Adiponectin ; blood ; Animals ; Fatty Liver ; pathology ; Rabbits

OBJECTIVES: The pathogenesis of nonalcoholic fatty liver in non-obese persons is poorly understood. We aimed to elucidate whether hyperinsulinemia and glucose intolerance are associated with development of fatty liver in patients with normal body weight. METHODS: Forty-seven patients with fatty liver were divided into non-obese (n = 25) and obese groups (n = 22) according to age adjusted body mass index. Inclusion criteria were as follows: (1) elevated transaminase levels during more than 3 months of follow up period, (2) no detectable HBsAg or anti-HCV in the serum, (3) alcohol consumption less than 40 gm/week, (4) no use of potential hepatotoxic drugs within 3 months and (4) sonographic evidence of fatty liver(moderate to severe degree). Baseline insulin levels and oral glucose tolerance test using 75gm of glucose were performed and the results were compared in each group of patients. RESULTS: Mean baseline insulin levels were elevated in both groups above the reference value, 9.3 +/- 3.5 microU/L in non-obese group and 9.9 +/- 3.5 microU/L in obese group (p = 0.26). Seventeen of non-obese patients (68%) had elevated basal insulin level and 16 of obese patients (73%) had elevated basal insulin level (p = 0.39). In oral glucose tolerance test, there was no difference in glucose level between non-obese and obese groups from O minute to 180 minutes (p > 0.05). Eleven patients from the non-obese group (44%) and 8 patients from the obese group (36%) had either impaired glucose tolerance or diabetes (p = 0.29). CONCLUSION: Our data suggest that hyperinsulinemia and glucose intolerance may play a role in the pathogenesis of fatty liver in patients with normal body weight as well as in patients with obesity.
Adult ; Body Weight ; Fatty Liver/pathology ; Fatty Liver/etiology* ; Fatty Liver/blood ; Female ; Glucose Intolerance/complications* ; Human ; Insulin/blood* ; Insulin Resistance ; Male ; Middle Age ; Obesity/complications

No abstract available.
Bilirubin/*blood ; Fatty Liver/*ultrasonography ; Female ; Humans ; Male

To investigate the effects of telmisartan on steatohepatitis (NASH) in rats by activating peroxisome proliferator-activated receptor gamma (r). Thirty male SD rats were randomized into normal control group, NASH control group and telmisartan prevention group. Normal control group was given standard food and the other two groups were given high fat diet for 16 weeks to induce NASH. Prevention group was given telmisartan (5 mg.kg-1.d-1) for 4 weeks by intragastric adminstration after 12 weeks. At the end of the 16th week, all the rats were sacrificed. Pathological changes of liver were observed by optical microscopy. Serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), fasting blood glucose(FBG), fasting insulin(FINS), HOMA-IR(homeostasis model assessment insulin resistance), Serum TNF-a and adiponectin were detected and analyzed.Western blot and RT-PCR were used to detect PPARr expression in hepatic tissues on protein and mRNA levels. (1) Rats were successfully modeled. The liver tissue samples were divided into 4 degrees (F0 - 4) based on total fatty degeneration of liver cells.There was one rat reached F3 and nine rats reached F4 in NASH group, one rat reached F1, six rats reached F2 and three rats reached F3 in prevention group. Inflammatory activity scores of hepatic tissues in the model group were 2.67+/-0.25, while that in the control group was 0 (U=15 and P is less than to 0.01), in the prevention group were 2.67+/-0.25 and 1.36+/-0.12 (U=24 and P is less than to 0.05 ). (2) The levels of serum ALT, AST, FBG, FINS, TNFa and HOMA-IR in the model group were increased than those in the control group( the vaules of q were 13.130, 6.472, 6.909, 26.619, 14.591 and 49.683 respectively, P less than 0.01). The levels of serum ALT, FINS, FBG, TNFa and HOMA-IR in the prevention group were decreased as compared to the model group (the vaules of q were 7.024, 4.145, 14.829, 13.195 and 31.991 respectively, P less than 0.01 ). (3) The serum adiponectin, PPARrmRNA and protein in liver tissues of the model group were lower than those in the control group (q values were 10.696, 8.679 and 16.762 respectively, P is less than to 0.05).The data in the prevention group were higher as compared to the model group(q values were 3.879,3.079,6.400, P is less than to 0.05 respectively). HOMA-IR was positively correlated with the expression of TNFa but negatively correlated with the expression of adiponectin (r = 0.927, P is less than to 0.01; r = -0.891, P is less than to 0.01, respectively). Telmisartan may has preventive effect on rats with steatohepatitis (NASH) by a mechanism of activating peroxisome proliferator-activated receptor r.
Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Fatty Liver ; Insulin Resistance ; Non-alcoholic Fatty Liver Disease ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the abdominal adipose area, serum adiponectin and leptin levels of nonalcoholic fatty liver disease in elderly males.

