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Aims: We aimed to construct a prediction model of type 2 diabetes mellitus (T2DM) in a Han Chinese cohort using a genetic risk score (GRS) and a nongenetic risk score (NGRS). Methods: A total of 297 Han Chinese subjects who were free from type 2 diabetes mellitus were selected from the Tianjin Medical University Chronic Disease Cohort for a prospective cohort study. Clinical characteristics were collected at baseline and subsequently tracked for a duration of 9 years. Genome-wide association studies (GWASs) were performed for T2DM-related phenotypes. The GRS was constructed using 13 T2DM-related quantitative trait single nucleotide polymorphisms (SNPs) loci derived from GWASs, and NGRS was calculated from 4 biochemical indicators of independent risk that screened by multifactorial Cox regressions. Results: We found that HOMA-IR, uric acid, and low HDL were independent risk factors for T2DM (HR >1; P<0.05), and the NGRS model was created using these three nongenetic risk factors, with an area under the ROC curve (AUC) of 0.678; high fasting glucose (FPG >5 mmol/L) was a key risk factor for T2DM (HR = 7.174, P< 0.001), and its addition to the NGRS model caused a significant improvement in AUC (from 0.678 to 0.764). By adding 13 SNPs associated with T2DM to the GRS prediction model, the AUC increased to 0.892. The final combined prediction model was created by taking the arithmetic sum of the two models, which had an AUC of 0.908, a sensitivity of 0.845, and a specificity of 0.839. Conclusions: We constructed a comprehensive prediction model for type 2 diabetes out of a Han Chinese cohort. Along with independent risk factors, GRS is a crucial element to predicting the risk of type 2 diabetes mellitus.

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Based on the high incidence of chronic kidney disease (CKD) in recent years, a better early prediction model for identifying high-risk individuals before end-stage renal failure (ESRD) occurs is needed. We conducted a nested case-control study in 348 subjects (116 cases and 232 controls) from the "Tianjin Medical University Chronic Diseases Cohort". All subjects did not have CKD at baseline, and they were followed up for 5 years until August 2018. Using multivariate Cox regression analysis, we found five nongenetic risk factors associated with CKD risks. Logistic regression was performed to select single nucleotide polymorphisms (SNPs) from which we obtained from GWAS analysis of the UK Biobank and other databases. We used a logistic regression model and natural logarithm OR value weighting to establish CKD genetic/nongenetic risk prediction models. In addition, the final comprehensive prediction model is the arithmetic sum of the two optimal models. The AUC of the prediction model reached 0.894, while the sensitivity was 0.827, and the specificity was 0.801. We found that age, diabetes, and normal high values of urea nitrogen, TGF-ß, and ADMA were independent risk factors for CKD. A comprehensive prediction model was also established, which may help identify individuals who are most likely to develop CKD early.

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BACKGROUND: Hypertension and high triglyceride are two of the most important risk factors for hyperuricemia. Epidemiological records show that hypertension and dyslipidemia often coexist and may significantly increase the risk of target organ damage. However, their combined effect on incident hyperuricemia is poorly understood. Thus, we aimed to investigate the separate and combined effect of hypertension and hypertriglyceridemia on the incidence of hyperuricemia. METHODS: A prospective cohort study of 6424 hyperuricemia-free participants aged 20 to 94 years between August 2009 and October 2017 was performed at Tianjin General Hospital of China. Participants were categorized into four groups by combining hypertension and hypertriglyceridemia status at baseline. The restricted cubic spline fitting Cox regression model was used to evaluate the relationship between blood pressure and triglyceride and hyperuricemia. Cox regression models were performed to calculate hazard ratios (HRs) and 95% confident intervals (CIs) to estimate baseline factors and their association with the incidence of hyperuricemia. A Kaplan-Meier survival analysis was performed to compare the incidence of hyperuricemia among subjects in each separate and combined hypertension and hypertriglyceridemia group. RESULTS: During the 8-year follow-up period, 1259 subjects developed hyperuricemia (20.6%). There existed positive relationships between blood pressure and triglyceride levels and hyperuricemia. This risk factor arising from a combination of the two (HR, 3.02; 95% CI 2.60-3.50) is greater than that from hypertension (HR, 1.48; 95% CI 1.28-1.71) or hypertriglyceridemia (HR, 1.84; 95% CI 1.55-2.18) separately. The Kaplan-Meier survival analysis indicated that combined effect of hypertension and hypertriglyceridemia may predict higher onset of hyperuricemia. CONCLUSION: The combined effect of hypertension and hypertriglyceridemia on the risk of hyperuricemia is much stronger than that by hypertension or hypertriglyceridemia separately. Hypertension combined with hypertriglyceridemia may be an independent and powerful predictor for hyperuricemia.

