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PubMed1993

A rat fatty liver transplant model.

A rat model of fatty liver transplantation has been developed to study primary nonfunction in fatty liver grafts. ACI rats were fed with a diet deficient in choline and methionine for 7, 14, 28, and 42 days. Fat content in the pretransplant livers was examined by gas chromatography and histology. The main constituent of the fatty droplets was determined to be triglyceride. The triglyceride concentration reached a maximum by day 14 and remained constant for an additional 28 days. Histology revealed an absence of necrosis in 14- and 28-day fatty livers but scattered hepatocytic necrosis and inflammation in 42-day fatty livers. After being given cold (UW stored, 4 degrees C) or warm (37 degrees C) ischemia, the fatty liver was orthotopically transplanted into normal ACI rats. The one-week survival of fatty liver grafts after 6, 12, 18, and 24 hr cold preservation was 5/5, 5/6, 3/8, 0/6 for 14-day fatty liver and 5/5, 4/6, 0/8, 0/6 for 42-day fatty livers. The survival of normal liver grafts was 5/5, 6/6, 5/9, 2/8, respectively. Increased survival rate was correlated with the absence of hepatocytic necrosis. The survival after 15 and 30 min warm ischemia prior to transplant was 5/5, 2/6 for normal liver grafts and 4/7, 0/6 for 28-day fatty liver graft, respectively. Fatty livers were less resistant to damage induced by cold or warm ischemia.

Animals↗
PubMed2003

Fatty liver in type 2 diabetes mellitus: relation to regional adiposity, fatty acids, and insulin resistance.

The current study was undertaken to examine metabolic and body composition correlates of fatty liver in type 2 diabetes mellitus (DM). Eighty-three men and women with type 2 DM [mean body mass index (BMI): 34 +/- 0.5 kg/m2] and without clinical or laboratory evidence of liver dysfunction had body composition assessments of fat mass (FM), visceral adipose tissue (VAT), liver and spleen computed tomography (CT) attenuation (ratio of liver to spleen), muscle CT attenuation, and thigh adiposity; these assessments were also performed in 12 lean and 15 obese nondiabetic volunteers. Insulin sensitivity was measured with a euglycemic insulin infusion (40 mU. m-2. min-1) combined with systemic indirect calorimetry to assess glucose and lipid oxidation, and with infusions of [2H2]glucose for assessment of endogenous glucose production. A majority of those with type 2 DM (63%) met CT criteria for fatty liver, compared with 20% of obese and none of the lean nondiabetic volunteers. Fatty liver was most strongly correlated with VAT (r = -0.57, P < 0.0001) and less strongly but significantly associated with BMI (r = -0.42, P < 0.001) and FM (r = -0.37, P < 0.001), but only weakly associated with subcutaneous adiposity (r = -0.29; P < 0.01). Fatty liver was also correlated with subfascial adiposity of skeletal muscle (r = -0.44; P < 0.01). Volunteers with type 2 DM and fatty liver were substantially more insulin resistant those with type 2 DM but without fatty liver (P < 0.001) and had higher levels of plasma free fatty acids (P < 0.01) and more severe dyslipidemia (P < 0.01), a pattern observed in both genders. Plasma levels of cytokines were increased in relation to fatty liver (r = -0.34; P < 0.01). In summary, fatty liver is relatively common in overweight and obese volunteers with type 2 DM and is an aspect of body composition related to severity of insulin resistance, dyslipidemia, and inflammatory markers.

Adipose Tissue↗
PubMed1991

A non-fatal case report of acute fatty liver of pregnancy.

Acute fatty liver of pregnancy (AFLP) is a potentially fatal disorder that typically complicates the third trimester of pregnancy. Unrecognised, acute fatty liver of pregnancy may rapidly progress to fulminant hepatic failure, disseminated intravascular coagulation, acute renal failure and death. The outcome is highly favourable, with complete hepatic recovery, if the diagnosis is made early and pregnancy terminated promptly. The diagnostic criteria of AFLP are met if third trimester jaundice is associated with hyperuricaemia, the presence of nucleated red blood cells in the peripheral blood film and hepatic attenuation values consistent with fatty infiltration by at least one imaging technique. We report here a 38 year old Chinese woman with acute fatty liver of pregnancy, a non-fatal case complicated by extrahepatic manifestations of disseminated intravascular coagulation, haemorrhage and renal dysfunction.

