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PubMed2005

Short-term overexpression of a constitutively active form of AMP-activated protein kinase in the liver leads to mild hypoglycemia and fatty liver.

AMP-activated protein kinase (AMPK) is a major therapeutic target for the treatment of diabetes. We investigated the effect of a short-term overexpression of AMPK specifically in the liver by adenovirus-mediated transfer of a gene encoding a constitutively active form of AMPKalpha2 (AMPKalpha2-CA). Hepatic AMPKalpha2-CA expression significantly decreased blood glucose levels and gluconeogenic gene expression. Hepatic expression of AMPKalpha2-CA in streptozotocin-induced and ob/ob diabetic mice abolished hyperglycemia and decreased gluconeogenic gene expression. In normal mouse liver, AMPKalpha2-CA considerably decreased the refeeding-induced transcriptional activation of genes encoding proteins involved in glycolysis and lipogenesis and their upstream regulators, SREBP-1 (sterol regulatory element-binding protein-1) and ChREBP (carbohydrate response element-binding protein). This resulted in decreases in hepatic glycogen synthesis and circulating lipid levels. Surprisingly, despite the inhibition of hepatic lipogenesis, expression of AMPKalpha2-CA led to fatty liver due to the accumulation of lipids released from adipose tissue. The relative scarcity of glucose due to AMPKalpha2-CA expression led to an increase in hepatic fatty acid oxidation and ketone bodies production as an alternative source of energy for peripheral tissues. Thus, short-term AMPK activation in the liver reduces blood glucose levels and results in a switch from glucose to fatty acid utilization to supply energy needs.

AMP-Activated Protein Kinases↗
PubMed1990

Fatty liver hepatitis and type 5 hyperlipoproteinemia in juvenile diabetes mellitus. Case report and review of the literature.

A 28-year-old man with poorly controlled juvenile-onset diabetes mellitus presented with jaundice and type 5 hyperlipoproteinemia. A liver biopsy showed fatty liver hepatitis (steatonecrosis). This case represents one end in a spectrum of lipid disorders and liver disease in diabetes mellitus. With increasing insulin deficiency, liver steatosis and the more common type 4 hyperlipoproteinemia pattern may progress to fatty liver hepatitis and type 5 hyperlipoproteinemia.

Adult↗
PubMed2005

The nutritional status modulates preservation-reperfusion injury in rat fatty liver.

BACKGROUND: Microcirculation disturbances are essential factors of preservation injury in fatty liver. However, hepatocyte injury is also markedly excessive in fatty liver resulting, at least in part, from energy metabolism impairment and oxidative stress. Thus, this study aimed to determine whether nutritional status influences preservation injury in fatty liver and whether energetic substrate supplementation, alone or with a vasodilator, is protective. MATERIALS AND METHODS: Normal or fatty livers induced by a choline-deficient diet were isolated from fed and fasted rats, preserved in University of Wisconsin solution at 4 degrees C for 18 h, and then reperfused with Krebs-Henseleit solution at 37 degrees C for 120 min. Fasted rats with fatty liver were also treated as follows: (1) Glucose supplementation: rats had access to a glucose solution for 18 h prior procurement; (2) Prostaglandin (PG): alprostadil was continuously infused during reperfusion; (3) Combined treatment: Glucose supplementation + PG. RESULTS: Fasting-induced liver injury was significantly greater in fatty than normal liver. In fatty livers from fasted rats, all treatments reduced the alanine aminotransaminase release. Hepatic oxygen consumption improved in the glucose and glucose + PG groups, while PG infusion had no effect. Glucose supplementation did not affect portal pressure, which, in contrast, was reduced in livers receiving PG. Finally, all treatments lowered oxidative injury. CONCLUSIONS: Preservation injury in fatty liver is greatly related to nutritional status. Energetic substrate supplementation may represent a clinically feasible protective strategy and a multistep approach adding vasodilators could offer further benefit by acting on different pathogenetic mechanisms.

Alanine Transaminase↗
PubMed2005

[Epidemiological survey of prevalence of fatty liver and its risk factors in a general adult population of Shanghai].