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BACKGROUND: Osteoporosis is one of the most closely related diseases associated with the elderly. In recent years, the studies found that gut microbiota can cause osteoporosis. We evaluated the role of Bacillus acidophilus in osteoporosis and its roles in proliferation and differentiation. METHODS: We selected 5 healthy people and 10 osteoporosis patients and analyzed their level of 25-hydroxyvitamin D and procollagen type I N-terminal peptide (PINP), the characteristic of gut microbiota. The effect of lactobacillus acidophilus and Lactobacillus rhamnosus supernatant and butanoic acids on proliferation, differentiation, and maturity of osteoblasts MC3T3-E1 and osteoclasts RAW 264.7 cells and the activity of alkaline phosphatase, concentration of osteocalcin, and the expression of RUNX2, RANK, NFATc1, cathepsin K, DC-STAMP, OSCAR, WNT2, and CTNNB1 were measured in the above cell lines. RESULTS: The diversity of gut microbiota in osteoporosis patients is decreased and imbalanced with lower abundance of lactobacillus and butyric acid bacteria; meanwhile, 25-hydroxyvitamin D and PINP of osteoporosis patient were significantly lower than the normal group. The proliferation, differentiation, and maturity of MC3T3-E1 cells were stimulated; the activity of alkaline phosphatase, concentration of osteocalcin, and the expression of RUNX2, NFATc1, cathepsin K, DC-STAMP, OSCAR, WNT2, and CTNNB1 were improved by supernatant of lactobacillus acidophilus, Lactobacillus rhamnosus and butanoic acids; however, the proliferation, differentiation, maturity, and the expression of RANK, NFATc1, cathepsin K, DC-STAMP, OSCAR, WNT2, and CTNNB1 in RAW 264.7 cells were suppressed. CONCLUSIONS: The lactobacillus acidophilus and Lactobacillus rhamnosus supernatant could stimulate the proliferation, differentiation, and maturation of osteoblasts; the production of butyric acid may be the potential mechanism.

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Background: Non-alcoholic fatty liver disease (NAFLD) has become a serious disease affecting people's health in the world. This article studies the causal relationship between NAFLD and serum uric acid (SUA) levels. Methods: During the 4 years of follow-up in a fixed cohort that was established in 2014, 2,832 follow-up subjects without NAFLD were finally included in this study. The study population was divided into four groups according to baseline SUA levels. Cox hazard regression model and Kaplan-Meier survival curves analysis were used to predict risk factors of NAFLD. The receiver operating characteristic curve analyses were used to determine SUA cutoffs for predicting NAFLD. Results: The cumulative prevalence rates of NAFLD were 33.97% (962/2,832), 38.93% (758/1,947) in males and 23.05% (204/885) in females. The results showed that males had a higher incidence of NAFLD (χ2 = 68.412, P = 0.000). The Cox regression analysis disclosed that the hazard ratios of NAFLD [95% confidence interval (CI)] were 1.431 (95% CI, 1.123~1.823), 1.610 (95% CI, 1.262-2.054), and 1.666 (95% CI, 1.287-2.157) across the second to the fourth quartile of SUA adjusted for other confounders. The SUA cutoffs, sensitivity, specificity, and area under the curve (AUC) (95% CI) were ≥288.5 µmol/L, 75.5, 46.5%, 0.637(0.616-0.658), respectively, for total; ≥319.5 µmol/L, 65.8%, 48.4%, 0.590 (0.564-0.615), respectively, for males; and ≥287.5 µmol/L, 51.0%, 75.6%, 0.662 (0.619-0.704), respectively, for females. Kaplan-Meier survival curves revealed that individuals with higher SUA level had an increased risk of NAFLD in comparison to lower SUA level (P = 0.000). Conclusion: Serum uric acid is positively correlated with NAFLD, and elevated SUA level can be used as an independent predictor for NAFLD.

