Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malnutrition is common among alcoholics because alcohol displaces protein-, vitamin-, and mineral-containing foods in the diet, and chronic alcohol consumption results in maldigestion and malabsorption of essential nutrients. In addition, alcohol exerts direct toxic effects on both the liver and gut, resulting in structural alterations in the intestine and the development of fatty liver, alcoholic hepatitis, and cirrhosis. Liver injury is preceded by an adaptive phase characterized by accelerated metabolism of drugs (including ethanol), and hyperlipemia, secondary to hypertrophy and hyperactivity of the smooth endoplasmic reticulum. Side effects include enhanced hepatotoxicity of CCI4 and possibly energy wastage. Alcoholics should not be led to beleive that correction or prevention of nutritional deficiency will prevent liver damage in the face of continued alcohol abuse.
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PMID:Alcohol and malnutrition in the pathogenesis of liver disease.. 117 54

10 to 20% of [1-14C] palmitate injected into pregnant guinea pigs was recovered in lipids of their fetuses. From these data and the rate of transport of palmitate in maternal blood, it appears that placental transport of free fatty acids can account for the accumulation of lipids in late gestational fetuses. About 80% of the labeled palmitate in the fetus appeared initially in lipids of the liver. 14C appeared in plasma triglyceride fatty acids after a few minutes and subsequently accumulated in lipids of white and brown adipose tissue, suggesting that much of the palmitate deposited in adipose tissue were derived from hepatogenous triglyceride fatty acids. By contrast, 14C was usually maximal in heart and carcass lipids before it appeared in plasma triglyceride fatty acids. Lipoprotein lipase activity in fetal adipose tissue was low, and activity of cofactor protein of lipoprotein lipase in fetal blood plasma was much lower than that observed in other mammalian species. On the basis of these and earlier observations, it is concluded that the accumulation of triglycerides in liver and blood plasma of fetal guinea pigs during late gestation is at least partly the result of the large uptake of maternally derived free fatty acids by the fetal liver accompanied by rapid synthesis and secretion of triglyceride-rich very low density lipoproteins into the blood. However, limited uptake of triglyceride fatty acids in adipose tissue may contribute to the fatty liver and hyperlipemia.
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PMID:Genesis of fatty liver and hyperlipemia in the fetal guinea pig. 119 88

The macroscopic and microscopic findings of a case of Zieve's syndrome are described (fatty liver, icterus, hyperlipemia and hemolytic anemia in chronic alcoholism). The outstanding macroscopic finding is milky turbidity of the blood in arterial and venous vascular channels as well as hepatomegaly and anaemia of internal organs. A prominent feature of the histological picture is the high-grade lipaemia of the large and small vessels (arteries and veins), capillary occlusions resembling fat embolism in all organs and severe diffuse fatty metamorphosis of the liver. Circulatory disorders and the cause of death are discussed.
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PMID:[Morphological findings in Zieve's syndrome (author's transl)]. 121 21

A model has been developed for the administration to rats and baboons of ethanol as part of a nutritionally adequate liquid diet. With this regimen, ethanol intake was much higher than with conventional procedures. All animals gained or maintained their body weight, and liver morphology was normal in the controls. Isocaloric substitution of carbohydrate by ethanol (36% of total calories in rats and 50% in baboons) resulted in the production of fatty liver in all animals, while the baboons also developed alcoholic hepatitis and cirrhosis with increased activities of serum glutamic oxaloacetic transaminase. Inebriation and manifestation of dependence upon withdrawal of the diet were observed in baboons and quantitated in the rat. Chemical alterations produced by ethanol at the fatty liver stage were characterized by hyperlipemia, striking triglyceride accumulation in the liver and enhanced activities of microsomal drug metabolizing enzymes, including the microsomal ethanol oxidizing system (MEOS). Ultrastructural changes of the mitochondria and the endoplasmic reticulum were already present at the fatty liver stage and persisted throughout the hepatitis and cirrhosis. The lesions were similar to those observed in alcoholics (including the inflammation and the central sclerosis), and differed strikingly from the alterations produced by other models of liver injury. In showing that all aspects of liver injury observed in alcoholics can be reproduced in animals by the feeding of pure ethanol with an adequate diet, this study incriminates ethanol itself as a cause for the hepatic complications. This new experimental model is proposed as a tool for the study of the pathogenesis and treatment of alcoholic liver injury and dependence.
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PMID:Alcoholic liver injury: experimental models in rats and baboons. 123 25

