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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic steatohepatitis (NASH) is the term used for a common form of fatty liver presenting in adults with varied clinical manifestations. The most common presentation is asymptomatic elevation of liver enzymes (AST or SGOT and ALT or SGPT), which can be discovered incidentally in the course of an annual checkup, life insurance examination, or as part of surrogate screening before blood donation. At the other end of the clinical spectrum is the patient with complications from cryptogenic cirrhosis, who also shows a lack of evidence of alcohol as an etiological factor in pathogenesis. Clinical associations of probable relevance include gender (female), obesity, diabetes, and hyperlipidemia, but many patients do not conform to any of these stereotypes (e.g., young men of normal weight with normal fasting glucose and lipid levels). Liver biopsy confirms the diagnosis of NASH, the association of steatosis with an inflammatory response being the sine qua non for the condition and "creeping fibrosis" being a variable but possibly sinister feature. Newer imaging techniques may provide convincing evidence of steatosis, but they give little insight into ongoing fibrosis, and liver biopsy therefore remains the gold standard. The mainstay of treatment remains judicious weight loss coupled with positive dietary advice, including the ingestion of adequate but not excessive vitamins. After initial encouraging data. the assessment of ursodeoxycholic acid currently being studied under randomized controlled conditions is eagerly awaited.
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PMID:Nonalcoholic fatty liver (NASH syndrome). 943 7

We studied the association of fatty liver with subcutaneous and visceral obesity in 46 male and 36 female patients with body mass index (BMI) over 22 kg/m2. The correlation coefficient between the ratio of the visceral adipose tissue to the subcutaneous adipose tissue (V/S) and the computed tomography (CT) number of the liver was -0.299 (P < 0.05) and that between the V/S ratio and the ratio of the CT number of the liver to that of the spleen (CT-L/CT-S) was -0.335 (P < 0.05) in the males. Partial correlation analysis after making correction for BMI showed an increased correlation coefficient of -0.485 (P < 0.05) between the V/S ratio and the CT-L/CT-S ratio in the males. The odds ratio in the males for CT-L/CT-S below 1.0 and V/S above 1.0 was 3.25 with a 95% confidence interval of 1.02 to 9.39. No such association between the V/S ratio and the CT-L/CT-S ratio was present in the female patients. Multiple regression analysis with serum level of alanine aminotransferase, a marker of fatty liver, as an independent variable revealed a partial regression coefficient of -17.7 for CT-L/CT-S (P < 0.05) in the males and -21.7 (P < 0.05) in the females, validating the CT-L/CT-S ratio as an index of fatty liver. The results indicate the association of fatty liver as determined by the CT-L/CT-S ratio with visceral obesity in males.
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PMID:Association of fatty liver with increased ratio of visceral to subcutaneous adipose tissue in obese men. 978 Dec 73

The detection and correction of dietary errors plays an important role in avian medicine. Examples of diseases caused in part by a deficiency or abundance of a nutrient include hypovitaminosis A in birds of the parrot (Psittacidae) family, hypocalcemia in the African grey parrot, goitre in budgerigars, and iron storage diseases in the minah and toucan. Hypovitaminosis A can lead to metaplasia of mucous membranes, which in turn can lead to chronic rhinitis and respiratory fungal infections. Vitamin A deficiency is caused by feeding a seed based diet. Seed mixtures are often deficient in calcium, and nutritional secondary hyperparathyroidism can develop if an additional source of calcium, in the form of ground shells, is not provided. Tetanic symptoms as a result of hypocalcemia are only seen in the African grey parrot and the timneh parrot. Over supplementation of vitamin D gives rise to poisoning with polyuria and polydipsia as common initial symptoms. The exact cause of iron storage diseases in toucans and minahs is not known. A diet low in iron and vitamin C is advised as therapy. Goitre can develop in budgerigars as a result of iodine-deficient drinking water and provision of a seed mixture based on millet. An unbalanced or multideficient diet can give rise to reproductive disorders, abnormal feathers, or infections as a result of diminished resistance. It is usually not possible to relate the cause of these diseases in a simple way to the composition of the diet. Obesity, which occurs in the galah, Amazon parrot, and budgerigars, can lead to fatty liver and lipoma. A gradual reduction in weight, by means of calorie restriction, is recommended. Commercially available nutritionally balanced bird food is often effective.
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PMID:[Nutrition-related problems in pet birds]. 992 97

