Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estramustine phosphate (Estracyt), a combination of estradiol and nitrogen mustard given to males with prostatic carcinoma, had the same effect on serum lipids, lipoproteins, and serum phosphoglyceride fatty acid composition as ethynyl estradiol (Etivex). The characteristic effects on serum lipids caused by both drugs, i.e., a reduction in serum cholesterol and an increase in serum phospholipids, were apparently expressions for reduced low density lipoproteins and increased alpha-lipoproteins. Serum lecithin fatty acid composition revealed during the administration of both drugs a characteristic increase in palmitic acid (16:0) and a decrease in stearic acid (18:0), interpreted as evidence for a cholestatic, although subclinical, liver involvement. Similar changes have earlier been revealed in women given ethynyl estradiol; however, the increase in serum triglycerides and very low density lipoprotein cholesterol in young women was not duplicated in aged males with prostatic carcinoma. Furthermore, in aged males, the administration of these estrogens did not change carbohydrate metabolism but did produce an increase in adipose tissue lipoprotein lipase.
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PMID:Treatment of oral estramustine phosphate (Estracyt) in prostatic carcinoma: influences on lipid and carbohydrate metabolism. 59 Dec 68

The lipid metabolic disorders in chronic renal insufficiency (CRI) are related to increased hepatic lipid synthesis, reduced triglyceride removal coupled with insulin insensitivity and impaired lipoprotein lipase activity. Growth hormone is lipolytic, and the effects of recombinant human growth hormone (rhGH) on the hypercholesterolemia of CRI are unsettled. To test this question, we gave rhGH for 14 days at a dosage of 3 units/day intraperitoneally to two-stage, 5/6 nephrectomized, male Sprague-Dawley rats (n = 18) compared to sex- and age-matched control (n = 27) and CRI (n = 40) rats. At the end of the study, CRI rats and those treated with rhGH had a similar degree of renal impairment, as assessed by serum concentrations (mean +/- SEM) of urea nitrogen (49 +/- 3 vs. 54 +/- 4 mg/dl), creatinine (0.9 +/- 0.0 vs. 1.0 +/- 0.1 mg/dl) and cumulative food intake (311 +/- 8 vs. 290 +/- 12 g). Serum urea nitrogen (16 +/- 4 mg/dl) and creatinine (0.4 +/- 0.1 mg/dl) concentrations as well as food intake (412 +/- 9 g) of control rats were significantly (p < 0.0001) different. Serum cholesterol concentration of CRI rats treated with rhGH (87 +/- 3 mg/dl) was not higher than those of CRI rats (81 +/- 2 mg/dl, p < 0.1338) but was significantly higher than in control rats (55 +/- 3 mg/dl, p < 0.0001). CRI rats treated with rhGH showed a similar serum albumin concentration and lower serum glucose than CRI rats (0.9 +/- 0.1 vs. 0.9 +/- 0.0 g/dl and 144 +/- 4 vs. 163 +/- 3 mg/dl, p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypercholesterolemia in rats with chronic renal insufficiency not aggravated by recombinant human growth hormone. 147 89

This study was designed to determine the effects of colostral fat on energy metabolism, fat oxidation and glucose homeostasis in newborn pigs maintained during the first 29h of life at thermal neutrality (34 degrees C) or in the cold (21 degrees C). Piglets were intragastric fed normal colostrum (NFC, 6% fat) or colostrum deprived of fat (LFC, less than 1% fat). A total of 21 meals of 15 to 18g colostrum/kg birthweight was given at 65- to 70-min intervals. Feeding NFC resulted in a higher amount of retained fat with the highest value being obtained in the 34 degrees C group (P less than 0.01). Fat oxidation represented 47% of the absorbed fat in NFC-fed piglets at 34 degrees C; it was 4.5 fold higher in piglets fed NFC than in those fed LFC (P less than 0.01), and 1.8 fold higher at 21 degrees C than at 34 degrees C (P less than 0.01). At both temperatures, feeding LFC resulted in a lower energy balance (P less than 0.01), whereas nitrogen balance was not affected by temperature and colostrum treatments. At 29 hours of age, rectal temperature was the lowest in piglets fed LFC at 21 degrees C (P less than 0.05). Postnatal enhancement of fat metabolism in relation to environmental and nutritional conditions was evidenced at the tissue level through an adaptation of lipoprotein lipase and cytochrome oxidase activities, especially in the red rhomboideus muscle and the liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of colostral fat to thermogenesis and glucose homeostasis in the newborn pig. 152 69