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BACKGROUND AND AIM: Recent clinical trials have confirmed that Helicobacter pylori infection is positively associated with nonalcoholic fatty liver disease (NAFLD), although some research has shown a negative association. Therefore, to confirm whether H. pylori eradication treatment is feasible for NAFLD patients in our hospital, we aimed to establish the association between H. pylori infection and NAFLD. METHODS: We enrolled 91 patients with NAFLD diagnosed by abdominal B-mode ultrasonography between January and December 2018. H. pylori infection was confirmed by C urea breath test, and liver function, glycometabolism, insulin sensitivity, lipid metabolism, as well as inflammatory reaction were assessed through blood biochemical analyses. RESULTS: A minority of NAFLD patients had liver dysfunction, increased fasting glucose and insulin levels, a score of insulin-resistance (HOMA-Ir), lipid metabolism, slight inflammatory response, fasting hyperglycemia and hypertension. Most patients were complicated with overweight/visceral obesity and dyslipidemia. Moreover, these abnormal indicators were closely associated with the severity of NAFLD and H. pylori infection. Notably, the prevalence of H. pylori infection showed a significant difference between mild, moderate and severe NAFLD, and hepatic steatosis with coexistent NAFLD also revealed a striking difference between H. pylori-positive and H. pylori-negative patients (P < 0.01). CONCLUSION: Our results suggest that H. pylori infection may be an independent risk factor in NAFLD progress.

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BACKGROUND: Although there is abundant evidence indicating the connection between triglyceride and type 2 diabetes mellitus (T2DM), few reports or cohort studies confirm that high TG concentration may predict the incidence of T2DM independently. Thus, we studied the association between triglyceride (TG) and T2DM in a male-dominated, middle and older aged cohort, Tianjin General Hospital Cohort. And we further verified our results in the China Health and Retirement Longitudinal Study (CHARLS). METHODS: We conducted an 8-year retrospective cohort study (2009-2017) with 7241 participants who were free from T2DM at baseline. Three groups were constructed based on baseline TG levels (normal, borderline-high, and high). We used a Cox proportional hazards model to evaluate the relationship between TG and T2DM after adjusting for possible risk factors. A Kaplan-Meier survival analysis was performed to compare the incidence of T2DM among subjects in each TG group. We also tested the association between TG and T2DM in the CHARLS cohort. RESULTS: In Tianjin General Hospital Cohort, 7241 participants (male 75.8%, female 24.2%) were included, mean age was 61.49 ± 13.85 years at baseline. The cumulative incidence of T2DM in our cohort study was 8.6% (9.2% in men and 6.6% in women). Compared with the normal TG group, the hazard ratios in the borderline and high group were 1.30 (95% CI 1.04-1.62) and 1.54 (95% CI 1.24-1.90). The Kaplan-Meier survival analysis indicated that higher TG levels may predict higher onset of T2DM. These results were verified in the CHARLS cohort, the hazard ratio with T2DM (95% CI) for logTG was 3.94 (2.64-5.87). CONCLUSIONS: Our findings suggest that the TG level may be an independent risk factor and predictor for T2DM.

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Rapid proliferation and migration are the main features of hepatocellular carcinoma (HCC) cells, which serve an essential role in carcinogenesis and are a hallmark of cancer therapy resistance. Previous studies have reported that tumor necrosis factor­α­induced protein­8 like­2 (TIPE­2) is involved in cancer initiation and the progression of HCC. The present study aimed to clarify the role of TIPE­2 in HCC carcinogenesis, growth and aggressiveness. The effects of TIPE­2 on HCC were determined using colony forming and cell cycle analyses. Cell apoptosis, and growth and aggressiveness of HCC cells, were investigated following TIPE­2 treatment. Treatment with TIPE­2 markedly suppressed HCC cell proliferation and increased the number of cells in S phase of the cell cycle. The results demonstrated that TIPE­2 significantly inhibited growth, migration and invasion of HCC cells via the downregulation of tumor metastasis-associated genes. Flow cytometric analysis indicated that TIPE­2 promoted apoptosis of HCC cells via regulation of apoptosis­associated gene transcription. In addition, TIPE­2 administration downregulated the expression of phosphoinositide 3­kinase (PI3K) and protein kinase B (AKT) in HCC cells. In addition, TIPE­2 selectively decreased neuroblastoma Ras viral oncogene and p27 expression in HCC cells. In vivo assays revealed that TIPE­2 significantly inhibited tumor growth and prolonged animal survival by promoting apoptosis of tumor cells. The results of the present study indicated that TIPE­2 acts as an inhibitor of HCC cell growth and aggressiveness, and promotes apoptosis, thus suggesting that TIPE­2 may inhibit the metastasis­associated PI3K/AKT signaling cascade and may arrest the tumor cell cycle. These findings provide a potential molecular mechanism by which TIPE­2 promotes apoptosis of HCC cells.

