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

A catabolic and hypolipemic effect of glucagon has been described in normal animals. We therefore studied the role of glucagon in genetically obese, hyperlipemic rats. Twelve genetically obese hyperlipemic LA/N-cp/cp (corpulent) rats and 12 lean littermates were fed either 54% starch or 54% sucrose for 12 weeks. Plasma glucagon and insulin levels and glucagon and insulin binding to liver membranes were measured. Comparing all corpulent and lean animals regardless of diet, a significant (P less than 0.0001) phenotypical effect (cp/cp greater than lean) was observed in plasma insulin levels (464 +/- 54 vs 70.3 +/- 7.6 muu/ml, mean +/- SEM). Insulin binding (2.68 vs 16.1%/50 micrograms protein) and glucagon binding (25.6 vs 47.3%/50 micrograms protein) were both significantly lower (P less than 0.0001) in corpulent rats as compared to their lean littermates. Sucrose feeding had marginal effect on plasma insulin or insulin binding. It, however, decreased glucagon binding in corpulent rats but not in their controls. A significant negative correlation was observed between plasma insulin and insulin binding, while a positive correlation was seen for plasma glucagon and glucagon binding. A significant negative correlation was observed between plasma glucagon and lipogenic enzymes (glucose-6-phosphate dehydrogenase and malic enzyme) in liver and between glucagon binding and these enzymes. We propose that in these genetically obese rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target cells may be an important contributor to the hyperlipemia and obesity. A further decrease in glucagon binding in rats fed sucrose indicates that sucrose, per se, may be an additional contributory factor.
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PMID:Genetic obesity and dietary sucrose decrease hepatic glucagon and insulin receptors in LA/N-corpulent rats. 300 53

Obese Zucker rats are hyperlipemic and mildly hyperglycemic. Because insulin and glucagon are involved in lipid and carbohydrate metabolism and they act via their receptors, we investigated the role of insulin and glucagon receptors in obese and lean female Zucker rats. Because dietary sucrose is more lipogenic than starch, we also studied the effect of dietary carbohydrates on the receptors. Significant phenotypic effect (obese greater than lean) was observed on plasma levels of glucose, triglyceride and insulin. Binding of insulin and glucagon to liver plasma membranes was significantly lower in obese rats than in lean rats. Lower insulin binding was due to a lower number of receptors as well as a lower affinity, whereas the lower glucagon binding was due only to a lower receptor number. Insulin binding in lean rats but not in obese rats was lower in sucrose-fed than in starch-fed rats. Diet had no effect on glucagon binding. We propose that in obese Zucker rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target tissues may be an important contributor to the hyperlipemia and obesity.
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PMID:Effect of dietary carbohydrates on glucagon and insulin receptors in genetically obese female Zucker rats. 303 87

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

A 3-year-old child with glycogenosis due to hepatic phosphorylase kinase deficiency is described. His clinical presentation was unusually severe. Biochemical studies revealed a lack of hypoglycemia, the presence of marked ketosis and hyperlipidemia, and a normal glycemic response to glucagon and to loading with galactose, fructose, and alanine. The ketosis was reversed by glucagon administration. Changes in plasma concentrations of lactate, pyruvate, beta-OH butyrate, and alanine in response to glucagon, galactose, fructose, and alanine administration are reported. The child responded poorly to a high protein diet. His condition improved markedly with a high carbohydrate diet. The significance of the findings is discussed.
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PMID:Clinical and laboratory observations in a child with hepatic phosphorylase kinase deficiency. 345 48

Circulating levels of insulin, glucagon, thyroid hormones as well as lipid levels were determined in an obese strain of chicken and their lean controls. Hepatic and muscle glycogen and lipids were also measured. Obese birds had higher plasma lipids accompanied by significantly higher insulin and lower glucagon levels compared to lean controls. Hepatic and muscle triglycerides were also higher in obese birds. Plasma T4 level was significantly higher in obese but T3 was not different in the two groups. Results suggest that genetically obese birds have significantly increased insulin/glucagon ratios as previously reported in the PTU induced hypothyroid-obese chicks (Horm. Metab. Res. 12: 51, 1980) and this could have causal relationship to hyperlipidemia and obesity observed in these birds.
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PMID:Possible role of pancreatic insulin and glucagon in the hyperlipidemia and obesity of obese strain of chicken. 351 30

1. GSD-I is described in a child with partial deficiency of hepatic glucose-6-phosphatase. 2. Growth retardation and hepatosplenomegaly were major clinical features. 3. Hyperlipidaemia, lactic acidaemia, hyperuricaemia and reduced uric acid clearance were major biochemical findings. 4. Although the glucose response to glucagon and galactose was impaired, there was a striking absence of hypoglycaemia which may be attributable to residual catalytic activity of the enzyme. 5. Preliminary studies of the crude liver enzyme showed it to have a normal pH inactivation profile and apparent Km with a reduced Vmax. 6. No evidence of increased PP-ribose-P availability in fresh liver tissue was detected. 7. Continuous glucose feeding resulted in accelerated growth without complete correction of lactic acidosis or hyperuricaemia. 8. GSD-I with partial deficiency of hepatic glucose-6-phosphatase should be considered in patients with gout or hyperuricaemia associated with hypertriglyceridaemia and lactic acidaemia even in the absence of hypoglycaemia.
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PMID:Clinical and enzymological studies in a child with type I glycogen storage disease associated with partial deficiency of hepatic glucose-6-phosphatase. 615 47

