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PubMed1994

Effect on ligand binding of arginine mutations in recombinant rat liver fatty acid-binding protein.

Rat liver fatty acid-binding protein is able to accommodate a wide range of non-polar anions in addition to long-chain fatty acids. The two arginine residues of rat liver fatty acid-binding protein, Arg122 and Arg126, have been mutated and the effect of mutation on ligand binding investigated. No significant decrease in affinity for the fluorescent fatty acid analogue, 11-(5-dimethylaminonaphthalenesulphonyl amino)undecanoic acid, or oleate was observed. However, the apparent affinity for oleoyl-CoA was slightly increased with the mutations Ala122 and Gln122 such that oleoyl-CoA rather than oleate became the preferred ligand for these mutants. Small changes in protein stability were observed with the Arg122 mutations. The lack of notable ionic involvement of the conserved internal residue Arg122 in ligand binding is consistent with the hypothesis that the mode of ligand binding in liver fatty acid-binding protein is markedly different from that of other members of this lipid-binding protein family.

Acyl Coenzyme A↗
PubMed1995

Effects of female sex hormones on mitochondria: possible role in acute fatty liver of pregnancy.

Acute fatty liver of pregnancy occurs in some women. As other cases of microvesicular steatosis are due to impaired mitochondrial oxidation of fatty acids, we investigated the effects of female sex hormones on liver mitochondria in female mice. Three hours after administration of both estradiol (36 mumol/kg) and progesterone (150 mumol/kg), the in vitro beta-oxidation of [U-14C]palmitic acid and the activity of the tricarboxylic acid cycle decreased 49 and 54%, whereas the in vivo oxidation of [U-14C]palmitic acid decreased 38%. One week of treatment with both sex hormones produced ultrastructural lesions of mitochondria, decreased the recovery of mitochondrial proteins by 34%, increased state 4 respiration by 54-77%, and decreased the activities per gram of liver of several enzymes involved in the activation, mitochondrial uptake, and oxidation of fatty acids by 34-54%. We conclude that female sex hormones have deleterious effects on liver mitochondria and suggest that these effects, together with other factors, may contribute to the development of acute fatty liver of pregnancy in some women.

Acute Disease↗
PubMed1998

The fatty liver dystrophy mutant mouse: microvesicular steatosis associated with altered expression levels of peroxisome proliferator-regulated proteins.

Fatty liver dystrophy ( fld) is an autosomal recessive mutation in mice characterized by hypertriglyceridemia and fatty liver during neonatal development. The fatty liver in fld/fld mice spontaneously resolves between the age of 14-18 days, at which point the animals develop a neuropathy associated with abnormal myelin formation in peripheral nerve. We have investigated the morphological and biochemical alterations that occur in the fatty liver of neonatal fld/fld mice. Studies at the light and electron microscopic level demonstrated the accumulation of lipid droplets and hypertrophic parenchymal cells in fld neonates, with no apparent liver pathology after resolution of the fatty liver. To better characterize the biochemical basis for the development of fatty liver in fld mice, we compared protein expression patterns in the fatty liver of fld mice and in the liver of phenotypically normal (wild-type) littermates using quantitative two-dimensional gel electrophoresis. We detected 24 proteins with significantly altered expression levels (P < 0.001) in the fld fatty liver, 15 of which are proteins that are altered in abundance by peroxisome proliferating chemicals. As these compounds characteristically elicit changes in the expression of mitochondrial and peroxisomal enzymes involved in fatty acid oxidation, we quantitated rates of fatty acid oxidation in hepatocytes isolated from fld and wild-type mice. These studies revealed that hepatic fatty acid oxidation in fld neonates is reduced by 60% compared to wild-type littermates. In hepatocytes from adult fld mice that no longer exhibit a fatty liver, oxidation rates were similar to those in hepatocytes from age-matched wild-type mice. These findings indicate that altered expression of proteins involved in fatty acid oxidation is associated with triglyceride accumulation in the fld fatty liver.

Animals↗
PubMed1999

Acute fatty liver in the second trimester.

