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

Six patients with congenital generalized lipodystrophy are described. They had generalized paucity of fat tissue, acanthosis nigricans, prominent superficial veins and muscle hypertrophy. They were mentally retarded. Three had corneal opacities. They had normal external genitalia and none was tall for age. Their bone age was advanced and some had minor skeletal anomalies and nephromegaly. The muscle histology on light microscopy was normal. The majority had elevated serum aldolase and to a lesser degree serum lactic dehydrogenase and creatinine phosphokinase. Four of five examined had a myopathic electromyogram. They had normal or deranged liver function tests. The fatty liver infiltration in one seems to be progressive. Four had a normal and two an abnormal metyrapone test. They had an age-dependent abnormality of growth hormone, insulin and carbohydrate homeostasis.
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PMID:Congenital generalized lipodystrophy. 16 54

In vitro hepatic synthesis of lipids starting from 1-(14)C-acetate was studied in rats made diabetic by subcutaneous alloxan administration (175 mg/kg b.w.). A second group of diabetic rats was treated with lente insulin. In the alloxan-treated rats, a decrese was observed in hepatic incorporation of 1-(14)C-acetate into phospholipids, triglycerides and esterified cholesterol; there was an increased incorporation into nonesterified fatty acids (NEFA) and free cholesterol. Insulin administration restored lipid synthesis values to normal. On histologic examination, an intranuclear glycogenesis was observed in the hepatocytes of the alloxan-treated rats, along with severe hepatic necrosis; the latter however, only in rats sacrified on the 3rd day. Hepatic steatosis with small, medium and large droplets was present in the insulin-treated rats; signs of cellular degeneration were less evident.
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PMID:Effects of insulin on hepatic lipid synthesis in alloxan diabetic rats. 39 74

Indirect calorimetric studies were performed during a 100 g oral glucose tolerance test in diabetic patients with varying degrees of endocrine pancreatic dysfunction and in a control group of normal subjects. In 3 obese diabetics the study was repeated after a 3 day protein sparing modiefied fast. In diabetic patients the results show alterations of oxidation and storage of carbohydrates, related to insulin secretion deficiency on the one hand, and to overweight on the other. Endocrine pancreatic insufficiency may account directly for alterations observed in individuals with decreased or absent insulin response to glucose load, wheras metabolic factors such as adipose mass, hepatic steatosis, and peripheral insulin resistance appear to be responsible for alterations in carbohydrate oxidation and storage in subjects with relative endocrine pancreatic insufficiency, particularly obese diabetics.
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PMID:[Changes in storage and oxydation of ingested glucose in obesity and diabetes mellitus]. 51 18

Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.
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PMID:[Alcoholic ketoacidosis (author's transl)]. 53 15

Plasma lipids and lipoproteins, glucose tolerance, plasma insulin response to glucose load, and liver function were examined in 81 relatives of 12 index cases with primary endogenous hypertriglyceridemia, hyperinsulinemia, and hepatic steatosis, as well as in 90 nonrelatives, including the spouses, as controls. Insulin hypersecretion (with or without glucose intolerance), endogenous hypertriglyceridemia, and abnormal liver function suggesting hepatic steatosis were shown to exist in the relatives mostly in combined fashion. Correlation analysis and stepwise multiple regression analysis revealed that the combined disorder developed on the basis of obesity. The incidence of diabetes mellitus was significantly high in the relatives (14.8 per cent) as compared with the normal Japanese population (3.5 per cent). Although the vertical transmission of the combined disorder was noted in almost all pedigrees, the frequency distribution analysis of insulin response, glucose tolerance, and plasma triglyceride showed the histograms of these variables similarly skewed to the right as compared with those of the controls, with no apparent bimodality. In view of the hitherto suggested role of insulin in triglyceride metabolism, it is concluded that hyperinsulinemia coupled with obesity seems to be the basic trait of this form of familial hypertriglyceridemia and hepatic steatosis, though the mode of transmission remains to be elucidated.
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PMID:Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia. 65 14

