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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-arteriosclerotic, virgin and arteriosclerotic, breeder rats were treated with aniline to suppress adrenal steroidogenic capacity and responsiveness to the stress of acute myocardial infarction. After two weeks of aniline treatment, some of the non-arteriosclerotic and arteriosclerotic animals were given two injections of isoproterenol, spaced 24 h apart, to induce massive myocardial infraction. On the 3 rd day, when myocardial necrosis reaches its zenith, the animals were sacrificed. Aniline-induced adrenal insufficiency caused increased mortality, absence of congestive heart failure, cardiac and adrenal enlargement but no evidence of the characteristic intense catabolism and increased corticoid production which attends acute myocardial infarction. Serum enzymes, e.g., SGOT, SGPT and LDH, triglycerides, but not glucose, free fatty acids and cholesterol, became acutely elevated in animals treated with aniline and isoproterenol. Animals developed a fatty liver, beta cell degranulation, post hypophy-sectomy-like changes in their adrenal cortices, unusually severe infarction, marked distention of intermuscular spaces, frequent foci of dystrophic calcification and cartilaginous metaplasia of the papillary muscles. It is believed that aniline-induced adrenal suppression altered the usual pathophysiologic response to acute myocardial infarction.
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PMID:Adrenocortical suppression and myocardial infarction in non-arteriosclerotic (virgin) and arteriosclerotic (breeder) rats. 126 59

The fatty liver often found in untreated kwashiorkor has been associated with highly variable concentration of circulating lipids. The effect on lipid metabolism of two isocaloric diets--one synthetic monomolecular (Vivonex) and one standard (Casilan)--which both initiated satisfactory clinical improvement was studied in 21 Ethiopian children with kwashiorkor during the first weeks of rehabilitation. Before treatment mean fasting values of all biochemical parameters were within normal ranges except for moderately elevated triglycerides--an unexpected finding-and low insulin. Individual values varied greatly; triglyceride between 0.39 and 3.49 mmol/1. FFA correlated both to glycerol, D-beta-hydroxybutyrate and triglyceride values. During treatment insulin, glucose and glycerol remained essentially unchanged and were similar in both dietary groups. In the Vivonex group only there was an initial marked, parallel fall of FFA and D-beta-hydroxybutyrate suggesting greater availability of carbohydrate and enhanced glucose utilization. This pattern of response seemed to occur without comparable inhibition of lipolysis. Triglycerides--like serum albumin--increased faster in the Casilan group. The highest mean triglyceride value was reached by day 8 in the Casilan group and by day 15 in the Vivonex group. Ten minutes following heparin injection triglycerides declined, FFA and glycerol increased indicating release of in vivo active lipase. LPL activity assayed in vitro was similar and unaffected by 2 weeks of dietary treatment in both groups. LPL activity was inversely correlated to triglycerides providing--beside the type of diet--another possible explanation for the wide variations seen in circulatory triglycerides.
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PMID:Dietary effects in the early recovery phase of kwashiorkor. Plasma levels of triglycerides, FFA, D-beta-hydroxybutyrate, glycerol, postheparin lipoprotein lipase (LPL), glucose and insulin. 127 67

A community health survey of 923 residents aged 30 years or more was performed in Putai Township of Taiwan. To elucidate the relationships between hepatitis C virus (HCV) and surrogate tests for non-A, non-B hepatitis in hyperendemic areas of hepatitis B virus (HBV) serum levels of alanine aminotransferase (ALT), triglycerides, cholesterol, hepatitis B surface antigen (HBsAg) and antibody to HCV (anti-HCV) were examined. Glucose tolerance tests and the history of diabetes treatment were used to define the diabetes status. Fatty liver was diagnosed by sonography. The prevalence of anti-HCV was 2.6% (95% confidence interval, 1.6-3.6%). Elevated ALT and fatty liver were significantly associated with anti-HCV in univariate analysis. Anti-HCV was not an associated factor for fatty liver after adjusting for serum triglycerides and cholesterol, sex, body mass index and diabetes status through multiple logistic regression. However elevated ALT was still associated with anti-HCV after adjusting for serum triglycerides, sex, body mass index, HBsAg and age through multiple linear regression. The anti-HCV prevalence was similar between HBsAg-positive and negative subjects. Aggregation of HCV infection was found among spouses. It was concluded that elevated ALT and intimate contact with HCV carriers might be associated factors for HCV infection, and that HBV infection and fatty liver were not related to HCV infection in Taiwan.
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PMID:Relationship between fatty liver, alanine aminotransferase, HBsAg and hepatitis C virus. 138 55

A fatal case of acute fatty liver of pregnancy (AFLP) is reported. After admission, the patient was delivered within 3 hours. Routine laboratory investigation revealed acute liver insufficiency with advanced coagulopathy. Despite substitution therapy, the severe coagulation defect progressed to lethal intracerebral bleeding. Advanced AFLP can only be satisfactorily diagnosed in time, if non-specific symptoms or icterus lead to studies of blood chemistry, especially liver function tests, coagulation parameters (including platelet count, fibrinogen, AT III), blood glucose and renal function (including uric acid). This will enable an adequate management of the patient. The clinical problem of AFLP still remains that of early diagnosis.
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PMID:[Fatal course of peracute fatty liver of pregnancy]. 139 61

