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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

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

The response to major trauma is characterized by a significant erosion of the body cell mass. Intensive nutritional support can decrease morbidity and mortality. Preservation and restoration of the body cell mass involves amino acid synthesis into protein, and this process requires nutrient energy. Newer methods of assessing energy expenditure have revised traditional concepts about energy requirements following trauma. The use of fat to meet some of the caloric requirements may obviate problems with ventilatory distress, glucose intolerance, and hepatic steatosis that occur with glucose-based nutritional regimens. Selection of the delivery method for intensive nutritional support should consider gastrointestinal integrity, physiologic tolerance, and cost. Enteral nutrition is superior to parenteral nutrition in maintaining gastrointestinal mucosal integrity, hormonal balance, and nutrient utilization. Furthermore, it is safer, more convenient, and more economical than parenteral nutrition.
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PMID:Postoperative nutritional support of patients with abdominal trauma. 219 Mar 43

Acute pancreatitis often results in a hyperdynamic, consumptive state. Hallmarks of this condition are decreased peripheral resistance with increased cardiac output. Hemodynamic and cardiovascular changes are accompanied by metabolic alterations. Increased protein catabolism, increased ureagenesis, glucose intolerance, increased lipolysis, and reduced servoregulation are metabolic changes commonly seen in this syndrome. To preserve organ structure and function, biochemical processes must be metabolically supported. Substrate needs change as stress level increases. The per cent of total calories provided as protein must increase. Branched-chain-enriched amino acid solutions have been shown to improve nitrogen utilization in hypermetabolic patients and may therefore be beneficial for the patient with acute pancreatitis. Glucose utilization decreases and free fatty oxidation increases. A mixed fuel system that provides fat, protein, and glucose is suggested for these patients. IV fat has been shown to be a safe energy substrate for patients with pancreatitis in the absence of hyperlipidemia. Failure to use fat as an energy substrate in conjunction with TPN may result in hepatic steatosis and excess carbon dioxide production. The decision of whether to use the parenteral or enteral route to nutritionally support the patient with pancreatitis remains controversial. TPN may allow maintenance of pancreatic rest. The role of enteral feedings is less clear. However, it has been shown that the further down the alimentary tract the feeding is infused, the less pancreatic stimulation occurs. Therefore, it seems wise to support the patient with TPN during severe acute pancreatitis. Jejunal enteral feedings should be initiated as a transitional feeding when the acute inflammatory episode begins to subside.
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PMID:Nutritional support in acute pancreatitis. 250 54

In a cross-sectional health screening 636 persons with negative urine glucose, a 75-g-oral glucose tolerance test was performed. We report the clinical features of the subjects with impaired glucose tolerance or diabetes mellitus. In 96 subjects with impaired glucose tolerance, the frequencies of alcohol dependency, fatty liver, and of increased levels of serum uric acid, cholesterol, triglycerides, total serum protein and gamma-glutamyl transpeptidase were significantly higher than in normal subjects. In 37 subjects with diabetes mellitus, the frequencies of fatty liver, hypertension and of increased erythrocyte sedimentation rate, triglycerides and gamma-glutamyl transpeptidase were significantly higher than in normal subjects. In addition, significant increases in serum gamma-glutamyl transpeptidase, triglycerides, serum total cholesterol and body mass index, and a significant decrease in high density lipoprotein cholesterol were also observed in subjects with impaired glucose tolerance and diabetes mellitus. These results suggest that alcohol dependency, fatty liver, obesity and hyperlipidemia are important concomitants of impaired glucose tolerance.
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PMID:Study on background factors associated with impaired glucose tolerance and/or diabetes mellitus. 278 10

Insulin responses to oral glucose loads were studied in patients with obstructive jaundice and compared with those of other liver diseases (fatty liver, chronic hepatitis and liver cirrhosis), pancreatic diseases, and definite diabetes mellitus. Compared with their corresponding glucose intolerance, high insulin responses were characteristic in fatty liver, chronic hepatitis and liver cirrhosis, and insulin responses and insulinogenic index decreased in chronic hepatitis and liver cirrhosis as glucose intolerance progressed. In obstructive jaundice with the pancreatic ducts stenotic or obstructed, insulin responses were suppressed in comparison with their corresponding glucose intolerance, and also insulinogenic index were below 0.5 in most of the cases. However, in obstructive jaundice with the pancreatic ducts intact, high insulin responses were observed in almost half of the cases with insulinogenic index above 0.5, and insulin response and insulinogenic index decreased as glucose intolerance progressed. While most cases of fatty liver, chronic hepatitis and liver cirrhosis with insulinogenic index above 0.5 were distributed in non-diabetes zone in sigma BS-sigma IRI plane (Kosaka's), those with insulinogenic index below 0.5 were distributed in intermediate zone. Most cases with obstructive jaundice with pancreatic ducts stenotic or obstructed, had insulinogenic index below 0.5 and were distributed in diabetes zone. However, half of cases with obstructive jaundice with pancreatic ducts intact, had insulinogenic index above 0.5 and their distribution in non-diabetes zone, while the other half had insulinogenic index below 0.5 and their distribution in diabetes zone. Therefore, it may be concluded that insulin responses increase at the early stage of obstructive jaundice mainly under influence of liver dysfunction itself, but that insulin response is suppressed at later stage of obstructive jaundice as pancreatic islets are affected.
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PMID:[Clinical study on glucose intolerance and insulin response in obstructive jaundice]. 388 96