METHODSA total of 238 elderly males (more than 60 years) were enrolled and divided into three groups: Nonalcoholic fatty liver disease (NAFLD) group (n = 76), matching group (age and body mass index matching with NAFLD group, n = 77), normal control group (n = 85). Serum levels of adiponectin and leptin were measured by RIA (radiological immunological assay). Abdominal adipose area was detected by computer tomography.

RESULT(1) body mass index (BMI), abdominal subcutaneous adipose area, visceral adipose area, total adipose area of NAFLD group and matching group were (26.87+/-2.62) kg/m2 and (26.63+/-1.97) kg/m2, (166.59+/-54.27) cm2 and (147.89+/-50.14) cm2, (148.94+/-53.72) cm2 and (150.06+/-45.47) cm2, (315.25+/-89.42) cm2 and (297.93+/-75.12) cm2, respectively; and were higher than those in control group (P less than 0.01). The abdominal subcutaneous adipose area is higher in NAFLD group than in matching group, however, the abdominal visceral adipose area and total adipose area were not significantly different between those two groups. (2) The serum leptin level in NAFLD group and matching group was significantly higher than that in control group, and serum leptin level was not significantly different between NAFLD group and matching group. The serum adiponectin of NAFLD group [(6.31+/-3.31)mug/ml] was significantly lower than that of matching group [(9.87+/-7.071)mug/ml, P less than 0.01] and control group (P less than 0.01). There was no difference in adiponectin level between matching group and control group. 3) AST, TG, abdominal subcutaneous adipose area, abdominal visceral adipose area were risk factors of NAFLD, while serum adiponectin was protective factor of NAFLD.

CONCLUSIONThese data indicate that elderly male NAFLD patients manifest abdominal obesity, high serum leptin, low serum adiponecin, and suggest that adiponectin may play a crucial role in the pathogenesis of NAFLD in elderly males.

Adiponectin ; blood ; Aged ; Body Mass Index ; Fatty Liver ; Humans ; Leptin ; Male ; Non-alcoholic Fatty Liver Disease ; Obesity ; blood

Animals ; Biomarkers ; blood ; Fatty Liver ; blood ; etiology ; Humans ; Leptin ; blood ; Obesity ; blood ; complications

OBJECTIVE: To investigate the relationship between serum 25(OH) vitamin D and liver fat content in nonalcoholic fatty liver disease (NAFLD). METHODS: A total of 120 patients with NAFLD admitted in our hospital between June and August, 2017 were enrolled and divided into 4 groups with different serum 25 (OH) vitamin D levels: >75 nmol/L (group A, =25), 50-75 nmol/L (group B, =35), 25-50 nmol/L (group C, =32), and < 25 nmol/L (group D, =28). For all the patients, serum 25 (OH) vitamin D level was measured by ELISA, and liver fat content was determined using in-phase opposed-phase TWI sequences. The measurement data were compared among the 4 groups to assess the association between serum 25(OH) vitamin D level and liver fat content. RESULTS: The liver fat content appeared to be higher in group B (28.66±6.45%) and group C (38.74±11.47%) than in group A (22.79 ± 6.10%), but the difference was not statistically significant (>0.05); the liver fat content in group D (54.79 ± 5.28%) was significantly higher than that in the other 3 groups (>0.05). Liver fat content increased significantly as serum 25(OH) vitamin D level decreased, showing an inverse correlation between them in these patients ( < 0.05, =-0.125). CONCLUSIONS In patients with NAFLD, a decreased serum 25(OH) vitamin D level is associated with an increased liver fat content, suggesting the value of serum 25(OH) vitamin D as a predictor of NAFLD.
Humans ; Liver ; pathology ; Non-alcoholic Fatty Liver Disease ; blood ; pathology ; Vitamin D ; blood

