Study On The Relationship Between Liver Fat Content And Metabolic Diseases In Elderly Patients In Changfeng Community

Like nitric oxide (NO) and carbon monoxide (CO), H2S has been shown to be the third gaseous transimitter, which is a toxic gas with the smell of rotten eggs and is found in multitudes of systems. Evidences show that H2S protects neurons from oxidative stress by increasing the reducibility of neurons. Our previous morphological experiments demonstrated that H2S in the rostral ventrolateral medulla (RVLM) lowered blood pressure and heart rate by inhibiting the activity of NADPH oxidase in the SHR, thus reducing the production of reactive oxygen species (ROS). In the present study, we use molecular biological techniques to explore the underlying mechanism how H2S protects neurons from oxidative stress induced by increased ROS level of medullary neurons.Primary cultured medullary neurons were used in all experiments. To detect whether CBS expressed in primary cultured medullary neurons or not, immunohistochemical method with fluorescence microscope was used.The result displayed that CBS could express in these nurons, providing the structural basis for studying the physiological effects of the central H2S. To investigate the effect of Ang Ⅱ (angiotensin Ⅱ) on the ROS level in medullary neurons, Dihydroethidium (DHE) staining was used and the activity of neurons was detected by CCK-8assay. The results showed that Ang Ⅱ (100nmol/L) significantly increased the level of ROS in medullary neurons(P<0.01), but had no effect on the activity of neurons(P>0.05), suggesting that Ang Ⅱ had no toxical effect on the medullary neurons. However,the effect of Ang Ⅱ could be significantly inhibited by NaHS (50μmol/L、100μmol/L、200μmol/L), especially100μmol/L NaHS (P<0.05),while NaHS alone did not change the level of ROS in these neurons. Background:Nonalcoholic fatty liver disease (NAFLD) is closely associated with type2diabetes mellitus. We investigated whether liver fat content is associated with glycemic abnormalities in people without prior known type2DM and determined to what extent liver fat content (LFC) contribute to impaired glucose profiles.Methods:The subjects were participants of the Changfeng Study from May2010to Jun2011. We excluded subjects with alcohol abuse, viral B hepatitis, prior known diabetes mellitus, incompleted data and other etiological hepatic disease. Finally,1608(596men and1012women) were included in the analyses. A standard interview (included life style, diseases history through questionnaires), anthropometrics (height, weight, waist and hip circumference, blood pressure), laboratory parameters (including serum lipid, fasting blood glucose(FBG),2h postload plasma glucose(PPG) after oral glucose tolerance test (OGTT)were conducted for each participant). The pictures with legible liver and renal were used to calculate liver fat content with software "image".Results:The median LFC value was6.12%(the range,0-48.02%), and34.20%of the subjects had LFC values exceeding9.15%. The cohort was stratified according to quintiles of LFC. PPG and FBG rose across the quintiles of LFC and increased significantly from the fourth and fifth quintile, respectively (from7.96,16.15%LFC, respectively). LFC was pronounced and continuous increase from NGT(7.7±0.3%), isolated IFG(10.0±0.8%), isolated IGT(11.8±0.5%) IFG±IGT(11.7±0.9%) to newly diagnosed diabetes mellitus(12.8±0.6%) after adjustment for age and sex(p<0.001). By logistic regression analysis,1%LFC increment independently predicted pre-diabetes and diabetes (OR1.034,1.025;95%Cl:1.019-1.050,1.007-1.044; P<0.001, P=0.007, respectively) after adjustment for sex, age, ALT, BMI, WHR, SBP, DBP. The optimal cut-off value of9.99%,11.54%for liver fat content might predict the occurence of pre-diabetes and diabetes.Conclusion:These results suggest that LFC is independently associated with pre-diabetes and diabetes. The optimal cut-off value of9.99%,11.54%for liver fat content might predict the occurence of pre-diabetes and diabetes. Background and Aim:Nonalcoholic fatty liver disease (NAFLD) is closely associated with several metabolic syndrome(MS) features and cardiovascular disease. We investigated whether liver fat