The metabolism of varying quantities of oleic acid was examined in isolated perfused livers from normal fed rats and from animals made diabetic by pretreatment with guinea pig antiinsulin serum (AIS). The data presented reemphasize the fact that the quantity of free fatty acid (FFA) coming to the liver is a necessary, but not the most important, factor affecting the subsequent metabolism of the FFA. Rates of ketogenesis and output of triglyceride and the terminal concentration of hepatic triglyceride were proportional to uptake of FFA in certain concentration ranges. For equal rates of uptake of FFA, ketogenesis was greater, and the quantity of triglyceride secreted or accumulated within the liver was less, with livers from diabetic animals than with livers from normal animals. In confirmation of previous data, the liver was observed to have a maximal capacity to secrete triglyceride. Triglyceride accumulated in livers from normal-fed and diabetic animals only when uptake of FFA was more than sufficient to saturate the secretory process. Since proportionately more FFA was catabolized by livers from AIS treated animals, greater uptake of FFA was required to produce maximal rates of output of triglyceride and accumulation in livers from diabetic than from normal animals. Rates of ketogenesis by livers from normal fed animals increased minimally with increasing uptake of FFA (up to 1.0 mM free fatty acid). Even when uptake increased considerably with FFA concentrations of approximately 2.5 mM, rates of ketogenesis by livers from normal animals were less than half those of livers from diabetic rats, and maximal rates were not achieved by the normal controls. It is evident that changes in hepatic metabolism of FFA in the intact diabetic animal result from simultaneous alterations of supply of FFA and hormonally induced metabolic changes in the liver. Moreover, although hepatic secretion and accumulation of triglyceride is greater in isolated perfused livers from normal rats than from diabetic animals when the livers are exposed to equal quantities of FFA, the diabetic livers can accumulate more triglyceride, secrete more triglyceride, and oxidize more FFA to ketone bodies than can the normal under conditions in which considerably more substrate is available to the diabetic rather than to the normal livers. These differences might also be expected to occur in the acutely insulin deficient intact animal, in which changes in hormonal status and substrate (FFA) availability occur simultaneously, and might, in part, explain the ketonemia, hypertriglyceridemia, and hepatic steatosis often observed in vivo.
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PMID:The metabolism of oleic acid by the perfused rat liver in experimental diabetes induced by antiinsulin serum. 72 30

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

Oral glucose tolerance tests (100 g glucose) and the intravenous tolbutamide test were carried out. The glucose tolerance was seen to be disordered even in acute infectious hepatitis, but returning to normal when cured. If chronic hepatitis develops, however, the proportion of manifest diabetes increases to 7.2% in chronic persistent hepatitis and to 16.3% in chronic progressive hepatitis, while 30% each have latent diabetes. The glucose tolerance is most impaired in fatty liver (stage III) and in active cirrhosis of the liver with portal hypertension, where more than half of all patients present manifest or latent diabetes. Conversely, glucose tolerance improves even in chronic hepatitis and in cirrhosis of the liver as the inflammatory activity subsides. The main cause for the development of "liver diabetes" is therefore likely to be the activity of the inflammatory process, the extent of portal hypertension, disorders of glucose regulation in the liver and the increased insulin inactivation in the cirrhotic liver.
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PMID:[Disorders of glucose tolerance in 2600 histologically confirmed acute and chronic liver patients (author's transl)]. 81 Jun 95

In 15 mongrel dogs, a mixture of exocrine and endocrine pancreatic tissue obtained by a simple procedure was implanted into the liver of the same animal through a branch of the portal vein. Five animals with partial pancreatectomy were used for a morphological study. In a second group of ten dogs, 5 delayed and 5 immediate pancreatectomies were performed. No diabetes appeared after the pancreatectomy. The subsequent blood glucose and insulin levels remained within or close to the normal range for several weeks in 9 animals and up to 10 months in a last one, still alive. In 9 out of 10 animals, the long term study was limited between 6 and 17 weeks by the development of a malnutrition syndrome with hepatic steatosis due to the lack of exocrine secretory function because of the pancreatectomy. The last animal still alive developed the malnutrition syndrome after a second complementary resection of a small pancreatic fragment left along the duodenum. This last animal without diabetes at the 45th week suggests that the endocrine function of the autotransplanted pancreatic tissue could be maintained over a long period of time.
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PMID:[Prevention of diabetes in pancreatectomised dogs by autotransplantation of pancreatic tissue in the liver]. 81 64

In order to investigate the combined effects of diabetes and hypertension on the pathogenesis of cardiovascular disease, adult male and female SHR rats which develop hypertension spontaneously were given a single, 10 mg or 15 mg/100 g body wt. injection of alloxan s.c. to induce moderate or severe diabetes. Insulin was deliberately withheld. Animals were examined by autopsy daily for 7 days post-alloxan and after 4 and 8 weeks. Mortality was high--only 52% of the males survived as against 80% of the females. Most deaths occurred on Day 5 and were associated with adrenal haemorrhage and hyperplasia, thymus galnd involution, fatty liver and marked hypotension despite elevated aldosterone levels. During the first week, corticosterone levels increased significantly in the male; in females they showed little change. After 4 weeks, the severly diabetic animals became emaciated and moribund; corticosterone and aldosterone levels fell to very low levels despite adrenal hyperplasia. The beta cells of the moderately diabetic animals eventually lost their ability to secrete insulin and these animals too became cachetic and moribund with concomitant elevation of lipid, glucose and BUN levels, as well as myocardial infarction, fatty liver, and generalized hyalin arteriolo-, arterio-, and nephrosclerosis. It is suggested that the combined hormonal and metabolic alterations of diabetes and hypertension reinforced one another in these spontaneously hypertensive rats, leading to intense stimulation of the hypothalamic-pituitary-adrenal system, the exacerbation of those cardiovascular degenerative changes known to be associated with uncontrolled diabetes or hypertension, eventual impaired adrenocortical steroidogenesis, hypotension and death.
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PMID:Alloxan diabetes in spontaneously hypertensive rats: gravimetric, metabolic and histopathological alterations. 86 Nov 67


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