Fatty liver is common in nonalcoholic, obese individuals and in lean people who consume alcohol chronically. Although fatty liver is typically benign, a subset of individuals with steatosis develop steatohepatitis and eventually cirrhosis. The disparate outcomes of fatty liver suggest that it reflects a generally beneficial, adaptive response to obesity or alcohol-related stress, but may also increase hepatocyte vulnerability to other challenges. Thus, both protective factors (e.g., Bcl-2 and Bcl-xL) and factors that promote hepatocyte death by apoptosis (e.g., Bax) or necrosis (e.g., UCP2) may be increased in fatty livers. To evaluate this possibility, hepatocyte apoptosis, necrosis, and the expression of factors that regulate cellular viability were assessed in two models of fatty liver (i.e., genetically obese [ob/ob] mice and ethanol [EtOH]-fed lean mice). Findings in mice with fatty livers were compared with lean, control mice that did not have hepatic steatosis. Immunohistochemistry showed striking induction of hepatocyte proteins that promote (e.g., Bax) and inhibit (e.g., Bcl-2 and Bcl-xL) apoptosis in both groups with fatty liver. Both models of fatty liver also increased hepatic transcripts for UCP2, a mitochondrial uncoupling protein, and the protein itself was induced in ob/ob hepatocytes. Despite the up-regulation of factors that threaten cell viability, hepatocyte death was not increased in either ob/ob or EtOH-fed mice, confirming that the liver's protective responses were sufficient under the conditions studied. However, if UCP2 induction reduces the efficiency of adenosine triphosphate (ATP) synthesis, this initially harmless response might enhance the vulnerability of hepatocytes to necrosis.
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PMID:Mitochondrial proteins that regulate apoptosis and necrosis are induced in mouse fatty liver. 1009 57

Nonalcoholic steatohepatitis (NASH) is an hepatic disorder with histologic features of alcohol-induced liver disease that occurs in individuals who do not consume significant alcohol. NASH is believed to be one of the most common explanations for abnormal liver chemistries in American adults. Risk factors for NASH include obesity, type II diabetes, hyperlipidemia, total parenteral nutrition, jejuno-ileal bypass surgery, and the use of certain drugs. However, some patients with NASH have no identifiable risk factors for the disease. Clinically, NASH is a diagnosis of exclusion that should be suspected as a cause of chronic hepatitis in patients who deny significant alcohol consumption and have negative serologic tests for congenital and other acquired causes of liver disease. The identification of fatty liver on imaging studies supports the diagnosis of NASH, which can be established definitively by liver biopsy. The latter also provides useful prognostic information since most patients with simple steatosis follow an indolent clinical course, whereas those with steatohepatitis, fibrosis, or cirrhosis are more likely to develop clinically significant complications of liver disease. Weight reduction and treatment of confounding medical conditions are the mainstays of therapy for NASH. However, there is little evidence that any of the current treatments prevent progression to more histologically advanced stages of NASH. Several experimental therapies, including treatment with bile acids, antibiotics, nutritional supplements, and antioxidants, have had anecdotal success in selected patients, but improved understanding of the pathogenesis and natural history of NASH will be required to develop generally effective therapy for the disorder.
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PMID:Nonalcoholic steatohepatitis. 1042 2

Fatty liver (FL) is a frequently diagnosed liver disease. There are presented the etiological factors causing FL, including the most frequent alcohol, obesity, diabetes mellitus, hyperlipoproteinemias and drugs. There are discussed some disturbances of lipid metabolism leading to FL. Morphologically we can distinguish FL with large or small fatty droplets. The more severe kind of the disease is FL with hepatitis (steatohepatitis). Symptoms of FL are not characteristic, as well as there are absent typical changes in biochemical analyzes. There are presented methods of the liver visualization (USG, CT) used in the diagnostics of FL. Treatment of FL includes of the elimination of etiological factors first of all, there is still under debate the supportive action of pharmacotherapy in FL.
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PMID:[Disturbances of lipid metabolism and fatty liver]. 1044 10