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BACKGROUND: Despite abundant evidence indicating that higher triglyceride (TG) levels are associated with increased risks of hyperuricemia (HUA), it is unclear whether TG levels can independently predict the incidence of HUA. OBJECTIVE: The aim of the study was to investigate whether TG is an independent risk factor of HUA in a cohort study. METHODS: We explored the relationship between TG levels and HUA in a dynamic cohort established in 2009. During the 6 years of follow-up, 5442 subjects without HUA were studied. We divided subjects into 4 groups based on baseline TG levels and used the Cox hazard regression model to estimate HUA risk by TG quartile, after adjustment for potential confounding factors. Kaplan-Meier survival analysis compared the risk of HUA incidence among individuals in each TG quartile. RESULTS: The incidence of HUA in this cohort was 25.9%. The hazard ratios (95% confidence intervals) for HUA in the second, third, and fourth TG quartiles, compared with the first quartile, were 1.19 (1.01-1.40), 1.33 (1.13-1.57), and 1.62 (1.37-1.92), respectively. The Kaplan-Meier survival analysis suggested that higher TG levels predicted higher incidences of HUA in a dose-dependent relationship. Stratification analyses showed that the association between TG levels and the presence of HUA was more pronounced in individuals aged <50 years, of obese, with normal estimated glomerular filtration rate, and with hypertension. CONCLUSION: Our findings suggest that TG level is a significant and independent risk factor for HUA.

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BACKGROUND: The prevalence of hyperuricemia has increased dramatically during the past several decades. Studies indicating uric acid is an independent risk factor for hypertension did not sufficiently control for other known risk factors. We explored this relationship in a comprehensive Chinese senior dynamic cohort. METHODS: To investigate the relationship between serum uric acid (SUA) levels and hypertension, we carried out a 6-year retrospective study (2006-2011) in a dynamic cohort with 3591 subjects free of hypertension. The first occasion of documented hypertension per subject was the index event. A Cox proportional hazards model assessed the relationship between SUA and hypertension. Kaplan-Meier survival analysis compared incidence of hypertension among individuals with each SUA quartile. Receiver operating characteristic curves were generated to obtain the area under the curve as a prediction of hypertension from SUA levels. RESULTS: The cumulative prevalence of hypertension in our cohort was 20.7 %. The prevalence of hyperuricemia was 17.5 %. Cox regression analysis showed that, compared with the lowest SUA quartile (<4.69 mg/dl), the 4.69-5.58, 5.58-6.52, and ≥6.52 mg/dl quartiles yielded hazard ratios (95 % confidence intervals) for hypertension of 1.652 (1.265-2.156), 2.195 (1.705-2.825), and 3.058 (2.399-3.899), respectively. Cumulative incidence of hypertension was consistently higher among individuals with hyperuricemia than among those with normal SUA levels. A Kaplan-Meier survival analysis showed that hyperuricemia predicted higher incidences of hypertension in a dose-dependent manner: hypertension onset significantly differed across SUA quartiles. SUA levels were significantly and independently associated with incidence of hypertension in our cohort. CONCLUSIONS: Our results, controlling for known risk factors, suggest that SUA level is an independent risk factor for hypertension and could be a useful indicator of hypertension.

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The underlying molecular pathogenesis of hepatocellular carcinoma (HCC) remains poorly understood. Mitogen-activated protein kinase kinase 3 (MKK3), has been reported as a novel tumor suppressor in breast cancer. However, its potential suppressive role in HCC has not been evaluated. In the current study, the biologic functions of MKK3 in HCC were investigated and a previously unreported cell cycle regulation mechanism was observed. MKK3 overexpression suppressed HepG2 and PLC­PRF­5 cell proliferation and induced cell cycle arrest in the two cell lines. In addition, MKK3 overexpression upregulated the cyclin-dependent kinase inhibitors, p16 INK4A and p15 INK4B in HCC cells. Their negative regulator, Bim­1, was downregulated following MKK3 overexpression. Moreover, MKK3 activated p38 in HCC cells and SB203580, a p38 inhibitor, reversed the tumor suppressive effect of MKK3. In conclusion, the results identify MKK3 as a tumor suppressor and highlighted the significance of p38 pathway aberration in HCC.