OBJECTIVE: To investigate the prevalence and major risk factors of fatty liver among adult residents in Shanghai. METHODS: A cross-sectional survey with multiple-stage stratified cluster and random sampling was performed. All residents aged 16 and above were invited to participate in the survey; they came from four communities of Yangpu District and Pudong New District. Questionnaire, physical examination, serum lipid-profile, and 75 gram oral glucose tolerance test and ultrasonographic examination of liver were undertaken. Analysis of data was performed through SPSS 11.0 for Windows statistical package. RESULTS: A total of 3175 residents took part in the survey, which was 75% of adult residents of the investigated communities and 2.26/10 000 of Shanghai municipal residents. Of the 3175, 1218 were males and 1957 were females. The mean age of the participants was 52.4+/-15.1 years and ranged from 16 to 88 years. Fatty liver was detected with ultrasound examination in 661 participants (20.82%), among which 3.48% had alcoholic fatty liver, 4.08% had suspected alcoholic fatty liver, and 92.43% had nonalcoholic fatty liver. The age-adjusted, sex-adjusted prevalence of fatty liver in Shanghai adult residents was 17.29%, the prevalence of alcoholic fatty liver, suspicious alcoholic fatty liver, and nonalcoholic fatty liver in Shanghai adult residents were 0.79%, 1.15%, and 15.35%, respectively. The prevalence of fatty liver was increased with aging in males and in females. Among participants younger than 50 years old, the prevalence of fatty liver in males was significantly higher than that in females, but in participants older than 50 years the case was just the opposite, higher in females. The mean age (years), body mass index (BMI), waist circumference, blood pressure, fasting and two hour serum glucose level, triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and the presence of obesity, diabetes mellitus, hypertension, dyslipidemia, and gallstones in the fatty liver group was significantly higher than those in the group without fatty liver, but the high-density lipoprotein cholesterol (HDL-C) level and the educational level were both lower in the fatty liver group. Logistic regression analysis demonstrated that the prevalence of fatty liver was only positively correlated to nine risk factors, including male sex, educational level, waist circumference, BMI, fasting glucose level, HDL-C, TG, hypertension and diabetes mellitus. In heavy drinkers, obesity increased the risk for fatty liver by 4.8-fold, but heavy drinking only increased the risk for fatty liver 1.5-fold (95% CI 0.9-2.6, P=0.1685). CONCLUSION: There is a high prevalence of fatty liver among adult residents in Shanghai, and nonalcoholic fatty liver is the major type. Metabolic disorders such as obesity and diabetes mellitus, hypertension and hyperlipidemia are more closely associated with fatty liver than heavy drinking in Shanghai.

Adolescent↗
PubMed2001

[Relationship between liver fibrosis criteria and syndrome-type of TCM in patients with non-alcoholic fatty liver].

OBJECTIVE: To explore the relationship between the liver fibrosis criteria and TCM Syndrome, type in the patients suffering from non-alcoholic fatty liver. METHODS: Seventy-nine patients with non-alcoholic fatty liver diagnosed by B ultrasonography were classified by TCM Syndrome Differentiation and their liver fibrosis criteria was determined and compared with those of the health subjects as control. RESULTS: Levels of procollagen III (PCIII), hyaluronic acid (HA), collagen IV (CIV) and laminin (LN) in the fatty liver group were significantly higher than those in the control group (P < 0.05, P < 0.01). In respect to the TCM Syndrome-types, PCIII, CIV and LN in patients of Phlegm-stasis combined type were significantly higher than those in patients of other two Syndrome-types (P < 0.05, P < 0.01), while HA was insignificantly different (P > 0.05). CONCLUSION: There was trend of liver fibrosis in fatty liver patients. It was indicated that the Phlegm-stasis combined Syndrome-type possibly was the main TCM pathologic factor of the increasing of fibrosis criteria for non-alcoholic fatty liver.

Adult↗
PubMed1979

Follow-up study on patients with non-alcoholic and non-diabetic fatty liver.

From a group of 424 patients with histologically verified fatty liver 92 patients without diabetes mellitus and alcohol abuse were subjected to follow-up examination for 3 1/2 years. 56 patients underwent second liver biopsy at this time; 20 of these patients had shown marked fatty liver at the initial liver biopsy examination. These 20 patients with marked fatty liver and 25 further patients with moderarte fatty liver could be followed up 5 and 7 1/2 years later; the clinical examination, the various liver function tests, liver scan and blind liver biopsy did not show any evidence of progression of fatty liver towards chronic inflammatory liver disorders or precirrhotic states. This clinical study therefore suggests the harmlessness of non-alcoholic fatty liver.