BACKGROUND: Acute fatty liver of pregnancy is a rare, potentially fatal disease that occurs in the late third trimester or early postpartum period. The case of a woman with acute fatty liver in the second trimester is presented. CASE: A 35-year-old woman, gravida 5, para 4, presented at 22 weeks' gestation with nausea, vomiting, malaise, weight loss, and moderately elevated liver transaminase levels. The differential diagnoses included viral gastroenteritis and cholelithiasis. During the next 12 days, her transaminase levels increased, jaundice developed, her sensorium changed, and coagulopathy appeared. After the patient was transferred to a tertiary care hospital, acute fatty liver of pregnancy was diagnosed. The woman rapidly improved after delivery. CONCLUSION: Although acute fatty liver of pregnancy usually occurs in the late third trimester or early postpartum period, it can occur in the second trimester.

Acute Disease↗
PubMed2005

Fatty liver and the metabolic syndrome among Shanghai adults.

BACKGROUND AND AIM: To explore the relationship between fatty liver and the metabolic syndrome in the adults of Shanghai and evaluate the value of fatty liver as a marker for risk factor clustering. METHODS: Questionnaires, physical examinations, laboratory tests (blood lipid and glucose) and real-time liver ultrasonographies were performed in Shanghai adults and analyzed using randomized, multistage, stratified cluster sampling. Prevalence of the metabolic syndrome was defined by the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATPIII) criteria with the exception of abdominal obesity (waist circumference > 90 cm in men and > 80 cm in women); fatty liver was diagnosed in accordance with the presence of an ultrasonographic pattern consistent with 'bright' liver (brightness and posterior attenuation of liver). RESULTS: The study population consisted of 3175 subjects (1218 men) with a mean (+/- SD) age of 52.4 +/- 15.1 years. Metabolic syndrome and fatty liver were found in 726 (22.87%) and 661 (20.82%) of sampled cases, respectively. After adjustment by age and sex, the prevalence of the metabolic syndrome and fatty liver in the general population of Shanghai were 15.30 and 17.29%, respectively. The risk for fatty liver in subjects with abdominal obesity, diabetes, dyslipidemia and hypertension increased 32.78-fold (95% confidence interval (CI) 14.85-72.35), 31.58-fold (95% CI 14.18-70.35), 22.64-fold (95% CI 10.26-49.99) and 23.25-fold (95% CI 10.54-51.30), respectively, compared with controls, whereas the risk for fatty liver in subjects with metabolic syndrome was increased by 39.33-fold (95% CI 17.77-87.05). After the 661 patients with fatty liver had been stratified by body mass index (BMI), the prevalence of abdominal obesity, hypertension and the metabolic syndrome were increased from 25.0, 47.2 and 36.1%, respectively, in people with normal BMI to 81.0, 73.8 and 55.4%, respectively, in obese persons. However, the prevalence of hypertriglyceridemia, high fasting glucose and low high-density lipoprotein-cholesterol showed no significant changes with increased BMI. Moreover, among fatty liver patients with normal BMI, the detection rate for one or more features of metabolic disorders was as high as 83.3% and that for five features was 2.8%. Compared with obesity (BMI > or = 25 kg/m2) and abdominal obesity, fatty liver had the highest clustering rate, specificity, positive predictive value and attributable risk percentage in detecting risk factor clustering in both sexes. CONCLUSIONS: There is a high prevalence of metabolic syndrome and fatty liver among Shanghai adults. Metabolic disorders are closely related to fatty liver; moreover, fatty liver appears to be a good predictor for the clustering of risk factors for metabolic syndrome.

Adolescent↗
PubMed1999

Reversible peripartum liver failure: a new perspective on the diagnosis, treatment, and cause of acute fatty liver of pregnancy, based on 28 consecutive cases.