Android obesity is associated with metabolic disorders, but the causality of this relationship remains unclear. We investigated the association of body mass index (BMI) and waist-to-hip ratio (WHR) with hormones, glucose tolerance, insulin sensitivity, serum lipoproteins, and the serum activity of hepatic enzymes in 40 healthy premenopausal women (BMI 19.2-46.1, mean 32.6 +/- 1.3 kg/m2; WHR 0.68-1.01, mean 0.82 +/- 0.02). BMI correlated with WHR (r = 0.52, P < 0.01). After correction for WHR, BMI was negatively correlated with high-density lipoprotein cholesterol and positively with total and very low density lipoprotein triglycerides, insulin sensitivity, blood glucose, serum insulin and glucagon. After adjustment for BMI, WHR was significantly associated with high-density lipoprotein cholesterol, total and very low density lipoprotein triglycerides, and the serum activities of hepatic enzymes but not with insulin sensitivity, blood glucose, serum insulin, or glucagon. According to these results, body fat distribution assessed by WHR is related to hypertriglyceridemia and alterations in hepatic function such as a fatty liver. WHR is not primarily related to glucose metabolism in healthy premenopausal women without preexisting metabolic disorders such as glucose intolerance. Therefore the observable association between android obesity and manifest impairment in glucose metabolism may develop secondarily during persisting hyperinsulinemia, which itself is primarily related to obesity. Thus an android body fat distribution may rather be an accompanying feature than a predictor of impaired glucose tolerance and insulin resistance.
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PMID:The waist-to-hip ratio corrected for body mass index is related to serum triglycerides and high-density lipoprotein cholesterol but not to parameters of glucose metabolism in healthy premenopausal women. 831 84

Fatty liver has prevailed by 14% in the healthy population of this country. The factors contributing genesis of fatty liver were gender (male), obesity, high alcohol consumption, glucose intolerance and hypertriglyceridemia. And hypertriglyceridemia seems to be the common underlying factor to all other causes. The mechanism for accumulation of triglycerides in the liver can be explained at least by increased HTGL activities and elevated apo A-II levels, a postulated co-factor of HTGL. An hypertriglyceridemic patients with fatty liver had the insulin resistance.
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PMID:Hypertriglyceridemia and fatty liver: clinical diagnosis of fatty liver and lipoprotein profiles in hypertriglyceridemic patients with fatty liver. 922 32

The prevalence of a mutation of the codon for tryptophan 64 to arginine (Trp64Arg) in the beta3-adrenergic receptor gene was investigated by genotyping 261 Japanese subjects. The allelic frequency of this mutation was 0.18. Subjects with the homozygous W64R mutant alleles had a significantly higher prevalence of fatty liver, BMI, serum gamma-glutamyl transpeptidase, and serum leucine amino transpeptidase levels than those without the mutation. Individuals with this mutation also showed a higher fasting blood glucose level than those without this mutation. However, the prevalence of diabetes mellitus was no different between the three groups. These results suggest a potential association of the Trp64Arg mutation with higher morbidity of fatty liver and mild glucose intolerance.
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PMID:Association of the Trp64Arg mutation of the beta3-adrenergic receptor with fatty liver and mild glucose intolerance in Japanese subjects. 969 85

To test the hypothesis that fatty liver coexists with other metabolic abnormalities of the insulin resistance syndrome, and responds to their amelioration, we prospectively studied 48 consecutive patients with chronically elevated liver enzymes and clinical, ultrasound and histological findings consistent with fatty infiltration of the liver. Most of the patients were overweight or obese (64%) with increased waist circumference which closely relates to visceral fat. Only 10% of the patients had normal glucose tolerance: 44% had diabetes mellitus, 29% impaired glucose tolerance, and 17% were hyperinsulinaemic. The most common dyslipidaemia found was hypertriglyceridaemia and/or low HDL-C (86%). Dietary intervention and follow-up (median 24 months), supplemented by oral hypoglycaemic or lipid-lowering drugs as needed, resulted not only in weight loss (mean 3.7 kg), decreased fasting blood glucose (p < 0.005) and improvement in serum lipid profile (p < 0.02 for both triglycerides or HDL-C) but also in an improvement of serum liver enzymes in 96%, which became normal in more than half of the patients. Thus, fatty liver was strongly associated with many features of the insulin resistance syndrome, and follow-up revealed a high potential for reversibility and a benign course.
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PMID:Fatty liver--an additional and treatable feature of the insulin resistance syndrome. 1020 58


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