The association of several risk factors, obesity, dyslipoproteinemia, hepatic steatosis, insulin resistance and hypertension with Type 2 (non-insulin-dependent) diabetes mellitus and myocardial infarction has long been known and has been termed the "metabolic syndrome". In 1988 Reaven introduced syndrome X as the link between insulin resistance and hypertension. It has been suggested that a critical factor in the association between obesity, Type 2 diabetes and cardiovascular morbidity is the mass of intraabdominal fat. Striking similarities exist between the metabolic syndrome and untreated growth hormone (GH) deficiency in adults. The central findings in both these syndromes are abdominal/visceral obesity and insulin resistance. Other features common to both conditions are premature atherosclerosis and increased mortality from cardiovascular diseases. These similarities indicate that undetectable and low levels of GH may be of importance in the metabolic aberrations observed in both these conditions. Recent investigations have found that abdominal/visceral distribution of adipose tissue is associated with endocrine disturbances including increased activity of the hypothalamic-pituitary-adrenal axis and a blunted secretion of GH and sex steroids. Theoretically, these endocrine perturbations can be a consequence of obesity, but the endocrine aberrations may have causal effects. We studied moderately obese, middle-aged men with a preponderance of abdominal body fat. As a group, they had slight to moderate metabolic changes known to be associated with abdominal/visceral obesity. Nine months of GH treatment reduced their total body fat and resulted in a specific and a marked decrease in both abdominal subcutaneous and visceral adipose tissue. Moreover, insulin sensitivity improved and serum concentrations of total cholesterol and triglyceride decreased. Diastolic blood pressure also decreased. The finding that GH replacement in men with abdominal obesity can diminish the negative metabolic consequences of visceral obesity suggests that low levels of this hormone are of importance for the metabolic aberrations associated with visceral/abdominal obesity.
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PMID:Growth hormone and the metabolic syndrome. 1044 70

Hepatic resection or transplantation in patients with fatty liver is associated with increased morbidity and mortality. The regenerative capacity of fatty livers after major tissue loss is unknown. Interleukin 6 (IL-6) is a potent inducer of hepatic regeneration in normal and ischemic livers. Therefore, we studied hepatic regeneration at day 1, day 2, and day 4 in a model of 70% hepatectomy in obese and lean Zucker rats, and obese Zucker rats pretreated with recombinant interleukin 6 (rIL-6). The mitotic cycle in hepatocytes was investigated by 4 different markers of regeneration representing distinct phases of mitosis (proliferating cell nuclear antigen [PCNA] = G(1) phase, bromodeoxy uridine [BrdU] = S phase, mitotic index, and regenerated liver weight = M phase). Obese Zucker rats had significantly decreased regenerative capacity compared with lean Zucker rats (PCNA, BrdU, mitotic index, regenerated liver weight) at days 1 and 2 after surgery. Four days after resection fatty animals showed an increase in the mitotic index indicating a delay of regeneration in steatotic livers. Animal survival after 70% hepatectomy was significantly decreased in obese rats compared with lean animals. Pretreatment of obese animals with rIL-6 normalized PCNA expression (G(1) phase) in steatotic hepatocytes but failed to increase DNA synthesis (BrdU, S phase), mitosis (mitotic index and regenerated liver weight, M phase), and animal survival. These results indicate major impairment of hepatic regeneration in steatotic livers. Two different blockages of regeneration must be present, one rIL-6 sensitive, at the level of IL-6 or upstream, and a second, rIL-6 resistant, at the level of G(1)/S-phase transition.
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PMID:Failure of regeneration of the steatotic rat liver: disruption at two different levels in the regeneration pathway. 1061 25

In lipoatrophic diabetes, a lack of fat is associated with insulin resistance and hyperglycemia. This is in striking contrast to the usual association of diabetes with obesity. To understand the underlying mechanisms, we transplanted adipose tissue into A-ZIP/F-1 mice, which have a severe form of lipoatrophic diabetes. Transplantation of wild-type fat reversed the hyperglycemia, dramatically lowered insulin levels, and improved muscle insulin sensitivity, demonstrating that the diabetes in A-ZIP/F-1 mice is caused by the lack of adipose tissue. All aspects of the A-ZIP/F-1 phenotype including hyperphagia, hepatic steatosis, and somatomegaly were either partially or completely reversed. However, the improvement in triglyceride and FFA levels was modest. Donor fat taken from parametrial and subcutaneous sites was equally effective in reversing the phenotype. The beneficial effects of transplantation were dose dependent and required near-physiological amounts of transplanted fat. Transplantation of genetically modified fat into A-ZIP/F-1 mice is a new and powerful technique for studying adipose physiology and the metabolic and endocrine communication between adipose tissue and the rest of the body.
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PMID:Surgical implantation of adipose tissue reverses diabetes in lipoatrophic mice. 1067 52

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.
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PMID:Altered hepatic lymphocyte subpopulations in obesity-related murine fatty livers: potential mechanism for sensitization to liver damage. 1070 53


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