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To study associations between type 2 diabetes (T2DM) candidate genes and microvascular complications of diabetes (MVCDs), we performed case-control association studies for both T2DM and MVCDs in Han Chinese subjects. We recruited 1,939 unrelated Han Chinese T2DM patients and 918 individuals with normal blood glucose levels as nondiabetic controls. Among T2DM patients, 1116 have MVCDs, 266 have a history of T2DM of >10 years but never developed MVCDs. Eighty-two single-nucleotide polymorphisms (SNPs) in 54 candidate genes were genotyped. Discrete association studies were performed by the PLINK program for T2DM and MVCDs. Significant associations were found among candidate gene SNPs and T2DM, including rs1526167 of the TOX gene (allele A, P = 2.85 × 10(-9), OR = 1.44). The SNP rs10811661 of the CDKN2A/B gene was also associated with T2DM (allele T, P = 4.09 × 10(-7), OR = 1.36). When we used control patients with >10 years of T2DM history without MVCD, we found that the G allele of SNP rs1526167 of the TOX gene was associated with MVCD (nominal P = 4.33 × 10(-4)). In our study, significant associations were found between TOX and CDKN2A/B gene SNPs and T2DM. The TOX polymorphism might account for the higher risk of T2DM and the lower risk of MVCDs in the Han Chinese population.

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PURPOSE: It is known today that sleep apnea hypopnea syndrome and its characteristic chronic intermittent hypoxia can cause damages to multiple organs, including the cardiovascular system, urinary system, and liver. It is still unclear, however, whether the damage caused by sleep apnea hypopnea syndrome and the severity of the damage are organ-specific. METHODS: This research observed the pathological effects of chronic intermittent hypoxia on rat's thoracic aorta, myocardium, liver, and kidney, under the condition of lipid metabolism disturbance, through establishing the rat model of chronic intermittent hypoxia with high-fat diet by imitating the features of human sleep apnea hypopnea syndrome. In this model, 24 male Wistar rats were randomly divided into three groups: a control group fed by regular diet, a high-fat group fed by high-fat diet, and a high-fat plus intermittent hypoxia group fed by high-fat diet and treated with intermittent hypoxia 7 h a day. At the end of the ninth week, the pathological changes of rat's organs, including the thoracic aorta, myocardium, liver, and kidney are observed (under both optical microscopy and transmission electron microscopy). RESULTS: As the result of the experiment shows, while there was no abnormal effect observed on any organs of the control group, slight pathological changes were found in the organs of the high-fat group. For the high-fat plus intermittent hypoxia group, however, remarkably severer damages were found on all the organs. It also showed that the severity of the damage varies by organ in the high-fat plus intermittent hypoxia group, with the thoracic aorta being the worst, followed by the liver and myocardium, and the kidney being the slightest. CONCLUSIONS: Chronic intermittent hypoxia can lead to multiple-organ damage to rat with high-fat diet. Different organs appear to have different sensitivity to chronic intermittent hypoxia.

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PURPOSE: Sleep apnea-hypopnea syndrome and its chronic intermittent hypoxia component may cause multi-system-targeted injury. The latest finding shows that liver is one of the injured organs. The purpose of the study is to observe the dynamic process of the influence that chronic intermittent hypoxia plays on rat liver enzyme, hepatic histology, and ultrastructure based on lipid disorders. METHODS: A total of 72 male Wistar rats were randomly divided into three groups. The control group was fed with a regular chow diet, the high fat group with a high fat diet, and the high fat plus intermittent hypoxia group with a high fat diet with a 7-h/day intermittent hypoxia treatment. Changes were observed in rat liver enzyme, hepatic histology, and ultrastructure of the three groups on the third, sixth, and ninth weeks, respectively. The liver paraffin sections were detected with myeloperoxidase. RESULTS: The liver function and structure of the control group were found to be normal; the liver enzyme level of the high fat group was significantly higher than that of the control group on the sixth and ninth weeks; and the liver enzyme level of the high fat plus intermittent hypoxia group was significantly higher than that of the control group and the high fat group on the third, sixth, and ninth weeks (all P < 0.01). Observed by a light microscope and a transmission electron microscope, the high fat group and the high fat plus intermittent hypoxia group were all characterized by nonalcoholic fatty liver disease: the high fat group was characterized by simple fatty liver on the third and sixth weeks and by steatohepatitis on the ninth week; the damage of the high fat plus intermittent hypoxia group was significantly more severe than that of the high fat group in all the monitoring points, characterized by steatohepatitis on the sixth week and by obvious liver fibrosis on the ninth week; the myeloperoxidase level of the high fat plus intermittent hypoxia group was significantly higher than that of the control group and the high fat group (all P < 0.01). CONCLUSIONS: Under the conditions of high fat and intermittent hypoxia, the injury to the liver function, hepatic histology, and ultrastructure is more severe than that of the high fat group. The injury mainly was characterized by nonalcoholic fatty liver disease and becomes more severe with increased exposure time. Oxidative stress may play an important role in the mechanism.

