Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 38-year-old female was admitted to our hospital because of dyspnea. The diagnosis of total lipodystrophy was made by following findings: (1) gaunt appearance; (2) insulin-resistant diabetes mellitus; (3) hyperlipidemia; (4) fatty liver. Chest X-ray demonstrated cardiomegaly, pulmonary edema and pleural effusion. Echocardiogram was characterized by left ventricular hypertrophy with asymmetrical septal hypertrophy and left ventricular dysfunction. Renal biopsy revealed focal glomerulosclerosis. We reported a patient with total lipodystrophy combined with heart failure and renal failure, which have been rarely associated with the disease.
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PMID:Total lipodystrophy with heart failure and renal failure: report of a case. 253 Mar 77

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

Feed restriction and dietary 1,3-butanediol were used with lactating goats in an attempt to induce metabolic changes characteristic of bovine lactation ketosis and fatty liver. In Experiment 1, midlactation goats were fed 80, 102, or 114% of metabolizable energy requirements and 0, 50, or 100 g/d of 1,3-butanediol. Concentration of beta-hydroxybutyrate in blood plasma decreased with increasing metabolizable energy but was increased greatly at 2 h after goats were fed 50 or 100 g butanediol and remained elevated at 6 h postfeeding with 100 g of butanediol. Concentration of glucose in plasma was decreased at 2 and 6 h postfeeding in goats fed 100 g of butanediol. In Experiment 2, goats in early lactation were fed for ad libitum intake or were restricted to 70% of ad libitum intake with 1,3-butanediol included at 10% of diet DM. The treatment decreased milk production, increased concentrations of beta-hydroxybutyrate and nonesterified fatty acids, and decreased the concentration of insulin and the insulin to glucagon ratio in plasma. Concentrations of glucose, acetate, and glucagon in plasma were not affected. After 28 d of treatment, concentration of total lipid in liver was increased, but concentrations of glycogen and triglyceride were unaffected. Changes caused in goats by feed restriction plus dietary 1,3-butanediol were characteristic of subclinical lactation ketosis in cows, but the response was more moderate than seen previously in cows.
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PMID:Metabolic responses of lactating goats to feed restriction and dietary 1,3-butanediol. 262 43

Hepatic steatosis and steatonecrosis occur in nonalcoholic individuals, usually in a setting of obesity, type II diabetes mellitus, and after jejunoileal bypass. We propose an hypothesis for the pathogenesis of these hepatic lesions based on an observation in peritoneal dialysis patients. Hepatic histology was examined at autopsy in 11 patients with type I diabetes mellitus and renal failure who had received i.p. insulin in conjunction with continuous ambulatory peritoneal dialysis (CAPD). Steatosis in a unique subcapsular distribution occurred in 10 of 11 patients treated with i.p. insulin and in 0 of 9 controls receiving CAPD without insulin. Three of the 11 had steatonecrosis, 2 of whom had Mallory bodies. We suggest that insulin has an important role in the pathogenesis of steatosis and steatonecrosis. In CAPD patients the lesions occurred only under the capsule where concentrations of insulin are high secondary to its i.p. administration. In obese patients the lesions occur throughout the liver where insulin concentrations are high because of elevated levels in the portal vein. Free fatty acids (FFA) are oxidized in the liver by a pathway that is blocked by insulin. In the presence of insulin, FFA are preferentially esterified into triglycerides which accumulate in large quantities leading to steatosis; small amounts of FFA escaping local control may lead to membrane injury and steatonecrosis. Steatosis and/or steatonecrosis will occur when there is insulin secretion sufficient to block FFA oxidation but not sufficient to block FFA mobilization from adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subcapsular steatonecrosis in response to peritoneal insulin delivery: a clue to the pathogenesis of steatonecrosis in obesity. 265 21