Fatty liver was often found concomitantly by the ultrasound during the follow up study of the gastric cancer operation. By ultrasound, development of postgastrectomy fatty liver was seen in 29 out of 176 patients (16.5%) with several gastrectomies. The number of the patients with postgastrectomy fatty liver was 12 out of 104 patients (11.5%) with distal partial gastrectomy with B-I reconstruction, while that was 17 of 72 patients (23.6%) with total gastrectomy with several reconstructions. The incidence of postoperative fatty liver change was significantly higher in the patients under 59 years old compared to the elders. Seventy-five g oral glucose test induced oxyhyperglycemia and hyperinsulinemia in patients with gastrectomy, especially with total gastrectomy. Integrated plasma insulin and triglyceride responses during first one hour in postgastrectomy patients were significantly higher than preoperative values. Moreover, plasma insulin and blood sugar in response to oral glucose test were significantly higher in patients with postgastrectomy fatty liver, compared to those in patients without fatty liver. These results suggested that the postgastrectomy fatty liver was resulted from the abnormality of the glucose metabolism.
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PMID:[Study of postgastrectomy fatty liver]. 144 45

To elucidate whether the presence of fatty liver influences ketogenesis in obesity, the metabolic and hormonal changes in basal and low-dose epinephrine (EPI)-stimulated states were studied in 12 obese patients (OB) with normal glucose tolerance, consisting of 6 without fatty liver (OBN) and 6 with fatty liver (OBF). In the basal state, the total ketone body (TKB) concentration and the TKB to free fatty acid (FFA) ratio were significantly (p < 0.01) lower in the OBF than in the OBN group, despite elevated, but comparable, FFA levels in both groups. The basal FFA level and the TKB/FFA ratio correlated with the degree of fatty liver (p < 0.05-0.01). EPI infusion resulted in accelerated lipolysis and diminished FFA-induced ketogenesis, similar to the findings of the basal data. These results suggest that fatty liver per se is related to diminished FFA-induced ketogenesis, leading to resistance to ketosis in obesity.
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PMID:Resistance to ketosis in moderately obese patients: influence of fatty liver. 147 71

Depression in feed intake during the final week before calving was hypothesized to be a major factor in the etiology of fatty liver development near parturition. Eleven cows were allowed to eat for ad libitum intake prior to calving (control), and 11 cows were maintained at the same level of DMI recorded during d 21 to 17 prior to calving by force feeding the feed refusals via rumen cannulas. Feed intake by control cows decreased 28% during the final 17 d prior to calving. Lipid triglyceride increased 227 and 75% for control and force-fed cows between d 17 prior to parturition and d 1 following calving. Dry matter intake prior to calving was correlated negatively with liver triglyceride immediately after calving (r = -.80). Plasma glucose concentrations for control and force-fed cows were 63 and 76 mg/dl 2 d prior to calving and also were related closely to liver triglyceride immediately after calving (r = -.50). By d 28 after calving, there were no differences in liver triglyceride between treatments. Cows that were force-fed prior to calving tended to yield milk with greater fat percentage (4.22 vs. 3.88%) and to yield more 3.5% FCM (46.1 vs. 41.7 kg/d) during the first 28 d postpartum.
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PMID:Effect of prepartum dry matter intake on liver triglyceride concentration and early lactation. 150 May 87

Diseases of intermediary metabolism include ketosis and fatty liver of dairy cattle and pregnancy toxemia of ewes. These conditions occur when there is a failure of the homeostatic mechanisms regulating the mobilization of fats and the conservation of carbohydrates. The therapeutic approach is to reestablish the normal homeostatic patterns of fuel utilization. Suppression of excessive ketogenesis is the most important factor in reestablishing homeostasis. Ketogenesis can be suppressed by a number of therapeutic agents that act either by suppressing the mobilization of fatty acids or by inhibiting the transport of fatty acids into the hepatic mitochondria, the site at which fatty acids are converted to ketone bodies. Useful therapies include bolus glucose infusions, glucose precursors, and glucocorticoids.
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PMID:Therapy of diseases of ruminant intermediary metabolism. 155 19

A case of clinically diagnosed acute fatty liver of pregnancy (AFLP) is reported. Hypoglycemia and coagulopathy were predominant in the clinical course. Serial studies on blood chemistry, especially blood glucose and coagulation parameters, in association with virus serology and ultrasound, can rule out common causes of jaundice in pregnancy. This contributes to reliability of the clinical diagnosis of AFLP in the absence of liver biopsy, and ensures adequate management of the patient.
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PMID:[Acute fatty liver of pregnancy--differential diagnosis and supportive therapy]. 160 87

AO-128 is a potent and structurally novel inhibitor of the intestinal disaccharidases, such as maltase and sucrase. Genetically obese-diabetic mice, KKA(y), were used to examine the acute or long-term effectiveness of this compound. AO-128 decreased a postprandial rise in blood glucose after sucrose solution loading dose-dependently; the ED50 to reduce a delta increment of blood glucose by 50% was 0.22 mg/kg. The intestinal sucrase and maltase activities were suppressed to 7 and 48% of the control levels, respectively, at a dose of 0.21 mg/kg. Four-week-old female KKA(y) mice were kept on a laboratory diet containing 10 or 50 ppm of AO-128 for 12 weeks. The high dose of AO-128 reduced food intake and body weight gain throughout the experimental period. On the other hand, the low dose reduced body weight gain for the first 4 weeks without any effect on food intake. Development of the hyperglycemia and hyperinsulinemia characteristic of KKA(y) mice was moderately prevented by the low dose, and completely by the high dose. Hypertriglyceridemia tended to be suppressed by the AO-128 treatment. The high dose decreased the hemoglobin A1 level and parametrial adipose tissue weight. Hepatomegaly and fatty liver were ameliorated by AO-128 dose-dependently. Nephropathy was ameliorated by the high dose. These findings indicate that AO-128 may be useful for treating human obesity and diabetes.
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PMID:Antiobesity and antidiabetic actions of a new potent disaccharidase inhibitor in genetically obese-diabetic mice, KKA(y). 162 84


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