Adult↗
PubMed1998

Acute fatty liver of pregnancy in triplet gestation.

BACKGROUND: Acute fatty liver is reported to be more common in twin than in singleton pregnancies. We report three cases of biopsy-proven acute fatty liver in triplet gestations. CASES: In all three cases of acute fatty liver complicating triplet pregnancies, the presenting features were vague abdominal complaints with elevated hepatic aminotransferase levels. A liver biopsy was performed in each case, and cesareans were performed immediately after the diagnosis was confirmed histologically. Clinical resolution occurred in all cases, and all infants did well in the neonatal period. CONCLUSION: Patients with triplet gestations should be monitored closely for the early signs of acute fatty liver. Triplet gestations may contribute to the onset of acute fatty liver by further stressing the fatty acid oxidation capabilities of the susceptible woman.

Acute Disease↗
PubMed1998

[Imaging manifestations of tumors metastasized in fatty liver].

OBJECTIVE: To evaluate the manifestations of tumors metastasized in fatty liver and the value of various imaging modalities, especially CT. METHODS: Nine cases of tumors metastasized in fatty liver were proved by clinical follow-up for 3-13 months. The primary neoplasms were breast carcinoma in 6 cases; ovarian carcinoma, malignant melanoma and colon carcinoma, one case for each. All had CT(19 episodes) and ultrasonography (US, 20 episodes). Four cases had MRI and 2 cases had DSA. RESULTS: Liver metastatic lesions were missed by US in 2 cases with moderate to marked fatty liver. On CT without contrast administrations, fatty liver was divided into marked, moderate and mild degree according to the density of hepatic parenchyma which was lower than that of the spleen; lower and higher than or equal to that of the intrahepatic blood vessels. Depending on the degree of fat infiltration(FI), the density of the metastatic lesions was high when FI was marked and low when FI was mild. However, when FI was moderate, the density of the metastatic lesions varied, being high, equal or low. On enhanced CT, all of the lesions were enhanced with moderate to marked fatty liver background. Lesions were heterogeneous in 4 cases. On plain CT, metastatic lesions had high-density rim, 2-6 mm in width in 4 cases. In SE sequence of MRI, metastatic lesions were hypointense on T1W and hyperintense on T2W, and moderately hyperintense on opposed-phase. CONCLUSION: Tumors metastasized in fatty liver show a broad spectrum of image manifestations. They are related to the degree of fat infiltration. On plain CT, isodense lesions are easily escaped detection when moderate degree of fatty liver is present. Contrast administrations is mandatory. Liver metastases is suggested if a lesion is found with hyperattenuating rim on plain CT, or appears heterogeneous after enhancement. MRI is of diagnostic help.

Adult↗
PubMedDate not supplied

Elevated pancreatic glucagon in moderately obese patients: relationship of fatty liver and hypertriglyceridemia.

To elucidate if the presence of fatty liver and hypertriglyceridemia (HTG) influences pancreatic A-cell function in obesity, basal and arginine-stimulated glucagon (IRG) secretions were studied in 7 normal subjects and in 28 moderately obese patients (OB) with normal glucose tolerance. The patients were divided into 4 groups, based on the presence of fatty liver and/or HTG. BMI was similar in all four obese groups. Basal IRG, as well as the sum of secretory response to arginine, namely sigma IRG values, were significantly (p less than 0.01) higher in the OB subgroup having both fatty liver and HTG than in the other three groups; these values were similar in subgroups of OB without fatty liver, and showed no significant difference from the normals. Basal and sigma IRG values in all OB correlated well with the degree of fatty liver and HTG, demonstrating that by stepwise analysis the effects of fatty liver and HTG were independent for basal and sigma IRG values. These results suggest that the combination of fatty liver and HTG may serve as a good predictor of hyperglucagonemia in simple obesity, and, hence, metabolic heterogeneity among obese patients should be considered in evaluating A-cell function.

Adult↗
PubMed2006

Fatty liver and transaminase changes with adjuvant tamoxifen therapy.