To elucidate if the presence of fatty liver in obesity influences hepatic insulin extraction under basal conditions, serum immunoreactive insulin (IRI) and C-peptide immunoreactivity (CPR) were measured in 20 obese patients with normal glucose tolerance and in 8 normal subjects. The obese patients were subdivided into two groups matched for age and body weight according to the presence or absence of fatty liver: 8 obese patients without fatty liver (OBN) and 14 with fatty liver (OBF). Basal levels of IRI and CPR were significantly greater in the obese patients than in the normals, but were similar in the two obese groups. In the OBF group, the CPR/IRI molar ratios, a relative measure of hepatic insulin uptake, were significantly lower than in the other two groups, while the ratios of the normal and OBN groups were similar. The CPR/IRI molar ratios in all obese patients correlated well with the degree of fatty liver (r = 0.785, p less than 0.001). These results suggest that hepatic insulin extraction in a subgroup of obese patients is either reduced or indistinguishable from that of non-obese subjects, and that basal CPR/IRI molar ratio may serve as a useful indicator of the presence of fatty liver in simple obesity.
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PMID:Altered basal C-peptide/insulin molar ratios in obese patients with fatty liver. 305 68

The effects of ethanol administration on activity and regulation of carnitine palmitoyltransferase I (CPT-I) were studied in hepatocytes isolated from rats fed a liquid, high-fat diet containing 36% of total calories as ethanol or an isocaloric amount of sucrose. Cells were isolated at several time points in the course of a 5-week experimental period. Ethanol consumption markedly decreased CPT-I activity and increased enzyme sensitivity to inhibition by exogenously added malonyl-CoA. Changes in enzyme activity occurred sooner than those in enzyme sensitivity. Fatty acid oxidation to CO2 and ketone bodies was depressed in hepatocytes from ethanol-fed animals during the first part of the treatment. At the end of the 35-day period, there were no longer differences in the rate of ketogenesis between the two groups. At that time, however, the rate of CO2 formation was still impaired in the ethanol-fed animals. Furthermore, addition of ethanol or acetaldehyde to the incubation medium strongly depressed CPT-I activity and rates of fatty acid oxidation in hepatocytes from ethanol-treated rats, whereas these effects were much less pronounced in cells from control animals. The response of CPT-I activity to insulin, glucagon, vasopressin, and phorbol ester was blunted in cells derived from ethanol-fed rats. These changes in the regulation of CPT-I activity corresponded with those observed in the rate of fatty acid oxidation. It is concluded that CPT-I may play a role in the generation of the ethanol-induced fatty liver.
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PMID:Effects of ethanol feeding on the activity and regulation of hepatic carnitine palmitoyltransferase I. 306 12

Sixteen patients given total pancreatectomy were experienced, and the essential points of postoperative management were reported. The morbid states after total pancreatectomy consist of: a deficiency of pancreatic endocrine function, a deficiency of pancreatic exocrine function, loss of the duodenum and upper jejunum, the influence of partial or total gastrectomy, and the influence of dissection around the superior mesenteric artery. These states influence each other and become more complicated. The management period is divided into five parts as follows; a period of intravenous nutrition, the early half; water replacement period, the late half; hyperalimentation period, a period of intravenous and enteral nutrition, a period of enteral, intravenous and oral nutrition, a period of oral and enteral nutrition, and a period of oral nutrition. In each period, a special form of management is needed. The essential points of long-term management are as follows: The use of suitable doses of pancreatic enzyme and antidiarrheal agents for the cure of severe maldigestion and malabsorption. Also, intermittent IVH or elemental diet are effective for recovery from deteriorative malnutrition. For the prevention of hypoglycemic attack, training of the patients and the maintainance of good nutrition are important. These patients have a high incidence of infection, and so speedy treatment must be given if this occurs. Fatty liver must be treated by intermittent IVH or elemental diet. As total pancreatectomy imposes a severe burden on the patient, including self-injection of insulin, the indications of this operation must be decided carefully giving due consideration to its radicality.
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PMID:[Postoperative management of total pancreatectomy]. 309 14