OBJECTIVE: We sought to describe our experience with the clinical diagnosis, management, and course of patients with acute fatty liver of pregnancy. STUDY DESIGN: Twenty-eight cases of acute fatty liver of pregnancy at the Los Angeles County and University of Southern California Medical Center from 1982 to June 1997 were identified, and presenting symptoms, clinical course, laboratory values, maternal complications, and neonatal outcomes were studied. RESULTS: The incidence of acute fatty liver of pregnancy was 1 in 6659 births. There were no maternal deaths. Initial presentation was at an average of 37 weeks of gestation with a characteristic prodrome of malaise, nausea, vomiting, and abdominal pain. No patient was admitted with the diagnosis of acute fatty liver of pregnancy. The condition was diagnosed most commonly on the second hospital day after laboratory results indicated coagulopathy, renal insufficiency, and liver function abnormalities. One patient underwent liver biopsy at cesarean delivery. Radiologic studies did not aid with the diagnosis. Twenty-one patients were admitted in spontaneous labor, and 16 labors were complicated by abnormal fetal heart rate patterns or meconium. There was 1 stillbirth and 1 neonatal death as a result of perinatal asphyxia. Maternal morbidity consisted of hypoglycemia, infection, renal insufficiency, coagulopathy, encephalopathy, and wound complications. All patients had evidence of disseminated intravascular coagulopathy with profoundly decreased antithrombin levels. All patients recovered normal liver function post partum. CONCLUSIONS: Reversible peripartum liver failure may be diagnosed and managed on the basis of clinical and laboratory criteria. With adequate support, these patients may have full recovery of hepatic function.

Acute Disease↗
PubMedDate not supplied

Enhanced tumor detection in the presence of fatty liver disease: cell-specific contrast agents.

It is assumed that hepatobiliary, cell-specific contrast agents will be adversely affected by the presence of diffuse liver disease. The diagnostic efficacy for tumor detection in the presence of fatty liver disease was experimentally studied at contrast-enhanced magnetic resonance (MR) imaging with manganese-DPDP (N,N'-dipyridoxylethylenediamine-N,N'-diacetate 5,5'-bis[phosphate]) and gadobenate dimeglumine (Gd-BOPTA/dimeg) and compared with conventional and chemical shift imaging. Carcinosarcoma was implanted into the liver of rats, and fatty liver was induced with L-ethionine. Without contrast agents, the tumor-fatty liver contrast-to-noise ratio (C/N) was increased on T1-weighted and decreased on T2-weighted MR images relative to tumor-bearing control rats without fatty liver. Chemical shift imaging (phase-contrast method) increased the tumor-fatty liver C/N from 2.3 +/- 1.0 to 6.1 +/- 1.7 (P < .001). Mn-DPDP and Gd-BOPTA/dimeg increased the tumor-fatty liver C/N from -5.4 +/- 1.6 to -11.0 +/- 1.9 and -9.8 +/- 3.4, respectively (P < .001). The hepatobiliary, cell-specific contrast agents were equally effective in both fatty and non-fatty liver and outperformed both chemical shift and conventional MR imaging in detecting liver tumors.

Animals↗
PubMed1995

Effect of weight control on hepatic abnormalities in obese patients with fatty liver.

This study was aimed at finding out whether weight reduction alone can improve liver function in obese patients with fatty liver. We did a longitudinal, clinical intervention study on weight reduction by behavior modification, diet and exercise. The study subjects were 25 patients referred to an obesity clinic in whom obesity is the sole factor causing abnormal liver function and fatty liver. Patients were weighed about one year later. We compared the degree of improvement in hepatic function between Group I that showed weight reduction and Group II that showed no-weight reduction. Group I (13) showed dramatic improvement in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, nearly all down to within normal levels. AST showed statistically significant improvement from 74 +/- 36 IU/l to 25 +/- 7 IU/l. ALT also showed statistically significant improvement from 109 +/- 67 IU/l to 30 +/- 14 IU/l. Group II (12) showed higher AST and ALT levels on follow-up visit than initial visit. AST showed statistically significant elevation from 43 +/- 11 IU/l to 59 +/- 23 IU/l. ALT also showed statistically significant elevation from 64 +/- 21 IU/l to 97 +/- 33 IU/l. If we can rule the other causes of hepatic abnormalities in obese patients with fatty liver, we suggest these patients would benefit by weight reduction.

Adolescent↗
PubMed2002

The metabolic abnormalities associated with non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is a common disorder in the Western hemisphere. It encompasses two histological lesions: fatty liver and steatohepatitis. A large body of literature indicates that insulin resistance is a key pathophysiological abnormality in patients with NAFLD. Insulin resistance results from a complex interplay between the major targets of insulin action, i.e. muscle, adipose tissue and liver, versus the ability of the pancreatic islet beta cells to compensate for insulin resistance by increasing insulin production. The metabolic and clinical profile associated with insulin resistance is thus defined by the factors that produce and maintain insulin resistance and the effects of decreased insulin sensitivity on various insulin-dependent pathways. The major metabolic defects associated with insulin resistance are increased peripheral lipolysis, increased hepatic glucose output due to increased gluconeogenesis and increased lipid oxidation. This is associated with an oxidative stress in the liver that may be compounded by additional pathophysiological abnormalities. While much work remains to be done, the current understanding of the pathogenesis of NAFLD provides direction for both future investigation and development of therapeutic trials.