Acute Disease↗
PubMed1988

Hepatic triacylglycerol synthesis during a period of fatty liver development in sheep.

Fatty liver was induced in six sheep by fasting and treatment with phloridzin and epinephrine. Treatment was associated with a rise in the concentration in serum and hepatic uptake of nonesterified fatty acid (NEFA) compared with pretreatment (P less than .01). At 24 h after the start of the treatment, concentrations of serum lipoprotein in each density class were not different from baseline, but all were elevated (P less than .01) by 120 h of treatment. Hepatic triacylglycerol (TG) concentration increased (P less than .01) 17-fold within the first 48 h of treatment, with no additional increase during the remaining 72 h. The activity of phosphatidate phosphohydrolase (PAP) in hepatic microsomes increased (P less than .01) fourfold over baseline by 48 h of treatment, then declined slightly by 120 h. The activities of diacylglycerol acyltransferase (DGAT) and glycerolphosphate acyltransferase (GPAT) in hepatic microsomes increased during treatment but appeared to follow a slightly different pattern from that of PAP. Activity of GPAT was not above baseline at 48 h, but was at 120 h (P less than .05); DGAT activity was increased (P less than .05) twofold at 48 h, with an apparent continued increase (P less than .01) to threefold over baseline by 120 h of treatment. Fatty liver appeared to develop during a period of rapid hepatic uptake of NEFA without a corresponding increase in serum lipoprotein concentrations. The activities of PAP, GPAT and DGAT, putative regulators of TG synthesis rate, all increased in liver microsomes during a period of high hepatic NEFA uptake, but that of PAP appeared to coincide most closely with the development of fatty liver.

Animals↗
PubMed2006

Relations between carotid artery wall thickness and liver histology in subjects with nonalcoholic fatty liver disease.

OBJECTIVE: Nonalcoholic fatty liver disease (NAFLD) is closely associated with several metabolic syndrome features. We assessed whether NAFLD is associated with carotid artery intima-media thickness (IMT) as a marker of subclinical atherosclerosis and whether such an association is independent of classical risk factors, insulin resistance, and metabolic syndrome features. RESEARCH DESIGN AND METHODS: We compared carotid IMT, as assessed by ultrasonography, in 85 consecutive patients with biopsy-proven NAFLD and 160 age-, sex-, and BMI-matched healthy control subjects. RESULTS: NAFLD patients had a markedly greater carotid IMT (1.14 +/- 0.20 vs. 0.82 +/- 0.12 mm; P < 0.001) than control subjects. The metabolic syndrome (according to Adult Treatment Panel III criteria) and its individual components were more frequent in those with NAFLD (P < 0.001). The marked differences in carotid IMT observed between the groups were only slightly weakened after adjustment for age, sex, BMI, smoking history, LDL cholesterol, insulin resistance (by homeostasis model assessment), and metabolic syndrome components. Notably, carotid IMT was strongly associated with degree of hepatic steatosis, necroinflammation, and fibrosis among NAFLD patients (P < 0.001 for all). Similarly, by logistic regression analysis, the severity of histological features of NAFLD independently predicted carotid IMT (P < 0.001) after adjustment for all potential confounders. CONCLUSIONS: These results suggest that the severity of liver histopathology among NAFLD patients is strongly associated with early carotid atherosclerosis, independent of classical risk factors, insulin resistance, and the presence of metabolic syndrome.

Adult↗
PubMed1991

Biochemical and immunohistochemical analysis of orotic acid-induced fatty liver.

