The relationship one-hour glycemia level at oral glucose tolerance test and non-alcoholic fatty liver disease /Oral glukoz tolerans testinde 1. saat glukoz seviyesi ve non-alkolik yagli karaciger hastaligi

2016 ◽  
Vol 23 (3) ◽  
pp. 297
Author(s):  
Evrim Cakir ◽  
Huseyin Demirci ◽  
Elif Menekse ◽  
Hatice Demir
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Alcoholic Fatty Liver ◽  
Glycemia Level ◽  
The Relationship ◽  
Alcoholic Fatty Liver Disease

scholarly journals Predictors of Impaired Glucose Regulation in Patients with Non-Alcoholic Fatty Liver Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Erifili Hatziagelaki ◽  
Drosos E. Karageorgopoulos ◽  
Athina Chounta ◽  
Anastasia Tsiavou ◽  
Matthew E. Falagas ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Density Lipoprotein ◽  
Tolerance Test ◽  
Glucose Regulation ◽  
Oral Glucose ◽  
Impaired Glucose Regulation ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Introduction. Many patients with non-alcoholic fatty liver disease (NAFLD) have impaired glucose regulation or type 2 diabetes mellitus (DM). We investigated characteristics of NAFLD patients associated with hyperglycemia.Methods. During a 2-hour oral glucose tolerance test (OGTT), serum glucose and insulin were measured in 152 NAFLD patients.Results. 48.7% of NAFLD patients had hyperglycemia. Age (odds ratio(OR)=1.08, 95% confidence interval (CI): 1.03–1.13), body mass index (BMI) (OR=1.12, 95% CI: 1.01–1.25), and lower high-density lipoprotein cholesterol (HDL-C) (OR=0.95, 95% CI: 0.92–0.98) proved to be independent predictors of hyperglycemia. After OGTT, 30 min insulin was lower in hyperglycemic patients (74.2±49.7versus94.5±53.9 μIU/mL,P=0.02), while 90 min insulin (170.1±84.6versus122.9±97.7 μU/mL,P=0.01) and 120 min insulin (164.0±101.2versus85.3±61.9 μIU/mL,P<0.01) were higher.Conclusions. NAFLD patients with higher BMI, lower HDL-C, or older age were more likely to have impaired glucose metabolism. An OGTT could be of value for early diagnosis of DM among this population.

scholarly journals Microbiota, type 2 diabetes and non-alcoholic fatty liver disease: protocol of an observational study

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Benedetta M. Motta ◽  
Christoph Grander ◽  
Martin Gögele ◽  
Luisa Foco ◽  
Vladimir Vukovic ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Liver Disease ◽  
Fatty Liver Disease ◽  
Liver Stiffness ◽  
Alcoholic Fatty Liver ◽  
Study Participants ◽  
The Relationship ◽  
Alcoholic Fatty Liver Disease

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is characterized by triglyceride accumulation in the hepatocytes in the absence of alcohol overconsumption, commonly associated with insulin resistance and obesity. Both NAFLD and type 2 diabetes (T2D) are characterized by an altered microbiota composition, however the role of the microbiota in NAFLD and T2D is not well understood. To assess the relationship between alteration in the microbiota and NAFLD while dissecting the role of T2D, we established a nested study on T2D and non-T2D individuals within the Cooperative Health Research In South Tyrol (CHRIS) study, called the CHRIS-NAFLD study. Here, we present the study protocol along with baseline and follow-up characteristics of study participants. Methods Among the first 4979 CHRIS study participants, 227 individuals with T2D were identified and recalled, along with 227 age- and sex-matched non-T2D individuals. Participants underwent ultrasound and transient elastography examination to evaluate the presence of hepatic steatosis and liver stiffness. Additionally, sampling of saliva and faeces, biochemical measurements and clinical interviews were carried out. Results We recruited 173 T2D and 183 non-T2D participants (78% overall response rate). Hepatic steatosis was more common in T2D (63.7%) than non-T2D (36.3%) participants. T2D participants also had higher levels of liver stiffness (median 4.8 kPa, interquartile range (IQR) 3.7, 5.9) than non-T2D participants (median 3.9 kPa, IQR 3.3, 5.1). The non-invasive scoring systems like the NAFLD fibrosis score (NFS) suggests an increased liver fibrosis in T2D (mean − 0.55, standard deviation, SD, 1.30) than non-T2D participants (mean − 1.30, SD, 1.17). Discussion Given the comprehensive biochemical and clinical characterization of study participants, once the bioinformatics classification of the microbiota will be completed, the CHRIS-NAFLD study will become a useful resource to further our understanding of the relationship between microbiota, T2D and NAFLD.

scholarly journals Relationship between triglyceride glucose index and the incidence of non-alcoholic fatty liver disease in the elderly: a retrospective cohort study in China

BMJ Open ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. e039804
Author(s):  
Chen Huanan ◽  
Li Sangsang ◽  
Adwoa Nyantakyiwaa Amoah ◽  
Bo Yacong ◽  
Chen Xuejiao ◽  
...  
Keyword(s):  
Cohort Study ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
The Elderly ◽  
Alcoholic Fatty Liver ◽  
Tyg Index ◽  
The Relationship ◽  
Alcoholic Fatty Liver Disease