Adiponectin ; blood ; Adolescent ; Child ; Fatty Liver ; blood ; Female ; Humans ; Male ; Obesity ; blood

OBJECTIVETo determine the efficacy of the plant-derived bioflavonoid, quercetin, for treating nonalcoholic fatty liver disease (NAFLD) by using a rat model, and to investigate the molecular mechanism underlying its therapeutic effects.

METHODSOne-hundred Sprague-Dawley rats were randomly assigned into the normal control group (normal group), untreated NAFLD model control group (model group), 75 mg/kg/day quercetin treatment group (low-dose group), and 300 mg/kg/day quercetin treatment group (high-dose group). The NAFLD rat model was established by providing four weeks of a high-fat diet; the normal group received normal rat chow diet. The quercetin treatments were administered for eight weeks after model establishment and control groups received simultaneous gavages of isotonic saline, with continuation of the respective diets. At the end of the eight weeks (experimental week 12), the rats were sacrificed for liver and serum collection. Intergroup differences in liver index, fasting blood glucose (FBG), triglycerides (TG), interleukin (IL)-18, IL-10, malondialdehyde (MDA), and histopathological features were assessed by independent samples t-test (normal vs. model), one-way ANOVA (model vs. treatments), and least significant difference t-test (pairwise comparisons); correlations were assessed by Pearson's correlation coefficient.

RESULTSCompared with the normal group, the model group showed significantly higher liver index (t=-2.327), FBG (t=-3.482), TG (t=-0.302), and serum IL-18 (t=-2.704) (all P less than 0.05), but significantly lower IL-10 (t=2.622, P less than 0.05); the MDA level was also higher in the model group, but the difference was not significant (t=-1.083, P less than 0.05). Livers from the model group showed obvious histological features of inflammation (lymphocyte and neutrophil infiltration) and steatosis (cytoplasmic lipid droplets). Inflammation was positively correlated with IL-18 (P less than 0.05), but negatively correlated with IL-10 (P less than 0.05), while steatosis was negatively correlated with IL-10 (P less than 0.05). Compared to the model group, quercetin treatment (both low- and high-dose) led to significant decreases in the liver index, FBG and IL-18 (all, P less than 0.01), and significant increase in IL-10 (P less than 0.05); however, the changes in liver index, FBG and IL-10 were not significantly different between the low- and high-dose treatment groups, but the high-dose of quercetin did induce a significantly greater decrease in IL-18 than the low-dose (P less than 0.05).

CONCLUSIONNAFLD rats have higher serum levels of IL-18 but lower levels of IL-10 than their healthy counterparts, and these differential cytokine expressions may be related to liver inflammation and steatosis. Quercetin treatment may help to delay the progression of NAFLD, possibly by adjusting the balance of inflammatory cytokines.

Animals ; Fatty Liver ; blood ; drug therapy ; Interleukin-10 ; blood ; Interleukin-18 ; blood ; Male ; Non-alcoholic Fatty Liver Disease ; Quercetin ; pharmacology ; therapeutic use ; Rats ; Rats, Sprague-Dawley

Adolescent ; Aminopeptidases ; blood ; Case-Control Studies ; Child ; Fatty Liver ; blood ; complications ; Female ; Humans ; Male ; Non-alcoholic Fatty Liver Disease ; Obesity ; blood ; complications