Orotic acid-induced fatty livers were examined by biochemical and immunohistochemical approaches. Lipid peroxide levels by the thiobarbituric acid method and glutathione-peroxidase (GSH-PO) activity in the liver homogenates from orotic administered rats were similar to those of controls. Immunohistochemical localization of GSH-PO in orotic acid-induced fatty liver was mainly observed in the portal zone of the hepatic lobules. This staining pattern of GSH-PO was similar to that of the controls. No remarkable changes in GSH-PO staining patterns were detected in orotic acid-induced fatty liver. Our data strongly suggested that no lipid peroxidation is actively involved in the genesis of fatty liver due to the administration of orotic acid, and GSH-PO a protective enzyme against lipid peroxidation, was not inhibited by orotic acid-induced fatty liver.

Animals↗
PubMed2004

Recent advances in alcoholic liver disease II. Minireview: molecular mechanisms of alcoholic fatty liver.

Alcohol has long been thought to cause fatty liver by way of altered NADH/NAD(+) redox potential in the liver, which, in turn, inhibits fatty acid oxidation and the activity of tricarboxylic acid cycle reactions. More recent studies indicate that additional effects of ethanol both impair fat oxidation and stimulate lipogenesis. Ethanol interferes with DNA binding and transcription-activating properties of peroxisome proliferator-activated receptor-alpha (PPARalpha), as demonstrated with cultured cells and in ethanol-fed mice. Treatment of ethanol-fed mice with a PPARalpha agonist can reverse fatty liver even in the face of continued ethanol consumption. Ethanol also activated sterol regulatory element binding protein 1, inducing a battery of lipogenic enzymes. These effects may be due in part to inhibition of AMP-dependent protein kinase, reduction in plasma adiponectin, or increased levels of TNF-alpha in the liver. The understanding of these ethanol effects provides new therapeutic targets to reverse alcoholic fatty liver.

AMP-Activated Protein Kinases↗
PubMed2006

Diagnostic evaluation of nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is a diagnostic consideration among patients with asymptomatic elevated aminotransaminases, patients with radiologic findings of hepatic fatty infiltration, or occasionally in the patient with "cryptogenic" cirrhosis. The diagnosis of NAFLD requires evidence of fatty infiltration of the liver in the absence of excessive alcohol ingestion. Clinical evaluation should examine for metabolic risk factors (central obesity, glucose intolerance, hypertension, hypertriglyceridemia, and low HDL cholesterol), which are suggestive but not specific for the diagnosis of NAFLD. Secondary causes of NAFLD, such as medications and intestinal bypass surgery, should be excluded as management of these conditions may differ. Confirmation of hepatic steatosis can usually be done by imaging studies, although occasionally liver biopsy is required. Among suspected NAFLD patients with chronically elevated aminotransaminases, clinical evaluation and serological testing should be performed to exclude other causes of chronic liver disease. Liver biopsy is required to stage fibrosis and distinguish between nonalcoholic steatohepatitis and steatosis. This is valuable for providing prognosis, excluding other liver disease, monitoring response to therapy or evaluating disease progression over time. Clinical features, particularly diabetes, obesity, and older age, can aid in stratifying patients at risk for advanced fibrosis but are not sufficiently accurate to replace liver biopsy.

Biopsy↗
PubMed1998

Fatty acid binding to rat liver fatty acid-binding protein is modulated by early glycolytic intermediates.

Fatty acid binding to rat liver fatty acid binding protein in the presence of glycolytic metabolites and at different pH (optimal 7.2) and ionic strength was studied. Binding decreased logarithmically with ionic strength. Glucose and glucose-6-phosphate increased fatty acid binding significantly with K0.5 within physiological ranges while glucose-1-phosphate and phosphate ion caused no effect.