ObjectiveNon-alcoholic fatty liver disease (NAFLD) is one of the major causes of liver-related diseases but relationship between triglyceride glucose (TyG) and NAFLD in the elderly is not reported yet. In this study, we investigated the role of TyG index for predicting the incidence of NAFLD in the elderly.Design and settingThis is a prospective cohort study in Henan, China, from 2011 to 2018.Participants and methodsIn total, 46 693 elderly who participated in a routine physical examination programme from 2011 to 2018 were included in this study. TyG index was calculated as ln (fasting triglyceride (mg/dL)×fasting plasma glucose (mg/dL)/2), while NAFLD was defined as hepatic steatosis after excluding other causes based on the results of abdominal ultrasonography; Cox regression model was performed to explore the relationship between TyG index and NAFLD. Also, mediation effect was used to analyse the role of the TyG index in WHtR (waist-to-height ratio) and NAFLD.ResultsDuring the 149 041 person-years follow-up, a total of 5660 NAFLD events occurred (3.80/100 person-years). After adjusting for potential confounding factors, quartiles 4 of TyG index significantly increased the incidence of NAFLD compared with quartile 1, the HRs and 95% CI were 1.314 (1.234 to 1.457). In addition, TyG index played a partial mediating role in the relationship between WHtR and NAFLD and indirect effect was 1.009 (1.006 to 1.011).ConclusionHigher TyG index was associated with higher risk of NAFLD in the aged, and therefore, TyG index may be a novel predictor for incidence of NAFLD. Further, regular examination and evaluation of the TyG index might be useful for controlling the occurrence of NAFLD.

scholarly journals Interplay between Oxidative Stress and Metabolic Derangements in Non-Alcoholic Fatty Liver Disease: The Role of Selenoprotein P

2020 ◽  
Vol 21 (22) ◽  
pp. 8838
Author(s):  
Gian Paolo Caviglia ◽  
Chiara Rosso ◽  
Angelo Armandi ◽  
Melania Gaggini ◽  
Fabrizia Carli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Fibrosis ◽  
Fatty Liver Disease ◽  
Gas Chromatography Mass Spectrometry ◽  
Oral Glucose ◽  
Selenoprotein P ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Background: Pathogenetic mechanisms involved in the progression of non-alcoholic fatty liver disease (NAFLD) are complex and multifactorial. We investigated oxidative stress through the measurement of selenoprotein P (SeP) in serum and we explored its relation to metabolic derangements and liver damage in a group of non-diabetic NAFLD subjects. Methods: 57 NAFLD patients underwent a double-tracer oral glucose tolerance test (OGTT). Insulin resistance (IR) components were calculated at baseline as follows: hepatic-IR = (endogenous glucose production*insulin); peripheral-IR = (glucose rate of disappearance(Rd)); adipose-tissue(AT)-IR as Lipo-IR = (glycerol rate of appearance (Ra)*insulin) or AT-IR = (free fatty acids (FFAs)*insulin). The lipid and amino acid (AA) profiles were assessed by gas chromatography–mass spectrometry. SeP levels were measured by enzyme immunosorbent assay. Results: Circulating SeP correlated with insulin (rS = 0.28), FFAs (rS = 0.42), glucose Rd (rS = −0.33) and glycerol Ra (rS = −0.34); consistently, SeP levels correlated with Lipo-IR and AT-IR (rS > 0.4). Among the AA and lipid profiles, SeP inversely correlated with serine (rS = −0.31), glycine (rS = −0.44) and branched chain AA (rS = −0.32), and directly correlated with saturated (rS = 0.41) and monounsaturated FFAs (rS = 0.40). Hepatic steatosis and fibrosis increased in subjects with higher levels of SeP. In multivariable regression analysis, SeP was associated with the degree of hepatic fibrosis (t = 2.4, p = 0.022). Conclusions: SeP levels were associated with an altered metabolic profile and to the degree of hepatic fibrosis, suggesting a role in the pathogenesis of NAFLD.

scholarly journals Non-alcoholic fatty liver disease and cardiovascular disease: assessing the evidence for causality

Diabetologia ◽  
2019 ◽  
Vol 63 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Martijn C. G. J. Brouwers ◽  
Nynke Simons ◽  
Coen D. A. Stehouwer ◽  
Aaron Isaacs
Keyword(s):  
Cardiovascular Disease ◽  
Liver Disease ◽  
Fatty Liver Disease ◽  
Plasma Lipids ◽  
Low Grade ◽  
Alcoholic Fatty Liver ◽  
Important Mediator ◽  
Low Grade Inflammation ◽  
The Relationship ◽  
Alcoholic Fatty Liver Disease

Abstract Non-alcoholic fatty liver disease (NAFLD) is highly prevalent among individuals with type 2 diabetes. Although epidemiological studies have shown that NAFLD is associated with cardiovascular disease (CVD), it remains unknown whether NAFLD is an active contributor or an innocent bystander. Plasma lipids, low-grade inflammation, impaired fibrinolysis and hepatokines are potential mediators of the relationship between NAFLD and CVD. The Mendelian randomisation approach can help to make causal inferences. Studies that used common variants in PNPLA3, TM6SF2 and GCKR as instruments to investigate the relationship between NAFLD and coronary artery disease (CAD) have reported contrasting results. Variants in PNPLA3 and TM6SF2 were found to protect against CAD, whereas variants in GCKR were positively associated with CAD. Since all three genes have been associated with non-alcoholic steatohepatitis, the second stage of NAFLD, the question of whether low-grade inflammation is an important mediator of the relationship between NAFLD and CAD arises. In contrast, the differential effects of these genes on plasma lipids (i.e. lipid-lowering for PNPLA3 and TM6SF2, and lipid-raising for GCKR) strongly suggest that plasma lipids account for their differential effects on CAD risk. This concept has recently been confirmed in an extended set of 12 NAFLD susceptibility genes. From these studies it appears that plasma lipids are an important mediator between NAFLD and CVD risk. These findings have important clinical implications, particularly for the design of anti-NAFLD drugs that also affect lipid metabolism.

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