Disease Progression↗
PubMed1997

A case of liver metastasis from colon cancer masquerading as focal sparing in a fatty liver.

Focal sparing in diffusely fatty liver is a well recognized entity. However, it occasionally creates some problems in the diagnosis of hepatic mass lesions. We recently experienced a case of liver metastasis from colon cancer which appeared as a wedge-shaped hyperdense area on non-enhanced CT (computed tomography). Other imaging techniques also demonstrated a wedge-shaped area which was difficult to distinguish from mere focal sparing in the fatty liver. CT arteriography and dynamic magnetic resonance images were useful for diagnosing this metastatic tumor. CT during arterial portography showed a wedge-shaped ischemic area in the anterior segment caused by intrahepatic portal vein blockade. The histological findings eventually revealed that the tumor, an adenocarcinoma, was surrounded by fibrotic tissue that mimicked focal sparing. We present the radiological features of this case and discuss how to arrive at a correct diagnosis.

Adenocarcinoma↗
PubMed1999

Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity.

BACKGROUND & AIMS: The spectrum of nonalcoholic fatty liver disease ranges from fatty liver alone to nonalcoholic steatohepatitis. Most previous studies have short follow-up and have not carefully delineated different histological types when determining clinical outcomes. The aim of this study was to compare clinical characteristics and outcomes of patients with different types of nonalcoholic fatty liver. METHODS: All liver biopsy specimens from 1979 to 1987 with fat accumulation were assessed for inflammation, ballooning degeneration, Mallory hyaline, and fibrosis. Biopsy specimens were also assessed for histological iron and hepatitis C RNA. Outcomes were cirrhosis, mortality, and liver-related mortality. RESULTS: Of 772 liver biopsy specimens, complete data were available in 132 patients. Fatty liver (type 1) did not differ from the other three types combined with respect to gender, race, age, or obesity. Cirrhosis was more common in the other types combined (22%) than fatty liver alone (4%; P </= 0.001). Overall mortality, histological iron, and hepatitis C did not differ between groups. Most of the liver-related deaths were in type 4. CONCLUSIONS: The outcome of cirrhosis and liver-related death is not uniform across the spectrum of nonalcoholic fatty liver. These poor outcomes are more frequent in patients in whom biopsies show ballooning degeneration and Mallory hyaline or fibrosis.

Adult↗
PubMed2000

Toremifene-induced fatty liver and NASH in breast cancer patients with breast-conservation treatment.

We have described fatty liver, diagnosed by computed tomography scanning (CT) in more than 30% of patients with breast cancer who received tamoxifen. Therefore, it is urgent to elucidate the frequency and the degree of fatty liver induced by toremifene, an analogue of tamoxifen, which is also used in breast cancer. We enrolled 52 breast cancer patients who were treated with breast-conservation treatment and administered oral toremifene for 3-5 years as adjuvant endocrine therapy. We evaluated the degree of fatty liver by abdominal CT performed annually. CT demonstrated toremifene-induced fatty liver in four (7.7%) of 52 breast cancer patients. Toremifene-induced fatty liver did not correlate with abnormal levels of AST, ALT, GGT or total cholesterol. One patient who demonstrated moderate fatty liver by CT was histologically diagnosed as non-alcoholic steatohepatitis (NASH) by liver biopsy. The incidence of toremifene-induced fatty liver was significantly lower than that induced by tamoxifen. Accordingly, in terms of fatty liver and NASH, toremifene is considered to be more appropriate agent than tamoxifen. Though toremifene is less likely to induce fatty liver, the possibility remains that toremifene-induced steatohepatitis occurs. Because the diagnosis of fatty liver or NASH can be easily missed if only a blood test is performed, it is necessary to screen fatty liver by annual CT examination for patients who receive an antiestrogen agent.