We investigated the time it took to develop fatty liver and changes in serum aspartate aminotransferase and alanine aminotransferase levels in patients with breast cancer treated with adjuvant tamoxifen. Liver sonography to detect fatty liver and measurement of serum aspartate and alanine aminotransferase levels were performed regularly for patients with early breast cancer. The results were compared in groups of patients with and without adjuvant tamoxifen as well as those on chemotherapy. Eighty-two of 156 patients treated with tamoxifen developed fatty liver, compared with eight of 62 patients not taking it. Fatty liver appeared as early as 3 months after beginning tamoxifen and was detected within 2 years in most cases. It persisted for 48 months after discontinuing tamoxifen in 17 of the 82 patients who developed it. The incidence of fatty liver in patients receiving both chemotherapy and tamoxifen was the same as that in patients receiving tamoxifen alone. While 115 patients had elevations of aspartate aminotransferase, alanine aminotransferase or both, the magnitude of the elevation was clinically significant in only 32 patients. Patients on both chemotherapy and tamoxifen had a higher incidence of elevated transaminases than those on tamoxifen alone. Adjuvant tamoxifen increases the incidence of fatty liver, but has only a minimal effect on aspartate aminotransferase and alanine aminotransferase. Fatty liver may appear as early as 3 months after beginning tamoxifen and may persist for more than 4 years after discontinuing it. Therefore, long-term follow-up is warranted. Chemotherapy is not clearly associated with fatty liver, but may cause a greater degree of hepatocellular damage than does tamoxifen.

Alanine Transaminase↗
PubMedDate not supplied

The pathology of post-parturient fatty liver in high-yielding dairy cows.

The pathology of post-parturient fatty liver has been studied in a group of 20 high-yielding dairy cows; 10 had less than 20 per cent fat in the liver cell and were classified as having a mild fatty liver and 10 had more than 30 per cent fat in the liver cell and were classified as having severe fatty liver. Severe fatty liver was accompanied by a number of morphological changes including the occurrence of lipogranulomas, increased liver cell volume, decreased volume of rough endoplasmic reticulum per liver cell and evidence of mitochondrial damage. The latter two changes were reflected in reduced albumin levels and increased activities of mitochondrial enzymes observed in the blood of cows with severe fatty liver. Reduced fertility may be one of the consequences of severe fatty liver in the dairy cow.

Animals↗
PubMed2000

Adipose tissue deficiency, glucose intolerance, and increased atherosclerosis result from mutation in the mouse fatty liver dystrophy (fld) gene.

The fatty liver dystrophy (fld) mutant mouse is characterized by neonatal fatty liver and hypertriglyceridemia that resolve at weaning, and neuropathy affecting peripheral nerve in adulthood. We now report additional significant manifestations of this single gene mutation, which include adipose tissue deficiency, glucose intolerance, and increased susceptibility to atherosclerosis. In adult fld/fld mice, both white and brown fat pads exhibit an 80% reduction in mass compared with wild-type controls, and consist of immature adipocytes as assessed by morphological and molecular criteria. The lack of lipid accumulation in fld/fld adipose tissue could be attributed, in part, to a failure to induce expression of lipoprotein lipase and enzymes involved in fatty acid synthesis, such as fatty acid synthase and acetyl-CoA carboxylase. Related to the deficiency of adipose tissue, fld/fld mice were also found to exhibit profound glucose intolerance, modest hyperinsulinemia, and reduced tissue response to insulin. As insulin resistance is a important risk factor in vascular disease, we examined susceptibility of fld/fld mice to diet-induced atherosclerosis. Mutant mice fed an atherogenic diet developed 2-fold greater aortic lesions than their wild-type counterparts, despite having a less atherogenic lipoprotein cholesterol profile. The fld adipose-deficient phenotype has both similarities to and distinctions from the group of rare human diseases known as lipodystrophies.

Abnormalities, Multiple↗
PubMed2002

Fatty liver in non-alcoholic non-overweight Japanese adults: incidence and clinical characteristics.