Obesity is associated either with hepatic steatosis, a well known and innocuous entity or with non alcoholic steatohepatitis. This latter lesion has been recently individualized. It affects mainly middle-aged, obese women, with diabetes and/or hyperlipidaemia. It is morphologically very similar to alcoholic hepatitis. We review the literature considering 1) histologic hepatic lesions of the obese, 2) epidemiologic, clinical and biological characteristics of the non alcoholic steatohepatitis, 3) evolution and treatment of the non alcoholic steatohepatitis and 4) present physiopathological considerations. We conclude by considering the clinician's attitude in front of an obese potentially afflicted by a non alcoholic steatohepatitis.
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PMID:[Obesity: danger for the hepatocytes?]. 133 21

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

Mortality, morbidity, liver function and regeneration were evaluated in dogs that had undergone simultaneous major resection of the liver and the pancreas. The 10-week survival rate was only 25% in the dogs that underwent 70% hepatectomy with more than 92% pancreatectomy, and many of them died of liver failure. Long-term survival was observed in more than 60% of the dogs after 70% hepatectomy with less than 92% pancreatectomy or after 40% hepatectomy with more than 92% pancreatectomy. The liver regeneration rate was reduced with the extent of the pancreatectomy, and the reduction was remarkable especially when more than 92% of the pancreas was resected. The frequency of diabetes was reduced when the pancreatectomy was combined with hepatectomy. Hyperlipemia and fatty liver were noted in all the dogs of the group that underwent more than 92% pancreatectomy alone. They were observed also in the postoperative diabetic groups but not in non-diabetic groups. The postoperative recovery of hepatic function and liver regeneration were delayed after simultaneous hepatectomy-pancreatectomy. Also, postoperative carbohydrate and lipid metabolism was better maintained in the hepatectomy-pancreatectomy groups than in the pancreatectomy-alone groups.
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PMID:Simultaneous extensive resection of the liver and the pancreas in dogs. 176 48

To determine whether the estrogen-induced hyperlipidemia is affected by fasting, male growing chicks were administered subcutaneously a single dose of 17 beta-estradiol (25 mg/kg body wt), and the hormone treatment lasted for 2 days with or without feed (Experiment 1). In the second experiment, chicks were initially fasted for 1 or 3 days, and then treated with the same dosage of 17 beta-estradiol as in Experiment 1 for 2 days without feed. Plasma and liver lipids, and the activities of hepatic malic enzyme, glucose-6-phosphate dehydrogenase, and hormone-sensitive lipase in the adipose tissue were determined. Compared with fed control chicks, estrogen treatment in fed birds resulted in a marked elevation of plasma lipids, especially triglyceride during the 2-day period (137 vs 2263 mg/dl). In fasted chicks, the present finding that estrogen also induced a marked hyperlipidemia is noteworthy. Upon estrogen treatment (Experiment 1), the level of plasma triglyceride in fasted birds increased about 16 times over that of the fasted control group (133 vs 2093 mg/dl). Even in chicks fasted for 5 days (Experiment 2), estrogen treatment resulted in a persistent hypertriglyceridemia (75 vs 1369 mg/dl). In fed chicks, estrogen treatment also induced a fatty liver with massive accumulation of triglyceride, but the liver of estrogen-treated/fasted chicks appeared to be normal. In both fed and fasted chicks, malic enzyme was found to be the major NADPH producing enzyme in the liver. Upon fasting, both malic enzyme and glucose-6-phosphate dehydrogenase activities decreased significantly (P less than 0.05). In fed chicks, the total activities of both enzymes increased with estrogen treatment, whereas the effect of hormone on these enzymes was less obvious in fasted chicks. The hormone-sensitive lipase activity in the adipose tissue was much lower in fed chicks compared with that of fasted birds (0.15 vs 0.33 nmol of oleic acid released/min/mg protein). Estrogen treatment in fed chicks had no effect on the hormone-sensitive lipase activity, but its activity was enhanced by the hormone treatment in fasted chicks. The present finding that hyperlipidemia persisted in estrogenized chicks during the fasting seems to indicate the complex nature of this hormonal influence on lipid metabolism.
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PMID:Estrogen induces hyperlipidemia in fasted chicks. 230 May 91

Zieve's syndrome (hyperlipidaemia, anaemia and fatty liver degeneration) may rarely occur with intracranial haemorrhage. Four patients suffering from both diseases are reported. Although it remains unclear whether there is a causal relationship between the two, it seems that hyperlipidaemia may be a major cause of intracranial bleeding. One reason for the small number of reported cases may be that hyperlipidaemic serum levels rapidly decrease after alcohol withdrawal.
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PMID:Zieve's syndrome and intracranial haemorrhage: coincidence or related disorders. 235 37

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


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