Alanine Transaminase↗
PubMed2004

[The assessment of nonalcoholic fatty liver disease detected by computed tomography in cases with obesity and overweight].

UNLABELLED: The pathogenesis of nonalcoholic fatty liver disease (NAFLD) has not been completely explained yet. There are no clear clinical indicators of the risk of NAFLD's occurrence. By means of computed tomography (CT) quantitative assessment of the fatty liver is possible and CT is therefore a suitable method of monitoring the effectiveness of the treatment in non-alcoholic fatty liver. AIM OF THE STUDY: The assessment of the influence of the clinical factors, such as: [1] overweight, [2] the fatty tissue distribution type, [3] the lipids profile, on the risk of NAFLD occurrence. INVESTIGATED GROUP AND METHOD. The examined group and the control group comprised 113 persons (59 women and 54 men) with overweight and obesity, who, due to different clinical indications, underwent CT of the abdomen. In the CT examinations the existence of fatty liver was assessed on the basis of the range of attenuation coefficient (in Hounsfield units), that was measured in four previously chosen areas of the liver. Additionally, two measurements of spleen tissue were conducted. The density of tissues, represented in Hounsfield units, once established makes it possible to assess the increase of fat percentage in the liver with respect to the norm. Excursion criteria: [1] ethanol consumption exceeding 20 g per day; [2] existence of other diseases which may cause derivative form of non-alcoholic fatty liver and/or different clinical features of other diseases of the liver; [3] existence of focal changes of the liver that could affect the measurements of the attenuation coefficient. In the group of 59 women in 23 of them (38.9%) the features of fatty liver have been found. The group with fatty liver in comparison with the group without fatty liver was marked by significantly higher WHR index (0.9 vs 0.8; p = 0.029), higher TG concentration (209.9 mg/dl vs 160.9 mg/dl; p = 0.032) and lower HDL-C concentration (37.7 mg/dl vs 46.1 mg/dl; p = 0.004). In the group of 54 men in 22 of them (40.7%) fatty liver has been affirmed. The group with fatty liver in comparison with the group without fatty liver was characterized by higher BMI (29.2.2 vs 27.4 kg/m2; p = 0.002) and, as in women, higher TG concentration and lower HDL-C concentration in serum. CONCLUSIONS: [1] CT examination with assessment of the range of attenuation coefficient is a useful tool for fatty liver evaluation and may be used in routine diagnostic procedure in patients with NAFLD. [2] The risk factors of NAFLD development are high TG concentration and low HDL-C concentration in serum. [3] In men the risk factor of NAFLD is obesity and overweight, whereas in women fatty liver correlates not only with the BMI value, but above all with central obesity.

Adipose Tissue↗
PubMedDate not supplied

Fatty liver: how frequent is it and why?

There is increasing evidence that fatty liver may be the most frequent liver disorder in Western countries. However, the epidemiology of fatty liver is still not fully understood and there is a clear need of better assessing and defining the potential role of the risk factors identified by clinical series in the general population. This article reviews the available data on the epidemiology of fatty liver and addresses some important questions that should be answered in much needed future research.

Alcohol Drinking↗
PubMedDate not supplied

The natural history and risk factors for progression of non-alcoholic fatty liver disease and steatohepatitis.

Nonalcoholic fatty liver disease (NAFLD) is a condition of increasing incidence in western Countries seldom associated to other diseases of high prevalence in general population (i.e. diabetes and obesity). NAFLD ranges from simple fatty liver to steatohepatitis (NASH), which may lead to cryptogenic cirrhosis and in some cases hepatocellular carcinoma (HCC). Natural history of NAFLD in humans is poorly understood and progression of liver disease seems to be due to interaction between hosting (i.e. genetic, gut flora, insulin resistance) and environmental factors (social and eating behaviours) that should be responsible of increased oxidative stress within hepatocytes. Even if we need non-invasive markers able to describe the progression of liver disease, only meaning of liver biopsy is useful to characterize the stigmata of worsening such as inflammation and fibrosis.

Animals↗
PubMed1996

Immunohistological study in cases of HELLP syndrome (hemolysis, elevated liver enzymes and low platelets) and acute fatty liver of pregnancy.