Changes in lipoprotein lipase (LPL) activity during pregnancy and lactation were followed in skeletal muscles and interscapular brown adipose tissue (BAT) of rats fed two diets differing in energy density (high carbohydrate or high fat). Rats were decapitated after 7, 19 or 21 d of pregnancy or after 3 or 12 d of lactation. Virgin rats and females separated from their litter just after delivery were used as nonpregnant and nonlactating controls, respectively. Blood was collected for determination of plasma glucose, triglycerides (TG) and nonesterified fatty acids (NEFA). Soleus, extensor digitorum longus (EDL), diaphragm and interscapular BAT were rapidly removed and frozen in liquid nitrogen for LPL activity measurement. LPL activity was not significantly higher in muscles and BAT of virgin rats fed the high fat diet than in those of rats fed the high carbohydrate diet. No significant change of skeletal muscle LPL activity was observed during pregnancy, regardless of the diet fed. Although BAT exhibited a transitory hypertrophy during pregnancy, its LPL activity was not significantly altered; during lactation BAT lost weight and its LPL activity dropped sharply when either diet was fed, leaving more TG available for milk production.
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PMID:Lipoprotein lipase activity in skeletal muscle and brown adipose tissue of pregnant and lactating rats. 355 50

Food availability was arranged so that episodes of feeding were separated by long periods of deprivation. Distinctly different contexts were associated with each condition. For other animals, relatively short periods of deprivation stood in contrast to relatively long opportunities to free-feed, and were also embedded in widely differing physical contexts. These temporal relationships among the conditions were adjusted to sharpen the saliency of each metabolic condition and thereby enhance its associability with the distinctive environment in which each occurred. To avoid the possibility of circadian entrainment, the feeding or deprivation episodes occurred at unpredictable times according to a variable-time schedule. Following several training cycles and an extended period of free-feeding in a neutral environment, the animals were reexposed to the various contexts and sacrificed for metabolite assays. The environment predictive of feeding elevated adipocyte lipoprotein lipase activity and lowered the levels of serum free fatty acids. The deprivation context boosted serum triglycerides and blood urea nitrogen. The conditioned responses were all of a compensatory nature: Feeding cues resulted in accelerated caloric deposition, deprivation cues elicited conditioned mobilization of stored energy. While protein catabolism and several indices of fat metabolism appear to be conditionable, no evidence of environmental control of glycemic responses was observed.
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PMID:Environmental control of energy metabolism in rats. 368 62

In malnutrition lipoprotein lipase activity in the liver and the beta-lipoprotein concentration in serum are reduced. The lipolysis is increased. One suspected a reduction of fat elimination in such patients. In 10 malnourished patients with a mean body weight of 73% ideal body weight an intravenous fat tolerance test was performed. The elimination rate was in mean 5.77%/min, that is in the normal range. Studies with radioactive triglycerides showed a metabolization of 30% of infused fat during 24 hours. These results were confirmed by measurements of gas exchange. Energy expenditure and nitrogen balance in malnourished patients correlate with the energy intake but not with the amount of fat in the parenteral nutrition. That could be confirmed in a prospective randomized study in 8 malnourished patients. The carbohydrate oxydation provided 70% to 80% of total energy expenditure independent from the dosage of fat in these patients. The minimum of fat needed in total parenteral nutrition to avoid essential fatty acid deficiency is 100 g per week. The tolerable maximum dose ist not known. In 10 malnourished patients with a mean time of 36 days of parenteral nutrition a dosage of 2.5 g/kg X d-1 was well tolerated and no side effects were seen. In 3 of these patients a previous cholostasis improved during parenteral nutrition.
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PMID:[Fat in the parenteral feeding of malnourished patients]. 641 15

In two separate trials male and female Wistar rats, 12 weeks of age, were either killed as a preliminary control group, ad lib.-fed or undernourished for 4 weeks until one-third of their 12-week body-weight was lost. Food intakes, urinary and faecal collections and measurements of standard metabolic rate were made at one-weekly intervals on both the ad lib.-fed and undernourished animals of both sexes. The bodies of the preliminary controls, the ad lib.-fed and the undernourished animals of both sexes were analysed for protein and fat, and the weights of four fat depots, two muscles and the major organs of all groups were determined. Measurements of lipid synthesis rate (LSR) and lipoprotein lipase (EC 3.1.1.34) (LPL) activity in the four fat depots and measurements of whole-body protein synthesis rates were carried out on animals of both sexes in each group. Although both sexes lost the same proportion of body-weight the females required more food on a body-weight basis than the males during the undernutrition period. The females absorbed significantly more energy on a body-weight basis during undernutrition and so were less efficient than the males at withstanding nutritional stress. There were no significant differences between males and females, on a body-weight basis, in the excretion of nitrogenous waste products (urinary nitrogen, creatinine, hydroxyproline or NT-methylhistidine) suggesting that there were no differences between the sexes in protein sparing during undernutrition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of male and female rats to undernutrition. 1. Changes in energy utilization, body composition and tissue turnover during undernutrition. 647 63

