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K.-C. Sung D.-C. Seo S.-J. Lee M.-Y. Lee S.H. Wild C.D. Byrne 《Nutrition, metabolism, and cardiovascular diseases : NMCD》2019,29(5):489-495
Background and aims
It is not known whether non alcoholic fatty liver disease (NAFLD) is a risk factor for diabetes in non obese, non centrally-obese subjects. Our aim was to investigate relationships between fatty liver, insulin resistance and a biomarker score for liver fibrosis with incident diabetes at follow up, in subjects who were neither obese nor centrally-obese.Methods and results
As many as 70,303 subjects with a body mass index (BMI) < 25 kg/m2 and without diabetes were followed up for a maximum of 7.9 years. At baseline, fatty liver was identified by liver ultrasound, insulin resistance (IR) by homeostatic model assessment of insulin resistance (HOMA-IR) ≥2.0, and central obesity by waist circumference (waist circumference ≥90 cm (men) and ≥85 cm (women). The Fibrosis-4 (FIB-4 score) was used to estimate extent of liver fibrosis. Cox proportional hazards models adjusted for confounders were used to estimate hazard ratios (aHRs) for incident diabetes. As many as 852 incident cases of diabetes occurred during follow up (median [IQR] 3.71 [2.03] years). Mean ± SD BMI was 22.8 ± 1.8 and 21.7 ± 2.0 kg/m2 in subjects with and without diabetes at follow up. In subjects without central obesity and with fatty liver, aHRs (95% CI) for incident diabetes at follow up were 2.17 (1.56, 3.03) for men, and 2.86 (1.50,5.46) for women. Similar aHRs for incident diabetes occurred with fatty liver, IR and the highest quartile of FIB-4 combined, in men; and there was a non significant trend toward increased risk in women.Conclusions
In normal weight, non-centrally obese subjects NAFLD is an independent risk factor for incident diabetes. 相似文献33.
《Nutrition, metabolism, and cardiovascular diseases : NMCD》2022,32(12):2883-2889
Background and aimsCoronary artery disease (CAD) is the principal cause of death in individuals with non-alcoholic fatty liver disease (NAFLD). The aim of this study was to use genetic epidemiology to study the association between de novo lipogenesis (DNL), one of the major pathways leading to NAFLD, and CAD risk.Methods and resultsDNL susceptibility genes were used as instruments and selected using three approaches: 1) genes that are associated with both high serum triglycerides and low sex hormone-binding globulin, both downstream consequences of DNL (unbiased approach), 2) genes that have a known role in DNL (biased approach), and 3) genes that have been associated with serum fatty acids, used as a proxy of DNL. Gene-CAD effect estimates were retrieved from the meta-analysis of CARDIoGRAM and the UK Biobank (~76014 cases and ~264785 controls). Effect estimates were clustered using a fixed-effects meta-analysis. Twenty-two DNL susceptibility genes were identified by the unbiased approach, nine genes by the biased approach and seven genes were associated with plasma fatty acids. Clustering of genes selected in the unbiased and biased approach showed a statistically significant association with CAD (OR:1.016, 95%CI:1.012; 1.020 and OR:1.013, 95%CI:1.007; 1.020, respectively), while clustering of fatty acid genes did not (OR:1.004, 95%CI:0.996–1.011). Subsequent exclusion of potential influential outliers did reveal a statistically significant association (OR:1.009, 95%CI:1.000; 1.018).ConclusionsDNL susceptibility genes are associated with an increased risk of CAD. These findings suggest that DNL may be involved in the pathogenesis of CAD and favor further development of strategies that target NAFLD through DNL. 相似文献
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目的了解长春西部地区过敏原特异性IgE分布情况。方法应用免疫印迹法检测1 258例患者的19种吸入性及食物性过敏原特异性IgE抗体,统计过敏原结果及种类。结果 1 258例患者,检出至少一种特异性IgE阳性率为34.0%。男性阳性率为33.5%;女性阳性率为34.5%。男女间阳性率差异无统计学意义(P> 0.05)。吸入性过敏原阳性率由高到低依次为:普通豚草14.2%、艾蒿11.4%、屋尘螨/粉尘螨8.1%、猫毛3.8%、狗上皮2.4%、柳树/杨树/榆树2.1%,屋尘1.6%、蟑螂1.6%、点青霉/分枝孢霉/烟曲霉/交链孢霉1.2%、葎草1.1%。食物性过敏原阳性率由高到低依次为:鸡蛋白2.9%、鳕鱼/龙虾/扇贝2.7%、牛奶2.3%、黄豆1.9%、蟹1.5%、虾1.3%、牛肉1.2%、花生1.0%、羊肉0.8%。混合过敏达到了相当高的比例。结论长春西部地区吸入性过敏原以普通豚草、艾蒿和屋尘螨/粉尘螨为主;食物性过敏原以鸡蛋白、鳕鱼/龙虾/扇贝、牛奶为主,明确过敏原,对过敏性患者的预防和治疗有重大意义。 相似文献
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《Clinical gastroenterology and hepatology》2020,18(7):1412-1416
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J. Rodríguez-Carrio A. Martínez-Zapico I. Cabezas-Rodríguez L. Benavente Á.I. Pérez-Álvarez P. López J.B. Cannata-Andía M. Naves-Díaz A. Suárez 《Nutrition, metabolism, and cardiovascular diseases : NMCD》2019,29(2):135-143