Animals↗
PubMed2006

Review article: Drug therapy for non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease represents a spectrum of liver diseases, characterized mainly by macrovesicular steatosis in the absence of significant alcohol ingestion. Non-alcoholic fatty liver disease includes both non-alcoholic fatty liver and non-alcoholic steatohepatitis. Non-alcoholic steatohepatitis once considered a benign process is now known to lead to progressive fibrosis and cirrhosis. Histologically indistinguishable from alcoholic liver disease, the exact aetiology of non-alcoholic fatty liver disease remains unknown, but the fundamental pathophysiological process appears to be insulin resistance and oxidative stress related to the metabolic syndrome. Therapy has focused on risk factors, weight reduction and pharmacological intervention. Promising pharmacological treatments have been demonstrated with antioxidants, insulin sensitizers, hepatoprotectants and lipid-lowering agents. However, without larger randomized studies, no pharmacological treatments can be recommended at this time.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

[A clinical and pathological study of nonalcoholic fatty liver disease].

OBJECTIVE: To study the pathological and clinical features of nonalcoholic fatty liver disease (NAFLD). METHODS: Grades and stages of liver lesions in 41 patients with NAFLD were analyzed. The relationships between pathohistological features of the livers, serum biochemical parameters, ultrasound examination and other clinical data of the patients were studied. RESULTS: Among the 41 patients with NAFLD (there were 21 with their liver fatty degeneration in grade 1, 15 in grade 2, and 5 in grade 3). There were 2 of grade 0, grade 1 had 25, grade 2 had 10, grade 3 had 3, and grade 4 had 1. Stage 0 of fibrosis was 20, stage 1 was 14, stage 2 was 4, stage 3 was 2, and stage 4 was 1. Degree of fatty degeneration was not positively associated with the body mass index (BMI) of the patients and the ultrasound findings in their livers. Grading of the inflammation was positively related to the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in the blood and ultrasound findings in their livers, but negatively to the platelet counts. Staging of fibrosis of the livers was positively related to the blood ALT, AST, GGT, and ALP, and negatively to triglyceride levels and platelet counts. CONCLUSIONS: Degree of liver fatty degeneration was not associated with grades of inflammation and staging of fibrosis of the liver. BMI, ALT and AST level, platelet counts, and ultrasound grades of fatty liver were associated with the liver histopathological changes of NAFLD patients. Liver biopsy is the essential way to make a diagnosis of NAFLD.

Adolescent↗
PubMed1958

Kwashiorkor type of fatty liver in primates.

Fatty livers resembling those seen in the early stages of kwashiorkor have been produced in primates. Monkeys were fed, for about 1 year, purified diets free from choline and betaine and low in methionine. Supplementation with choline slightly improved food consumption and gain in weight. Choline prevented the appearance of any stainable lipide in the liver of the control animals. The extent to which the slightly greater intake of protein, including methionine, in the choline-supplemented animals contributed to the prevention of the periportal accumulation of fat in the liver is being determined.

Animals↗
PubMed1986

Palmitic acid oxidation and incorporation into triglyceride by needle liver biopsy specimens from control subjects and patients with alcoholic fatty liver disease.

A micro-technique was developed to measure fatty acid oxidation in vitro and to investigate its possible derangement in alcoholic fatty liver disease. Percutaneous liver biopsy specimens were obtained from nine control subjects and 28 alcoholic patients with mild to severe fatty liver. Fresh tissue (10-15 mg) was incubated at 37 degrees C for 90 min in a sealed reaction flask containing 1.92 mmol/l [1-14C]palmitic acid (1-2 microCi) and 1% essentially fatty acid free albumin in Krebs-Henseleit buffer, pH 7.4. Radiolabelled CO2 and perchloric acid-soluble ketone bodies were isolated and counted. CO2 production was markedly reduced in alcoholic patients with mild and severe fatty liver compared with controls. This depression was reversed by the addition of malate to the reaction flask but not by carnitine or coenzyme A. Ketone body production was similar in controls and patients with mild and severe fatty liver. After the incubation in vitro, the tissue was extracted with chloroform/methanol and the triglyceride fraction isolated by thin layer chromatography and counted for radioactivity. The rate of palmitic acid incorporation into triglyceride was higher in alcoholic patients, particularly those with severe fatty infiltration, compared with controls. It is suggested that alcoholic fatty liver is accompanied by a progressive reduction in palmitic acid oxidation with the major defect occurring in the tricarboxylic acid cycle. In contrast, the rate of palmitic acid esterification into triglyceride is enhanced.