Apart from being a stimulator of longitudinal growth, growth hormone (GH) regulates fuel metabolism in children and adults. A halfmark is mobilization of lipids, which involves an inhibition of lipoprotein lipase activity in adipose tissue and activation of the hormone sensitive lipase. Suppression of basal glucose oxidation and resistance to insulin are other important effects. This may cause concern during GH substitution in GH-deficient adults, some of whom may present with insulin resistance due to concomitant abdominal obesity. However, there are data to suggest that the GH-induced reduction in fat mass and increase in lean body mass may offset the insulin antagonistic actions of the hormone. The nitrogen-retaining effects of GH seem to involve a direct stimulation of protein synthesis in addition to secondary effects such as generation of insulin-like growth factor-I (IGF-I), hyperinsulinemia, and promotion of lipolysis. Thus, during periods of substrate affluence, GH acts in concert with insulin and IGF-I to promote protein anabolism. Postabsorptively, GH is primarily lipolytic and thereby indirectly protein-sparing. This effect becomes further accentuated with more prolonged fasting. In that sense, GH is unique by its preservation of protein during both feast and famine. These fuel metabolic effects add merit to the principle of GH substitution in hypopituitary adults.
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PMID:Fuel metabolism in growth hormone-deficient adults. 747 1

We examined the effects of dietary n-3 polyunsaturated and saturated fatty acids on the development of the atherogenic process in mice and on the macrophage ability to secrete several effector molecules that may be involved in the atherogenic process. The secretion of inflammatory proteins such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) and the production of lipoprotein lipase (LPL), nitrogen oxide (NO2), and prostaglandin E2 (PGE2) were evaluated in peritoneal macrophages isolated from atherosclerosis-susceptible C57BL/6J mice. The mice were assigned at random to three experimental groups: the first group was fed a semi-defined control diet (control diet); the second group was maintained on the control diet supplemented with 10% menhaden oil (menhaden diet); and the third group received the control diet supplemented with 10% palm oil plus 2% cholesterol (saturated fat diet). Macrophages derived from mice fed the menhaden diet showed a suppression of their basal TNF-alpha mRNA expression and production. They also presented a dramatically decreased ability to express TNF-alpha and IL-1 beta mRNAs in response to exposure to lipopolysaccharide (LPS) compared with the macrophages from the control group. LPL mRNA and protein expression were downregulated after 6 and 15 weeks of menhaden-diet feeding. Significantly higher NO2 production in response to interferon gamma was found, both after 6 and 15 weeks of diet feeding, in the menhaden group compared with the control group. In addition, prostaglandin production and macrophage tumoricidal activity in response to LPS were decreased in this group compared with the control group. Macrophages derived from the saturated fat group did not show any significant alterations in TNF-alpha, LPL, NO2, or PGE2 secretion compared with controls. Interestingly, we observed a progressive increase of the LPS-induced IL-1 beta gene expression and secretion among macrophages harvested from mice receiving the dietary supplement of saturated fatty acids. At 6 and 15 weeks histologic examination of the atherosclerotic lesions did not reveal any important lesions in the control and menhaden groups, whereas a gradual development of fatty streaks was observed in the menhaden experimental diets for 10 additional weeks resulted in a major development of lesions in the control group, whereas only slight lesions were observed in the menhaden group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dietary n-3 polyunsaturated fatty acids prevent the development of atherosclerotic lesions in mice. Modulation of macrophage secretory activities. 839 89

Most patients with diabetes die from macrovascular complications. Little is known about the pathogenesis of diabetic vascular disease, but recent advances in molecular genetics and oxidation chemistry provide clues to the mystery of diabetes and atherosclerosis. Genetic variants of well-known proteins such as lipoprotein lipase and apolipoprotein E are common. These proteins are suitable candidates for mediating diabetic vascular risk because their variants can produce hypertriglyceridemia, a risk factor for atherosclerosis in diabetes. However, mutations could have different effects on lipoprotein flux across arteries depending on whether expression is dominant in the vascular space or the vascular wall. Lipoproteins retained in the arterial wall are subject to oxidative modification, which could be dependent on glycoxidation, the enzyme myeloperoxidase, or reactive nitrogen species derived from nitric oxide. Accelerated vascular disease in diabetes is likely the result of complex interactions between metabolic derangements such as hyperglycemia, mutations in genes controlling lipid metabolism, and antioxidant defense mechanisms.
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PMID:The mystery of diabetes and atherosclerosis: time for a new plot. 903 85


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