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

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

Marked fatty liver was found to develop in both KK and KK-Ay (yellow KK) mice when they were allowed free access to a 15% ethanol solution as drinking fluid. The present studies were undertaken to elucidate the characterization of the fatty liver and associated changes. Chemical analysis showed that accumulated lipids were mainly triglycerides, whose fatty acid composition was changed with increases in palmitoleic and oleic acids, indicating augmentation in endogenous lipogenesis. An accumulation of small fat droplets was histologically observed in centrolobular hepatocytes extending to perilobular zones. Among the tested mice of seven strains, only KK and KK-Ay mice developed the ethanol-induced fatty liver, and the latter mice were more susceptible. Growth, food and alcohol intakes, plasma levels of glucose, triglycerides, and immunoreactive insulin were also surveyed during the development of the alcoholic fatty liver. In contrast to high energy diet, ethanol induced neither development of obesity nor exaggeration of diabetic states. A possible correlation between the pathogenesis of the fatty liver and the genetic factor inherited in KK mice is discussed.
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PMID:Induction of fatty liver by ethanol drinking in KK and KK-Ay mice. 115 19

Young, adult, female Sprague-Dawley rats were fasted for 18 h and then given a single s.c. injection of alloxan (10 mg/100 g body weight) which promptly induced a severe state of diabetes. The animals were killed at frequent time intervals during the 7-day study period in order to record the dynamic changes in their capacity for adrenal steroidogenesis and secretion as measured by fluorometric determination of their circulating corticosterone (Cmpd B) levels as well as by thin layer chromatographic identification of cortical lipid moieties used for steroidogenesis. In addition to severe polydypsia, polyuria and polyphagia, these animals manifested super-normal glucose, triglycerides, free fatty acids and cholesterol in their blood, severe hepatic steatosis, adrenal hyperplasia with lipid depletion from the mineralocorticoid producing z. glomerulosa, thymus gland involution and complete degranulation of their insulin producing islet beta cells. Despite an initial high output of Cmpd B and despite progressive cortical hyperplasia, the serum Cmpd B levels became reduced and many of the animals succumbed suddenly, due most likely to inadequate adrenocortical steroidogenesis. Adrenocortical lipids showed a progressive accumulation of free fatty acids, di- and triglycerides, suggesting that some lipid enzymatic defect could be responsible for the lack of conversion of these lipid entities essential for proper steroidogenesis.
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PMID:Adrenal glandular lipids and circulating corticosterone in severely diabetic rats. 117 54

Two trials were to study alloxan diabetes in goats. The data were grouped: 1) normal fed goats (10); 2) 48-h fasted goats (5); 3) fed goats sampled 96 h after alloxan treatment (5); and 4) goats treated with alloxan following a 48-h fast and sampled 96 h after alloxan treatment with continued fasting (3). Groups 1 and 4 exhibited the following means: serum insulin 43.9, 16.4, 9.4, and 6.7 muU/ml; blood glucose 55.0, 47.3, 219.6, and 485.6 mg/100 ml; blood ketones 4.3, 2.6, 36.6, and 28.6 mg/100 ml; blood acetate 4.7, 4.0, 42.7, and 4.9 mg/100 ml; plasma-free fatty acids 1.8, 10.0, 14.4, and 40.5 mg/100 ml; and plasma triglyceride 13.3, 7.0, 47.6, and 12.2 mg/100 ml. Liver samples from five fed goats before and 12 days after alloxan treatment exhibited the following means: phospholipid 27.5 and 26.1 mg/g; triglyceride 21.2 and 98.9 mg/g; and percent lipid 7.2 and 14.4. The diabetes was accompanied by fatty liver development and probably reduction in utilization of acetate and triglyceride in the fed animals.
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PMID:Blood and liver metabolites in fed and fasted diabetic goats. 124 92

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

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

Hepatic steatosis in rats is associated with an infusion of excessive carbohydrate calories. Previous work from this laboratory suggested that this is associated with an elevated portal insulin/glucagon molar ratio (I/G) and is reversed by parenteral glucagon administration. Although hepatic steatosis is not related to essential fatty acid deficiency, addition of lipid to total parenteral nutrition (TPN) has been reported as being protective against the development of hepatic steatosis. Therefore, we propose that lipid may exert its salutary effect via an alteration of the I/G ratio. To test this hypothesis, adult rats (seven per group) received internal jugular catheters: group 1, saline (3 mL/h) plus chow ad libitum; group 2, 25% dextrose base TPN; group 3, 17% dextrose base TPN + 2.5% lipid; group 4, 25% dextrose base TPN + 2.5% lipid. At 7 days, portal and peripheral venous blood was drawn for insulin and glucagon radioimmunoassay and liver function tests; livers were removed for histology and lipid content determination. Panlobular vacuolization, on histology, and lipid content were excessive in group 2, and the portal I/G was increased because of elevated portal insulin. In contrast, portal venous insulin and I/G did not increase, and hepatic steatosis was absent in groups 3 and 4. The results suggest that the addition of lipid to TPN in rats decreases the portal insulin level and lowers the portal I/G, and thereby prevents hepatic steatosis.
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PMID:Addition of lipid to total parenteral nutrition prevents hepatic steatosis in rats by lowering the portal venous insulin/glucagon ratio. 155 3

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

Previous research has shown that a combination of feed restriction and dietary 1,3-butanediol starting at 14 d post-partum resulted in fatty liver and ketosis. Sixteen multiparous Holstein cows were used to determine effects of feed restriction or 1,3-butanediol as separate treatments. Treatments during d 14 to 42 postpartum were 1) control (ad libitum intake), 2) 20% feed restriction, or 3) control plus dietary 1,3-butanediol (5.5% of DM). From d 43 to 56, cows assigned to treatments 2 and 3 received a combination of feed restriction and butanediol. One cow on treatment 2 developed ketosis, but not fatty liver, after only 4 d of feed restriction. No other cows developed fatty liver or ketosis. Both treatments decreased milk production compared with controls. Feed restriction increased the extent of negative energy balance and caused transient increases in concentrations of NEFA, acetate, and beta-hydroxybutyrate in plasma. Concentrations of beta-hydroxybutyrate and insulin in plasma were increased by butanediol, which is a potent ketone body precursor. Concentration of glycogen in liver was less in feed-restricted cows, whereas glycogen and total lipid were greater in cows given butanediol separately. Gluconeogenic capacity of liver slices was not different among groups. Addition of 1,3-butanediol to in vitro incubation media decreased oxidation of propionate to CO2. Neither feed restriction nor dietary 1,3-butanediol as separate treatments induced the fatty liver and ketosis observed in earlier experiments in which the two treatments were given together.
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PMID:Metabolic changes in blood and liver of dairy cows during either feed restriction or administration of 1,3-butanediol. 178 95


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