Adult↗
PubMedDate not supplied

Nonalcoholic fatty liver disease.

The definition of nonalcoholic fatty liver disease has evolved in recent years. Today, it is considered a nonspecific term encompassing several clinicopathologic entities (steatosis alone, steatonecrosis, steatohepatitis and histologic alcoholic-like hepatitis) that are similar to alcoholic liver disease. Studies of nonalcoholic fatty liver disease have come to conflicting conclusions about the course of the disease. It can be argued that the disparate results are largely the result of nonuniform definitions. When histologic features such as hepatocyte ballooning, necrosis, and Mallory hyaline are seen, nonalcoholic fatty liver disease has been shown to be associated with an aggressive outcome. Steatosis alone, in contrast, appears to be benign. The current understanding of nonalcoholic fatty liver disease, the limited treatments available, and two theories of the pathogenesis of the disease are also reviewed here.

Diagnosis, Differential↗
PubMed2001

Fatty liver and nonalcoholic steatohepatitis.

Fatty liver is a relatively common incidental finding on imaging studies. Although generally a benign condition, fat in the liver can be troubling for clinicians because it can cause persistently elevated liver enzyme levels. The finding of fatty liver may also indicate the presence of nonalcoholic steatohepatitis (NASH). NASH is a histologic diagnosis applied to a constellation of liver biopsy findings that appear similar to alcoholic liver disease but are found in the absence of alcohol abuse. NASH is typically identified during the evaluation of elevated aminotransferase levels after exclusion of viral, metabolic, and other causes of liver disease. Obesity is a major risk factor; the role of diabetes is less certain, although evidence is accumulating that hyperinsulinism may play an important pathophysiologic role. About 15% to 40% of NASH patients develop hepatic fibrosis, a precursor to cirrhosis. Exactly how many patients with NASH progress to cirrhosis is unknown, but 1% to 2% of liver transplants are now performed because of a pretransplant diagnosis of NASH. Specific and effective treatments are needed but until the pathogenesis of this common liver disease is better understood, weight loss will remain the mainstay of treatment for obese patients.

Diabetes Complications↗
PubMed2000

Altered hepatic lymphocyte subpopulations in obesity-related murine fatty livers: potential mechanism for sensitization to liver damage.

Although obesity-related fatty livers are vulnerable to damage from endotoxin, the mechanisms involved remain obscure. The purpose of this study was to determine if immunologic priming might be involved by determining if fatty livers resemble normal livers that have been sensitized to endotoxin damage by Propionibacterium acnes infection. The latter induces interleukin (IL)-12 and -18, causing a selective reduction of CD4+NK T cells, diminished IL-4 production, deficient production of T-helper type 2 (Th-2) cytokines (e.g., IL-10), and excessive production of Th-1 cytokines (e.g., interferon gamma [IFN-gamma]). Liver and spleen lymphocyte populations and hepatic cytokine production were compared in genetically obese, ob/ob mice (a model for obesity-related fatty liver) and lean mice. Obese mice have a selective reduction of hepatic CD4+NK T cells. Serum IL-18 is also increased basally, and the hepatic mRNA levels of IL-18 and -12 are greater after endotoxin challenge. Thus, up-regulation of IL-18 and IL-12 in fatty livers may reduce hepatic CD4+NK T cells. In addition, mononuclear cells from fatty livers have decreased expression of the adhesion molecule, leukocyte factor antigen-1 (LFA-1), which is necessary for the hepatic accumulation of CD4+NK T cells. Consistent with reduced numbers of hepatic CD4+NK T cells, mononuclear cells from fatty livers produce less IL-4. Furthermore, after endotoxin treatment, hepatic induction of IL-10 is inhibited, while that of IFN-gamma is enhanced. Thus, fatty livers have inherent immunologic alterations that may predispose them to damage from endotoxin and other insults that induce a proinflammatory cytokine response.

Animals↗