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OBJECTIVE: To study the effects of high-fat plus ethanol diet on myocardial ultrastructure in rats. METHODS: 40 male SD rats in seventy-eight-week old were randomly divided into four groups: group A was control group, fed with common feedstuff; group B was high-fat diet group, freely foraging high-fat feedstuff; group C was ethanol group, the rats were intragastrically administered 60% ethanol solution twice a day by 1 ml/kg; group D was high-fat diet and ethanol group, the rats freely foraged high-fat feedstuff, and ethanol solution was intragastrically administered as before. After 12 weeks, blood samples were taken through jugular vein, the concentration of blood cholesterol (TG), triglycerides (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL) were determined. The cardiac index was also determined for all groups and the cardiac morphous were observed by high resolution Doppler ultrasound, and myocardial ultrastructure was observed by transmission electron microscope. RESULTS: After experiment, TG levels of groups A, B, C, D were (1.07 +/- 0.21), (2.34 +/- 0.72), (1.33 +/- 0.42) and (1.75 +/- 0.65) mmol/L, respectively (F = 8.323, P = 0.000); TC levels were (1.74 +/- 0.38), (5.66 +/- 1.74), (1.70 +/- 0.44) and (5.65 +/- 2.95) mmol/L, respectively (F = 13.670, P = 0.000); HDL levels were (0.65 +/- 0.11), (2.99 +/- 0.54), (0.52 +/- 0.13) and (2.06 +/- 0.26) mmol/L, respectively (F = 112.225, P = 0.000); LDL levels were (0.74 +/- 0.22), (1.87 +/- 0.90), (0.60 +/- 0.26) and (1.54 +/- 0.78) mmol/L, respectively (F = 7.318, P = 0.001); Apo-A1 levels were (0.25 +/- 0.10), (0.31 +/- 0.14), (0.21 +/- 0.05) and (0.36 +/- 0.11) g/L, respectively (F = 3.015, P = 0.047); Apo-B levels were (0.18 +/- 0.03), (0.11 +/- 0.04), (0.16 +/- 0.03) and (0.39 +/- 0.13) g/L, respectively (F = 15.621, P = 0.000); ALT levels were (111.25 +/- 20.18), (447.13 +/- 89.25), (173.13 +/- 44.01) and (198.25 +/- 39.81) U/L, respectively (F = 58.708, P = 0.000); AST levels were (105.50 +/- 9.99), (483.00 +/- 16.80), (120.75 +/- 5.09) and (276.88 +/- 10.48) U/L, respectively (F = 1906.624, P = 0.000);TBIL levels were (1.35 +/- 0.12), (1.66 +/- 0.18), (1.89 +/- 0.15) and (2.68 +/- 0.35)U/L, respectively (F = 55.006, P = 0.000); cardiac indexes were (3.02 +/- 0.22)%, (3.21 +/- 0.16)%, (3.26 +/- 0.26)% and (3.43 +/- 0.27)%, respectively (F = 16.150, P = 0.000). There were changes of cardiac morphous in group C and D, but not in group A and B; the myocardial ultrastructure was normal in Group A, but light to heavy changes were found in group B, C and D. CONCLUSION: High-fat diet and excessive intake of ethanol significantly induce abnormal lipid metabolism. High-fat diet induces the changes of myocardial ultrastructure before cardiac morphous and electrocardiogram, and intake of ethanol changes cardiac muscle in microstructure and macroscopy. High-fat diet plus ethanol may worsen this injury farther.

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