BACKGROUND AND AIMS: Fatty liver is not uncommon in many countries, including Japan, and is mainly caused by alcohol usage and obesity. The aim of this study was to determine the incidence and causative factors of fatty liver in Japanese adults. METHODS: The clinical characteristics of 3432 Japanese adults who visited our hospital between January and December 2000 for thorough medical examinations were recorded including sex, age, body mass index (BMI), percentage body fat measurement using a bipedal bioimpedance instrument, history of alcohol intake, blood pressure, serum levels of aspartate aminotransferase, alanine aminotransferase (ALT), gamma-glutamyl transpeptidase, total cholesterol, triglyceride, uric acid, fasting blood glucose (FBG), and liver status by ultrasonography (USG). RESULTS: Of 3432 participants, 747 (21.8%) were diagnosed as having fatty liver by USG, 1873 (54.6%) were 'daily alcohol drinkers', and 698 (20.3%) were overweight (BMI >or= 25 kg/m2). Fatty liver was more frequent in men and overweight subjects (P < 0.01), whereas there was no significant difference in the proportion of the 'daily alcohol drinker' between fatty liver and non-fatty liver participants. The logistic regression analysis showed that BMI, ALT, and triglyceride were independent predictors of fatty liver in both sexes, and FBG, uric acid, percentage body fat, and total cholesterol were independent predictors of fatty liver only in men. It was noted that 319 (9.3%) were non-alcoholic individuals with fatty liver, and 141 (4.1%) were non-alcoholic and non-overweight individuals with fatty liver. The logistic regression analysis showed that percentage body fat was an independent predictor of fatty liver in non-alcoholic and non-overweight participants in both sexes, although non-significant in women in the whole group. CONCLUSIONS: In our study population, 21.8% had fatty liver diagnosed by USG, 9.3% were non-alcoholic with fatty liver, and 4.1% were non-alcoholic and non-overweight with fatty liver. Our results suggest that central body fat distribution can correlate with the development of fatty liver, and that measurement of percentage body fat is useful to assess the etiology of fatty liver in non-alcoholic and non-overweight participants, particularly women.

Adipose Tissue↗
PubMed2004

[Computerized tomography in the diagnosis of nonalcoholic fatty liver--comparison with liver biopsy].

The frequency of nonalcoholic fatty liver disease (NAFLD) is high, an estimated 10-25% of the population in different countries. Due to the lack of specific symptoms or irregularities in laboratory examinations the major role in diagnosis is played by, apart form liver biopsy, the imaging examinations. AIM: The assessment of the correlation between intensity of fatty liver in computed tomography (CT) and in liver biopsy. INVESTING GROUP AND METHOD: The initial group comprised of 147 patients who had undergone CT of the abdomen. Within this group the range of attenuation coefficient in Hansfield units was measured in certain areas of liver and spleen. Density of the tissues being given (in Hansfield units) the increase of the fat content in the liver above the norm (tKT) was calculated, according to the formula: tKT = [(spleen density in OH units + 4 OH units) - liver density in OH units] x 0.8 = fat above norm in mg/l g of the liver tissue. Out of this group 12 patients (8 men and 4 women, average age 45.9 +/- 14.5 years) with clinical features of NAFLD on clinical indications for liver biopsy were selected. RESULTS: 3 patients the received value of tKT was found to be correct, that is tKT < 0. In these patients the estimated percentage of hepatocytes affected by steatosis (%TB) reached 5-20%. In the subgroup that comprised if the folio wing 6 patients %TB ranged from 30 to 70% and tKT--from 3.2 to 10. In the group of patients with the highest %TB, reaching 100%, the tKT value reached respectively 5, 10.8 and 13.6. The analysis of the relation between %TB and tKT showed a linear correlation of these two parameters. Following the increase of the intensity of the fatty liver in the biopsy the value of tKT rises. CT of the liver with the range of attenuation coefficient marked (in Hansfield units) is a useful tool for quantitative assessment of the fatty pulp.

Adult↗
PubMed2006

Vulnerability of experimentally induced fatty liver to heat stress in rats.

BACKGROUND: The aim of this study was to confirm the vulnerability of fatty liver to heat stress using fatty liver rats from the viewpoint of the induction of apoptosis. METHODS: We exposed rats with and without a fatty liver to heat stress and then looked for apoptotic cells within the liver tissue using two apoptosis detection kits. We also determined the mRNA expression of heat shock protein (HSP) 70, caspase-3, bcl-2, and bax using a quantitative reverse transcription-polymerase chain reaction method. RESULTS: Following heat stress, apoptosis was strongly visible in the fatty liver comparing with that noted in the normal liver. The expression of HSP70 was increased following heat stress in both livers, but the volume of its expression was significantly less in the fatty liver than in the normal liver. The ratio of bcl-2/bax expression tended to increase in the normal liver but decrease in the fatty liver following heat stress. Caspase-3 demonstrated no significant change following heat stress in both livers. CONCLUSIONS: The detection of apoptosis, together with changes in the mRNA expression of HSP70 and the expression ratio bcl-2/bax mRNA may indicate vulnerability of a fatty liver to heat stress and may support the hypothesis that morphologic change is induced in a fatty liver by exposure to heat stress. These results suggest that fatty liver may be more vulnerable to heat stress than normal liver.

