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

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

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

To evaluate the role of insulin in familial hypertriglyceridemia, 34 relatives of the pedigrees of 3 index cases of endogenous hypertriglyceridemia and hepatic steatosis as well as 9 spouses were examined for plasma lipids and responses of blood glucose and plasma insulin during oral glucose tolerance tests. The combined disorders of hypertriglyceridemia and hyperinsulinemia plus glucose intolerance--insulin resistance--were most commonly found among the relatives, which were often accompanied by an impaired liver function. Some relatives showed hyperinsulinemia without hypertriglyceridemia. Obesity was frequent, but its incidence was similar to the controls. Thus, the observed form of familial hypertriglyceridemia was apparently coupled with insulin resistance; and hyperinsulinemia, or insulin resistance by itself, might be a basic genetical trait in this form of lipid disorder.
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PMID:Evidence for a familial form of hypertriglyceridemia as disorders coupled with insulin resistance. 96 Jan 7

Among 31 nonobese or obese patients with endogenous hypertriglyceridemia, hepatic steatosis was found by histologic examination of the biopsied specimen in 17 patients, and it was severe in six patients, They had no history of excessive alcohol intake. Chemical analysis revealed that the lipid accumulated in the liver was triglyceride. The hypertriglyceridemic patients, with or without histologic steatosis, showed significantly increased responses of both plasma insulin and blood glucose to oral glucose load compared with control subjects. The responses were more exaggerated in the hypertriglyceridemic patients with steatosis than in the hypertriglyceridemic patients without steatosis. Analysis of correlations between five variables (liver triglyceride, plasma insulin, blood glucose, body weight index, and serum triglyceride) was done on 15 subjects whose liver triglyceride values were quantified, and highly significant correlations were found between liver triglyceride and plasma insulin, blood glucose, or body weight index. A step wise multiple regression analysis performed on the five variables with liver triglyceride as the dependent variable revealed that the plasma insulin level was the most closely related variable, and the blood glucose level the next. The prediction equation for liver triglyceride as a function of plasma insulin and blood glucose levels (r = 0.91, p greater than 0.001) accounted for 84 percent of the total variance of liver triglyceride. It was shown that the decay of intravenously injected insulin in plasma was not delayed in the hypertriglyceridemic patients with steatosis, while the insulin sensitivity examined after intravenous insulin injection significantly decreased in the hypertriglyceridemic patients with or without steatosis, thus suggesting that the hyperinsulinemia in the hypertriglyceridemic patients was due to an increased insulin secretion associated with the decrease in the insulin sensitivity. Therefore, the elevated plasma insulin and blood glucose levels--or the insulin insensitivity by itself--might be the essential abnormalities in patients with endogenous hypertriglyceridemia, which, in extreme cases, might lead to massive triglyceride accumulation in the liver.
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PMID:Hepatic steatosis and the elevated plasma insulin level in patients with endogenous hypertriglyceridemia. 112 34

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

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

Intraperitoneal and subcutaneous routes of administration for diabetics on CAPD were compared. The comparison included: (1) Control of blood glucose concentration: both methods can provide satisfactory glycemic control for most patients. Changing the method of insulin administration is warranted when one method fails. (2) Effect on plasma insulin levels: intraperitoneal administration can produce a plasma insulin profile similar to the normal profile. This is unusual with subcutaneous administration. Consequences of hyperinsulinemia (hyperlipidemia, hypertension) seem, however, to be similar between the two methods of insulin administration. (3) Effect on peritoneal permeability: permeability characteristics are maintained unchanged, usually, with either method after long-term CAPD. However, insulin is mitogenic in vitro. Theoretically, intraperitoneal insulin could lead to peritoneal fibrosis. (4) Effect on infectious complications of CAPD: a difference in the rate of peritonitis or overall PD catheter-related infections has not been convincingly demonstrated between the two methods of insulin administration. Exit site and tunnel infections with staphylococcus aureus may be more frequent in diabetics receiving insulin subcutaneously. (5) Effect on hepatic structure and function: subcapsular hepatic steatosis was described in diabetics receiving insulin intraperitoneally. The clinical significance of this finding remains to be demonstrated. We conclude that both methods can be applied for insulin administration in diabetics on CAPD. The intraperitoneal method should be tried first in most instances. Prospective studies comparing the two methods are needed.
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PMID:Subcutaneous versus intraperitoneal insulin in the management of diabetics on CAPD: a review. 168 Apr 63