content(LFC) quantified by ultrasound is independently associated with carotid artery intima-media thickness (CIMT) and also evaluated the contribution of LFC to increased CIMT.Methods:The subjects were participants of the Changfeng Study from May2010to Jun2011. We excluded subjects with alcohol abuse, viral B hepatitis, incompleted data and other etiological hepatic disease. Finally,1809subjects (682men and1127women) were included in the analyses. A standard interview(included life style, diseases history through questionnaires), anthropometrics (height, weight, waist and hip circumference, blood pressure), laboratory parameters (including serum lipid, fasting blood glucose(FBG),2h postload plasma glucose (PPG)after oral glucose tolerance test (OGTT)were conducted for participants without diabetes mellitus). Carotid artery ultrasonography was performed using a10-MHz linear transducer on the LOGIC P5scanner. Three measurements of the common carotid artery were taken, and the average measurement of two sides was used. All measurements were carried out by a single sonographer. The pictures with legible liver and renal were used to calculate liver fat content with software "image".Results:The median LFC value was6.13%(the range,0-48.02%), and34.49%of the subjects had LFC values≥9.15%. The cohort was stratified according to quartiles of LFC. Carotid IMT and the frequency of plaques increased across the quartiles of the LFC, both of them increased significantly when LFC exceeded14.21%(both P value<0.001).Notably, average common carotid IMT and max common carotid IMT were strongly associated with degree of LFC(β0.316,0.314, respectively, both P<0.001) after adjustment by age, sex, smoking, SBP, DBP, FBG.PPG, BMI, WHR, LDL-c, TG, HDL-c. By logistic regression analysis,1%LFC increment independently predicted plaques (OR1.026,95%Cl1.012-1.036; P<0.001) after adjustment for all potential confounders.Conclusions:These results suggest that LFC is independently associated with carotid atherosclerosis in Chinese, and even slightly elevated LFC is related with increased risk for atherosclerosis. Background:Non-alcoholic fatty liver disease (NAFLD) is associated with an increased prevalence of chronic kidney disease. We investigated whether liver fat content (LFC) is independently associated with microalbuminuria in normotensive and euglycemic people and to determine to what extent LFC contribute to increased microalbuminuria.Methods:The subjects were participants of the Changfeng Study from May2010to Jun2011. We excluded subjects with alcohol abuse, viral B hepatitis, abnormal glucose level or blood pressure, urinary tract infection, incompleted data and other etiological hepatic disease. Finally,550(174men and376women) were included in the analyses. A standard interview (included life style, diseases history through questionnaires), anthropometrics (height, weight, waist and hip circumference, blood pressure), laboratory parameters (including serum lipid, fasting blood glucose,2h postload plasma glucose after oral glucose tolerance test were conducted for each participant. The urinary albumin excretion rate was measured from an early morning urine sample as the albumin-to-creatinine ratio (ACR). Standardized hepatic-renal echo-intensity indices were used to assess LFC.Results:The median LFC value of this population was5.26%(the range,0-48.02%), and23.09%of the subjects had LFC values≥9.15%. The cohort was stratified according to quartiles of liver fat content. The prevalence rates of microalbuminuria increased across quartiles after adjustment for age and sex(P=0.012). Notably, IgACR was strongly associated with degree of LFC (β0.541, P=0.010) after adjustment for age, sex, smoking history, LDL-c,BMI, SBP, DBP, FBG, PPG, TG and HDL-c. Similarly, by logistic regression analysis,1%LFC increment independently predicted microalbuminuria (OR1.086,95%CI1.012-1.165; P=0.022) after adjustment for all potential confounders. The optimal cut-off value of6.82%for liver fat content might predict the occurence of microalbuminuria.Conclusion:These results suggest that LFC is an independent risk factor for microalbuminuria. And even slightly elevated LFC is associated with increased microalbuminuria.