Animals↗
PubMed2005

Histological progression of non-alcoholic fatty liver disease in Chinese patients.

BACKGROUND: Non-alcoholic fatty liver disease is an important cause of chronic hepatitis and cryptogenic cirrhosis. The natural history of non-alcoholic fatty liver disease is not well understood especially in Asian populations. AIM: To investigate the histological progression in Chinese patients with biopsy-proven non-alcoholic fatty liver disease. METHODS: Chinese patients who had liver biopsy at least 3 years ago and confirmed to have non-alcoholic fatty liver disease were invited for a second liver biopsy. Clinical and laboratory parameters related to their liver function and metabolic syndrome were recorded and analysed. Liver biopsies were scored for the degree of steatosis, necroinflammation and fibrosis. Correlation coefficients were calculated to assess the association between changes in histological scores and metabolic parameters. RESULTS: Seventeen patients who had been followed up for a median period of 6.1 (range: 3.8-8.0) years underwent a second liver biopsy. Nine (53%) patients had progressive disease with worsening of fibrosis score. No statistically significant correlation was found between the changes in histological scores and metabolic parameters. Seven patients developed hypertension or diabetes mellitus during the period of follow-up. CONCLUSIONS: Non-alcoholic fatty liver disease is a progressive disease in Chinese patients as in their Caucasian counterparts. Diagnosis of non-alcoholic fatty liver disease may predate development of new components of metabolic syndrome.

Adult↗
PubMed2005

Sonographic fatty liver, overweight and ischemic heart disease.

AIM: To demonstrate the prevalence of sonographic fatty liver, overweight and ischemic heart disease (IHD) among the male workers in Taiwan, and to investigate the possible association of these three factors. METHODS: From July to September 2003, a total of 2 088 male aircraft-maintenance workers aged from 22 to 65 years (mean 40.5) underwent an annual health examination, including anthropometrical evaluation, blood pressure measurement, personal medical history assessment, biochemical blood analysis, abdominal ultrasonographic examination and digital electrocardiography (ECG). The Student's t-test, chi(2) test and multivariate logistic regression analysis were utilized to evaluate the relationship between IHD and salient risk factors. RESULTS: The all-over prevalence of overweight was 41.4%, and that of fatty liver was 29.5% (mild, moderate and severe fatty liver being 14.5%, 11.3%, and 3.7%, respectively); while the prevalence of ischemic changes on ECG was 17.1% in this study. The abnormal rates for conventional IHD risk factors including hypertension, dyslipidemia, hyperglycemia and overweight increased in accordance with the severity of fatty liver. Overweight and severity of fatty liver were independently associated with increased risks for developing IHD. Overweight subjects had a 1.32-fold (95%CI: 1.01-1.73) increased IHD risk. Participants with mild, moderate, and severe fatty liver had a 1.88-fold (95%CI: 1.37-2.6), 2.37-fold (95%CI: 1.66-3.37) and 2.76-fold (95%CI: 1.62-4.72) increased risk for developing IHD. The prevalence of ischemic ECG for the fatty liver-affected subjects with or without overweight was 30.1% and 19.1%, while that of overweight subjects free from fatty liver was 14.4%. Compared to the subjects without fatty liver nor overweight, IHD risk for the three subgroups above was as follows: OR: 2.95 (95%CI: 2.31-4.09), OR: 1.60 (95%CI: 1.07-2.39) and OR: 1.11 (95%CI: 0.78-1.56), respectively. CONCLUSION: The presence of fatty liver and its severity should be carefully considered as independent risk factors for IHD. Results of the study suggest the synergistic effect between fatty liver and overweight for developing IHD. Abdominal sonographic examination may provide valuable information for IHD risk assessment in addition to limited report about liver status, especially for overweight males.

Adult↗