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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In experiments on albino rats it was found that the partial alloxan elimination of the pancreatic incretory elements followed by the normal diet and long-term adaptation of a healthy organism to excessive readily assimilating food carbohydrates are accompanied by a series of morphofunctional shifts, indicating the development of early diabetes mellitus stages, which are characterized by a recurrent increase in the glycemia level over 100 mg/100 ml, in the presence of sugar curves, changed according to a questionable type, hyperinsulinism and hyperlipemia arising. Some pancreatic islets are hypertrophied, whereas their beta-cell number decreases.
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PMID:[Morphofunctional characteristics of the initial phase of the development of experimental diabetes mellitus]. 637 95

To elucidate the pathogenesis of hyperlipidemia in chronic renal disease in children and adolescents, we have measured serum triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C) and activities of postheparin plasma lipoprotein lipase and hepatic triglyceride lipase (EC 3.1.1.3) in nine patients with transplants, and nine hemodialyzed and 18 conservatively treated patients with chronic renal failure. In 29 of 36 patients, serum insulin levels both in fasting and in response to oral glucose load were measured. The lipase activities were measured separately, utilizing antiserum against hepatic triglyceride lipase. All groups of patients had hypertriglyceridemia. The patients with endogenous creatinine clearance less than 20 ml/min/m2 had a low HDL-C level. The HDL-C level was correlated inversely with serum triglyceride level and positively with glomerular filtration rate. The lipoprotein lipase activities were low in patients with endogenous creatinine clearance less than 20 ml/min/m2. Although hepatic triglyceride lipase activities were not significantly low in any groups of patients, they were correlated with glomerular filtration rates in the conservatively treated patients with chronic renal failure. A defective triglyceride removal due to low lipase activities may contribute to uremic hypertriglyceridemia in these patients. On the other hand, patients with transplants had almost normal lipase activities and exhibited hyperinsulinemia; overproduction of triglyceride due to hyperinsulinemia may contribute to their hypertriglyceridemia.
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PMID:Lipid profiles and lipase activities in children and adolescents with chronic renal failure treated conservatively or with hemodialysis or transplantation. 638 39

We have previously reported that normal Wistar rats fed an isocaloric, sucrose-rich (63%) diet (SRD) developed glucose intolerance and elevated triglyceride levels in plasma as well as in heart and liver tissue. This metabolic state was accompanied by hyperinsulinism both in vivo and in vitro, suggesting that a state of insulin resistance has developed. The aim of this study was to gather information on the various plasma post-heparin lipolytic activities in rats fed a SRD. Hepatic triglyceride lipase (H-TGL) was evaluated by both, protamine sulfate inhibition (PSI) of extrahepatic lipoprotein lipase (LPL) and heparin-Sepharose affinity chromatography (H-SAC). Both methods rendered comparable results. Total triglyceride lipase (T-TGL) was measured after Krauss et al. and monoglyceride hydrolase (MGH) after Vogel et al. Our results have shown a significant decline of plasma T-TGL (5.32 +/- 0.34 means +/- SEM vs. 7.48 +/- 0.64 mumol glycerol ml-1 h-1; p less than 0.01), H-TGL (3.71 +/- 0.28 vs. 5.05 +/- 0.69; p less than 0.05), LPL (1.61 +/- 0.26 vs. 2.42 +/- 0.41; p less than 0.05) and MGH (558 +/- 108 mumol glycerol l-1 min-1 vs. 1,165 +/- 45; p less than 0.001) activities. Thus, feeding a sucrose-rich diet induced a state of hyperlipemia and insulin resistance in which not only plasma T-TGL but also H-TGL and MGH activities were significantly decreased. This suggests that the latter two enzymes are also under nutritional and/or hormonal control.
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PMID:Post-heparin plasma hepatic triglyceride lipase and monoglyceride hydrolase activities in hyperlipemia induced by a sucrose rich diet. 661 28

In psoriatic patients with hyperlipidemia we studied the hepatic lipid synthesis from (1-(14)C)-acetate in human liver biopsy specimens in vitro by a thin-layer radio-chromatography. In psoriatics type IV (according to Fredrickson) a significant increase in (1-(14)C)-acetate hepatic incorporation especially into phospholipids (25%) and triglycerides (52%) was observed; in type IIb increased lipogenesis was phospholipids (24.5%), free cholesterol (44.4%) and triglycerides (29%). Abnormal lipid metabolism often coexists with glucose intolerance in psoriasis; no correlation between hyperinsulinemia and augmented (1-(14)C)-acetate incorporation into hepatic triglycerides was found.
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PMID:Lipid synthesis from the liver in patients with psoriasis. 701 Dec 16

Experiments on rats with hyperlipemia induced by carbohydrates have been shown that synthesis of apoprotein B by the liver and its relative content in very low-density proteins (VLDP) of the liver and blood increase. This is accompanied by accelerated metabolism of C-III in blood VLDP and by hyperinsulinemia suggesting that hyperinsulinemia may be regarded as one of the mechanisms by which there occurs hyperlipemia under high carbohydrate diets.
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PMID:[Etiologic mechanisms of carbohydrate-induced hyperlipemia]. 702 Jul 94