We immunohistologically studied the hepatic tissue sections in cases with the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome; n = 2) and acute fatty liver of pregnancy (AFLP; n = 2) compared to necropsy controls. Unlike in the AFLP cases, a marked infiltration of neutrophils in liver tissues was found in both cases of the HELLP syndrome. Immunostaining with the antihuman (polyclonal) TNF-alpha, IL-1 beta, IL-8 and antihuman neutrophil elastase (monoclonal antibody) was performed in paraffin-embedded hepatic tissue sections. Liver tissues in HELLP syndrome patients were stained strongly with TNF-alpha and neutrophil elastase antibody. The strongest staining pattern was observed in the eclamptic case, whereas in the AFLP cases, as in the necropsy controls, a very weak staining for anti-TNF-alpha and elastase antibody was found. The liver sections of the HELLP syndrome cases were moderately stained with polyclonal IL-1 beta and IL-8 antibodies whereas AFLP and controls had a very faint staining. Significant correlations were found between the numbers of necrotic hepatocytes and elastase dots in the same microscopic fields (randomly selected) of liver sections from two cases of HELLP syndrome (r2 = 0.63; p < 0.0001), which might suggest a neutrophil-mediated tissue damage in such a disease. This study suggests that a cytokine- and neutrophil-mediated liver injury occurs in the HELLP syndrome but not in AFLP.

Adult↗
PubMed2005

Nonalcoholic fatty liver disease in the pediatric population: a review.

PURPOSE OF REVIEW: Nonalcoholic fatty liver disease is a common condition that may progress to end stage liver disease. It is closely associated with obesity and insulin resistance, two conditions whose prevalence is increasing dramatically in children. This could potentially make nonalcoholic fatty liver disease the most common liver disease in the pediatric population. This review will focus on the current knowledge regarding the epidemiology, clinical presentation, diagnosis, pathogenesis, and management of nonalcoholic fatty liver disease in children. RECENT FINDINGS: Recent studies suggest that nonalcoholic fatty liver disease is an increasingly recognized condition during childhood, especially in overweight and obese children. Although limited information is currently available on the natural history of the disease in the pediatric population, few cross-sectional studies and a single longitudinal cohort study with follow up data up to 16 years, showed that as in adults, nonalcoholic fatty liver disease in children may have a progressive clinical course with the development of cirrhosis. Emerging data from small pilot studies suggest weight loss through lifestyle modifications as well as insulin sensitizing and antioxidant medications may be of benefit. Moreover, recent advances in the understanding of nonalcoholic fatty liver disease pathogenesis may result in novel therapeutic targets to treat this disease. SUMMARY: Nonalcoholic fatty liver disease is probably the most common form of chronic liver disease in children and may continue to rise with the increasing prevalence of childhood obesity and metabolic syndrome. Recent studies have provided new insights regarding this condition in children. There is still much progress to be made in terms of the description of pediatric nonalcoholic fatty liver disease, its demographics, pathogenesis, and treatment as well as natural history and long-term prognosis.

Adolescent↗
PubMed1999

The FLS mouse: a new inbred strain with spontaneous fatty liver.

BACKGROUND AND PURPOSE: A new strain of mouse, named FLS (fatty liver Shionogi), which develops spontaneous fatty liver without obesity, was established by inbreeding. Morphologic, physiologic, and genetic characterization of the strain was done. METHODS: Characteristics of male FLS mice were compared with those of the sister strain, dd Shionogi (DS), which does not develop spontaneous fatty liver. A genetic cross experiment was performed by mating FLS with C3H/He/Shi mice. RESULTS: The hepatocytes of neonatal FLS mice contained fine lipid droplets throughout the lobules, and large lipid droplets appeared as mice aged. Liver triglyceride concentrations of FLS mice were fivefold higher than those of DS mice, but serum lipid concentrations and the lipoprotein profile did not indicate abnormalities. Higher plasma aspartate transaminase and alanine transaminase activities in FLS, compared with DS mice, suggested hepatocellular lesions. The genetic cross experiment suggested that the fatty liver formation is a complex polygenic trait. CONCLUSION: The FLS mice develop a progressive hepatic steatosis without obesity and diabetes. The FLS mouse might be a good model for investigating hepatic disorders accompanied by fatty liver unrelated to alcoholism or obesity.

Adipose Tissue↗