): 4070-4076.
[32] Saisho Y, Butler AE, Meier JJ, et al. Pancreas volumes in humans from birth to age one hundred taking into account sex, obesity, and presence of type2 diabetes[J]. Clin Anat, 2007, 20(8): 933-942.
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