The possibility that postprandial hyperinsulinemia could play a role in the development of hepatic lipid disturbances during convalescence from influenza B infection was explored in the ferret as a possible model of the steatosis of Reye's syndrome. Postprandial hyperinsulinemia was produced by feeding young ferrets glucose/water and a regular diet (glucose-treated group), as reflected by the mean serum insulin levels attained, which were 57 and 135 microU/ml during control and postinfluenza periods, respectively. By comparison, ferrets fed water and a regular diet (untreated group) had mean insulin levels of 19 and 22 microU/ml, while postprandial glucose levels were comparable in the two groups of animals for each period. In contrast to untreated animals, grossly visible fatty livers were found in glucose-treated ferrets during convalescence. The total lipid content of these livers had doubled compared with preinfection samples and compared with livers of untreated ferrets. By electron microscopy hepatic mitochondria showed striking changes with diminution of matrix density and reduction in cristae surface area only in convalescent samples from glucose-treated animals. Serum free fatty acid (FFA) levels were considerably higher in the glucose-treated animals during fasting before influenza and also after feeding during convalescence. Serum triglyceride (TG) levels were also high during convalescence in the glucose-treated group. Adipose tissue lipoprotein lipase activities were similar between groups, but hormone-sensitive lipase activity was twelvefold higher in glucose-treated ferrets before and after influenza B. These findings indicate that for a given stimulus, glucose-treated ferrets would mobilize more FFA than untreated ferrets. The total capacity for beta-oxidation of FA by the mitochondrial pathway was identical in all groups of animals. Total carnitine palmitoyl transferase (CPT) activity was the same in both control groups, but was significantly diminished in glucose-treated animals during convalescence. As CPT regulates the entry of FA into the mitochondrial matrix, its reduction in response to higher insulin concentrations would limit the oxidation of FA and stimulate TG accumulation. Therefore, the accumulation of lipid in the liver in this model is regarded to have been caused by the simultaneous occurrence of increased lipolysis and increased hepatic TG synthesis owing, in part, to diversion of activated FA by CPT, which is reduced in activity due to the regulatory action of insulin. These findings may have pathophysiologic relevance for the lipid changes that occur in Reye's syndrome and to fatty liver formation in hyperinsulinemic states.
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PMID:Hepatic steatosis during convalescence from influenza B infection in ferrets with postprandial hyperinsulinemia. 220 96

Steatohepatitis (fatty liver hepatitis), histologically identical to alcoholic disease, occurs in some obese patients after jejunoileal bypass. A similar lesion occurs rarely in obese patients without bypass surgery, but the risk factors are poorly understood. Hepatic steatosis, steatohepatitis and fibrosis were sought in 351 apparently nonalcoholic patients at autopsy and various risk factors were evaluated. Incidence of steatosis and steatohepatitis correlated with the degree of obesity. Steatohepatitis was found in 18.5% of markedly obese patients and 2.7% of lean patients. Additional risk factors for steatohepatitis were type II diabetes, weight loss in the preterminal period shortly before death and intravenous glucose therapy in the last week of life. Severe fibrosis was found in 13.8% of markedly obese patients and in 6.6% of lean patients; this difference was largely explained by the higher prevalence of diabetes in obese groups. The risk factors defined in this study are known to be associated with abnormalities of free fatty acid metabolism. Obesity, type II diabetes and intravenous glucose therapy are associated with hyperinsulinemia, which may inhibit fatty acid oxidation. Obesity and weight loss increase the presentation of fatty acids to the liver. Similar metabolic changes may occur in obese patients after jejunoileal bypass surgery. Thus this study supports the hypothesis that fatty acids have a role in the hepatocellular necrosis found in some obese individuals.
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PMID:Fatty liver hepatitis (steatohepatitis) and obesity: an autopsy study with analysis of risk factors. 222 7

In a large sample of 1379 adult patients and, in addition, in a smaller group of 223 other patients in whom a glucose tolerance test with measurement of serum insulin was carried out, an increase of blood pressure, pulse rate, relative body weight and serum insulin was found which correlated significantly with that range of gamma glutamyltransferase (GGT) values which erroneously so far is considered to be normal. The really normal range of the GGT is not up to 28 (measured at 25 degrees C), but only up to 10 U/l. Persons with GGT 9-12 U/l have a significantly higher blood pressure than persons with GGT up to 8 U/l. The relationship between blood pressure and GGT is the same in males and females although the females show a higher GGT for the same amount of alcohol consumed; in both, males and females, the steepest increase is just in the low GGT range between 9 and 25 U/l. The nature of this ethanol-effect is toxic, not caloric. Daily alcohol in "normal" ("social") amounts causes hyperinsulinemia (and thus increased sodium reabsorption in the Kidney) as well as increased catecholamine excretion. "Normal" alcohol consumption leading to hepatic steatosis as the "normal" condition of the population, has more health hazards than so for assumed. A GGT higher than 10 U/l (measured at 25 degrees C), is besides hyperinsulinemia the most sensitive test for pathologic changes of the metabolism and the cardiovascular parameters due to hepatic steatosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The normal values of gamma-glutamyltransferase are falsely defined up to now: on the diagnosis of hypertension, obesity and diabetes with reference to "normal" consumption of alcohol]. 256 44


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