Although young infants are at greater risk for total parenteral nutrition (TPN)-related liver disease than adults, previous studies on the effect of the TPN energy source on the development of hepatic steatosis have been carried out in adult rats and adult humans. We studied the effect of a glucose and a glucose/fat TPN energy regimen on hepatic chemical composition and the development of steatosis in newborn miniature pigs. Twenty miniature pigs were randomized at 10 days of age to receive a TPN regimen which utilized either glucose (group A) or glucose/fat (group B) as the non-nitrogen energy source. After 8 days, blood was drawn for insulin, glucagon, SGPT, albumin, and bilirubin determinations. Samples of liver were obtained at 9 days. Plasma insulin levels were significantly higher and glucagon levels lower in group A piglets than in those in group B. Normal values were obtained for SGPT, albumin, and bilirubin, and no differences were found between groups. Chemical analysis of the livers revealed no differences between groups in the concentrations of glycogen, fat, protein, DNA, and RNA. Group A animals had significantly higher concentrations of water than group B (group A: 0.75 +/- 0.01 liter/kg; group B: 0.74 +/- 0.01; p less than 0.03). A significant correlation was found in group B between the plasma insulin/glucagon ratio and the hepatic glycogen concentration (r = 0.73, p less than 0.05). Group A animals had fat vacuoles in centrilobular hepatocytes, in contrast with group B animals who had visible fat only in Kupffer cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Liver composition and histology in growing infant miniature pigs given different total parenteral nutrition fuel mixes. 311 Apr 45

Hepatic steatosis is an ongoing problem in total parenteral nutrition (TPN). The etiology of this deranged hepatic morphology is unclear, but lack of enteral stimulation and excess carbohydrate calories have been suggested as altering the intestinal hormone profile. In this study, adult male Sprague-Dawley rats (n = 28) received internal jugular catheters: group 1 (n = 7) received saline (3 cc/hr) and chow ad libitum; groups 2, 3, and 4 (n = 7) received 15, 20, and 25% dextrose-base TPN solutions, respectively, in quantities matching the caloric intake of paired ad libitum animals. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay, and livers were removed for histologic examination and determination of total hepatic lipid content. Portal and peripheral insulin levels rose in a linear fashion with increasing dextrose concentration. Lipid content increased with elevated portal venous insulin/glucagon ratio in groups 3 and 4. Periportal fatty infiltration increased with increasing dextrose concentrations. The results suggest that the liver's response to altered portal insulin/glucagon ratio may play an important role in changes of hepatic morphology associated with TPN.
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PMID:Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in rats. 313 73

Hepatic steatosis is one of the two principal hepatic complications of total parenteral nutrition (TPN), the other being cholestasis. While the cause is uncertain, an excess of carbohydrate calories in rats leads to an elevated portal insulin/glucagon (I/G) molar ratio, periportal fatty infiltration, and increased total hepatic lipid content. Insulin causes fatty acid biosynthesis, whereas glucagon causes hepatic release and inhibition of fatty acid synthesis. Thus we attempted to add glucagon to lower the I/G to see if this would affect the degree of hepatic fatty infiltration by encouraging hepatic fat mobilization. Adult rats (n = 21) received internal jugular catheters; Group 1 (n = 7) was given saline solution (3 ml/h) and chow ad libitum; Group 2 (n = 7), 25% dextrose-base (D25W) TPN solution; Group 3 (n = 7), D25W TPN + 33 micrograms/100 gm/day glucagon. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay and blood glucose determination; livers were removed for histologic study and lipid determination. Blood glucose did not differ in any group. Hepatic lipid and peripheral and portal venous I/G were increased and periportal fatty infiltration was extensive in Group 2, whereas hepatic lipid and I/G were decreased and periportal fatty infiltration was absent in glucagon-infused rats (Group 3). An abnormally high I/G ratio in portal blood elicited by high-glucose TPN may be responsible, at least in part, for hepatic steatosis. By increasing hepatic lipid export, addition of glucagon to TPN may play a major role in decreasing hepatic steatosis.
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PMID:Addition of glucagon to total parenteral nutrition (TPN) prevents hepatic steatosis in rats. 313 27


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