The response of the thoracic aorta to balloon-catheter-induced endothelial denudation was studied in two animal models of diabetes: the obese Zucker rat and the streptozotocin-treated Wistar rat. The obese Zucker rat, an animal with a metabolic profile similar to that of noninsulin-dependent human diabetics, was characterized by excessive body weight, hyperinsulinemia, hyperlipidemia, and a mild increase in plasma glucose levels. In Zucker rats sacrificed 3 weeks after endothelial denudation, the cross-sectional areas of the fibrocellular intimal lesions were found to be approximately twice as large as those of the lean control. In all other respects, the morphology of the lesions in the obese rats, as assessed by both light and transmission electron microscopy, was similar to that of the lean control rats. In streptozotocin-treated Wistar rats, neither the cross-sectional areas nor the morphology of the intimal lesions differed from those in control rats. These results indicate that, in the obese Zucker rat, the response to aortic intimal injury is altered.
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PMID:Response of the aorta of the obese Zucker rat to injury. 702 12

The fa-gene was transferred from the Zucker rat (13 M strain) to the Wistar Kyoto (WKY) rat. The survey, performed at the 10th generation of backcrossing, showed that Wistar fatty rats (fa/fa), a congenic strain of WKY, developed obesity and obesity-related features, such as hyperinsulinemia and hyperlipemia, in the same manner as Zucker fatty rats. Males, but not females, showed hyperglycemia, glucosuria, and polyuria as early as 8 wk of age. Tolerance and insulin response to oral glucose were decreased with advancing age in males. The diabetic changes appeared to be caused by an interaction between predisposition to develop diabetes in the WKY rat and fa-induced obesity. This is because WKY rats were found to be less sensitive to insulin than Zucker rats by both the glucose tolerance test and the steady-state blood glucose method which estimates overall insulin sensitivity.
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PMID:A new genetically obese-hyperglycemic rat (Wistar fatty). 703 Aug 30

Changes in a number of morphological and biochemical parameters were observed in genetically obese Zucker rats and in lean controls between 3 and 58 weeks of age. By 3 weeks, the genetically obese rats had higher proportional (wt/100 g body wt) and absolute amounts of adipose tissue, hyperlipemia affecting all the lipid fractions, and hyperproteinemia compared to lean controls. Obesity, hepatomegaly, high concentrations of hepatic lipids and hyperinsulinemia did not appear until the fifth week. In obese animals, liver lipid concentration reached a maximum at 17 weeks of age and then declined. During this time, the triacylglycerol concentration in the serum remained stable, whereas the cholesterol and phospholipid concentrations continued to increase. The glycogen concentration in obese animals increased, both absolutely and compared to lean controls, between the 12th and 43rd weeks of age. From weaning, the Zucker rats, compared to lean controls, exhibited characteristics of obesity (accumulation of adipose tissue, hyperlipemia and hyperproteinemia), which persisted to the age of 58 weeks.
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PMID:Age-related changes in biological parameters in Zucker rats. 703

Chromium deficiency may cause insulin resistance, hyperinsulinemia, impaired glucose tolerance, and hyperlipidemia, recovered by chromium supplementation. The effect of chromium supplementation on serum lipids and glucose tolerance was tested in a double-blind 12-wk study of 23 healthy adult men aged 31 to 60 yr. Either 200 micrograms trivalent chromium in 5 ml water (Cr) or 5 ml plain water (W) was ingested daily 5 days each week. Half the subjects volunteered for glucose tolerance tests with insulin levels. At 12 wk high-density lipoprotein cholesterol increased in the Cr group from 35 to 39 mg/dl (p less than 0.05) but did not change in the water group (34 mg/dl). The largest increase in high-density lipoprotein cholesterol and decreases in insulin and glucose were found in those subjects having normal glucose levels together with elevated insulin levels at base-line. The data are thus consistent with the hypothesis that Cr supplementation raises high-density lipoprotein cholesterol and improves insulin sensitivity in those with evidence of insulin resistance but normal glucose tolerance.
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PMID:Effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein of adult men. 703 73

The spiny mouse Acomys cahirinus, which exhibits beta-cell hyperplasia but low insulin secretion in captivity responded with hyperlipidemia without obesity or diabetes on a sucrose diet and became obese, and glucose-intolerant on a diet of fat-rich seeds. A three-month sucrose diet induced a marked rise in the activity of regulatory enzymes of glycolysis and lipogenesis in the liver but not in adipose tissue. There was also increased energy waste on this diet evident from a three-fold rise in the activity of hepatic mitochondrial FAD-glycerophosphate oxidase associated with an elevation in circulating triodothyronine. The obesity in mice maintained for three months on fat rich seeds was associated with moderate hyperglycemia, mild hyperinsulinemia and little change in circulating lipids. There was a decrease in the activity of glycolytic and lipogenic enzymes both in the liver and adipose tissue. Adipose tissue lipoprotein lipase activity rose, suggesting that the chylomicrons carrying the exogenous fat were better assimilated than the very-low-density lipoproteins synthesized from the dietary carbohydrate. Along with adipose tissue gain, triglyceride deposition was apparent in several muscles, accompanied by increased tissue free fatty acid, citrate and glycogen content. This suggested relation of increased muscle fat utilization with decreased glucose metabolism and insulin sensitiveness. Diverse responses to diets were thus elicited, which were particularly discernible in desert animals surviving on a limited caloric intake. Detailed follow up of these enzymatic and endocrine adaptation patterns to selective nutritional affluence may promote the understanding of the mechanisms leading to hyperlipidemia with leanness and normal glucose homeostasis versus obesity with diabetes but without hyperlipidemia.
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PMID:Intermediary metabolism during the development of obesity and diabetes in the desert rodent Acomys cahirinus. 711 67


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