The effect of long-term oral synthetic protease inhibitor (FOY 305) administration on fasting blood sugar (FBS), body weight, glucose tolerance, plasma insulin and glucagon levels, pancreatic insulin and glucagon contents, hepatic enzyme activities, and plasma lipids in normal and streptozotocin (STZ)-induced diabetic rats was studied. Normal rats treated with oral FOY 305 for 9 weeks were found to have pancreatic hypertrophy and decreased body weight gain as compared with the untreated normal controls. FBS, glucose tolerance, plasma insulin and glucagon levels, pancreatic insulin and glucagon contents, and plasma lipids were uninfluenced in FOY 305 treated normal rats. STZ-induced diabetic rats treated with oral FOY 305 were found to have decreased FBS for 5 weeks after the beginning of FOY 305 administration as compared with the untreated diabetic controls, whereas at the 7th and 9th week after treatment there was no difference in FBS between FOY 305 treated and untreated diabetic rats. In the metabolic balance observed at the 4th week after treatment, a slight improvement of the diabetic state was found in FOY 305 treated diabetic rats. There was no apparent difference in the blood sugar curve and insulin response following oral glucose load between diabetic rats treated for 7 weeks and untreated diabetic rats. All the rats were sacrificed after 9 weeks of treatment. Diabetic rats treated with oral FOY 305 for 9 weeks showed pancreatic hypertrophy and decreased plasma glucagon level and decreased pancreatic glucagon content as compared with the untreated diabetic controls, whereas there was no difference in body weight, plasma insulin level and pancreatic insulin content between FOY 305 treated and untreated diabetic rats. Furthermore, oral FOY 305 treatment improved hyperlipidemia in STZ-induced diabetic rats and also significantly improved the hepatic pyruvate kinase and phosphoenlpyruvate carboxykinase activities of diabetic rats. These improvements might partly be due to a decreased pancreatic content and secretion of glucagon and/or a direct action of the synthetic PI, FOY 305 to tissues.
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PMID:[The effect of oral synthetic protease inhibitor (FOY 305) on endocrine pancreas and carbohydrate and lipid metabolism in normal and streptozotocin-induced diabetic rats]. 638 47

Is is well known from laboratory investigations and acute intervention studies that glucagon is involved in lipid metabolism. The present study was undertaken in order to evaluate a possible sustained effect of zinc-protamin-glucagon in moderately hyperlipidaemic patients. 4 patients were investigated after an acute bolus dose of glucagon 5 mg intravenously and 16 patients were given zinc-protamin-glucagon 5 mg subcutaneously, b.i.d. for 5 days. A similar degree of decrease of plasma cholesterol and triglycerides was obtained in the acute and chronic study, while the increase in fasting blood sugar and plasma insulin seen in the acute study was not present after 5 days treatment. The effect on plasma triglycerides was much more variable than the effect on plasma cholesterol. Five days after treatment the lipid concentrations had returned to the pretreatment values. The effect could not be predicted from the pretreatment lipid concentrations, neither by the type of hyperlipidaemia present. The decrease in plasma cholesterol and triglycerides were not correlated. The drug might prove useful in the long term research of lipid metabolism and the various complex hormonal interactions.
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PMID:Sustained effect of zinc-protamin-glucagon in hyperlipidaemic patients. 663 8

Individuals with type Ia glycogen storage disease (glucose-6-phosphatase deficiency) frequently develop hepatic adenomas. Potential complications involving these adenomas include malignant transformation and hemorrhage. Five of 9 patients with this disease had evidence of hepatic filling defects on radionucleotide liver scan when first evaluated at our hospital. Dietary therapy aimed at preventing hypoglycemia was begun in 7 of the 9 patients. Prevention of hypoglycemia resulted in the correction of all of the metabolic abnormalities (lactic acidosis, hyperlipidemia, hyperuricemia, and growth retardation). Treatment also corrected the marked elevation in plasma glucagon concentrations. A disappearance of the hepatic lesions occurred in 2 of the treated patients, and a marked reduction in size of the adenoma occurred in the third patient. The hepatic filling defects remained present in the two untreated patients. None of the affected patients receiving dietary therapy have developed hepatic adenomas. One of these patients is now 22 yr old and has received dietary therapy for 7 yr. Early dietary therapy seems to be effective in preventing development of adenomas as well as inducing their resolution.
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PMID:Regression of hepatic adenomas in type Ia glycogen storage disease with dietary therapy. 694 8

Resistance to both insulin and glucagon have been considered as possible causes of primary hypertriglyceridemia. In the present research, we have compared insulin and glucagon secretion in five hyperlipidemic patients with familial dysbetalipoproteinemia with five normolipidemic control subjects matched for age, sex and adiposioty. Plasma insulin and glucagon concentrations mesaured during standard oral glucose tolerance and arginine infusion tests were similar in the two groups. Blood glucose fell transiently in the controls, but not in the patients, during the Himsworth test (100 g glucose orally plus 0.05 U insulin per kg body weight intravenously). There were no significant differences in plasma FFA concentrations and responses during all tests between the groups. The percentage reduction in plasma triglyceride concentration during infusion of arginine was similar in the two groups. These results suggest that the patients with familial dysbetalipoproteinemia were slightly less insulin sensitive than the controls. However, primary insensitivity to glucagon or insulin does not appear to be fundamental to the pathogenesis of hyperlipidemia in familial dysbetalipoproteinemia.
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PMID:Pancreatic alpha and beta cell function in familial dysbetalipoproteinemia. 700 Jun 52


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