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)

Metabolism of ruminant adipocytes involves the synthesis and mobilization of lipids. Rates of lipid synthesis from the uptake of preformed fatty acids (via lipoprotein lipase) and de novo synthesis of fatty acids are related to the energy balance. Acetate is the major carbon source for fatty acid synthesis with NADPH originating from the pentose cycle and the isocitrate cycle. Ruminant adipose tissue lacks the ability to utilize for lipogenesis those substrates that generate mitochondrial acetyl CoA because of an absence of ATP citrate-lyase and NADP-malate dehydrogenase. Lipid mobilization in ruminant adipocytes is apparently regulated via cAMP levels and a summary of the compounds investigated for lipolytic responses is presented. The control of lipid synthesis and mobilization is interrelated in ruminant adipose tissue. The coordinated manner in which these two functions are regulated is examined with regard to adipocyte responses to insulin and epinephrine. In both lipid synthesis and lipid mobilization, ruminant adipocytes are uniquely different from nonruminant adipose tissue. The physiological significance and possible basis for these species differences in adipose metabolism are discussed.
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PMID:Intermediary metabolism of adipose tissue. 18 55

The association between feed intake and lipogenic activity in adipose tissue was investigated in growing cattle. Twenty-five 300-kg steers were allotted by BW to one of five levels of intake of a single high-energy corn-corn silage-based diet. Steers were adapted to diets over 4 wk and intakes were adjusted weekly to achieve steady but varying rates of growth. Daily intakes (% of BW) averaged .92, 1.15, 1.64, 2.28 and 2.69 and resulted in growth rates over the final 3 wk of -.28, .07, .71, 1.67 and 1.69 kg/d, respectively. Lipogenic activities in biopsied tissue and circulating concentrations of glucose and insulin were lowest at maintenance feeding and below but increased linearly (P less than .01 for lipogenesis; P less than .1 for glucose and insulin) as intake increased above maintenance. Mean minimal and maximal rates (mumoles.-min(-1).10(6) cells(-1)) or concentrations were fatty acids synthesis ([14C]acetate---fatty acid)), .065 and .723; fatty acid synthetase (NADPH oxidized), .266 and 2.97; lipoprotein lipase (fatty acid released), .048 and .359; glucose (mg/dl), 60.4 and 70.7 and insulin (ng/ml), .70 and 1.66. In a preliminary study with the same 25 steers fed ad libitum, nearly 25% of the variability in adipose tissue lipogenesis was accounted for by variation in feed intake. Results indicate that activities of lipogenic enzymes and lipogenic capacity in growing steers coordinately adapt to the level of feed consumed and that nutrient availability and(or) insulin concentrations may participate in this adaptation.
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PMID:Adipose tissue lipogenesis in growing steers adapted to different levels of feed intake. 268 16

Fetuses were decapitated in one uterine horn in each of 14 sows at 45 d of gestation. Control (C) and decapitated (D) fetuses were removed by Caesarean section from three sows at 65 d of gestation (total of 10 D and 10 C fetuses), two sows at 85 d (six D and six C fetuses) and nine sows at 110 d (nine C and nine D fetuses) of gestation (Exp. 1). In Exp. 2, four to six fetuses were removed from each of two Ossabaw (O) gilts and three crossbred (C, Landrace X Yorkshire) gilts at 70 d of gestation, from three C and O gilts at 90 d of gestation and from three C and two O gilts at 110 d of gestation. In Exp. 1, one semitendinosis muscle was removed for histochemistry, whereas the contralateral muscle was removed and weighed. A medial portion of biceps femoris muscle was removed and used for histochemistry in Exp. 2. In both experiments, transverse sections (cryostat) of muscle were stained for lipid, glycogen (PAS) and the following enzymes: acid ATPase, NADH-TR, NADPH-TR, malate dehydrogenase (NAD- and NADP-dependent reactions; MDH), succinate dehydrogenase (SDH), alpha-glycerol phosphate dehydrogenase (with and without NAD; alpha-GPDH), isocitrate dehydrogenase (NAD dependent; ICDH), esterase, lipoprotein lipase and lipase. In Exp. 1, body and muscle weights of the two groups were not significantly different (P greater than .05) at 65 d of gestation, whereas D fetuses were smaller and had lighter weight muscles (P less than .05) at 85 d of gestation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enzyme histochemical studies in an ontogeny study of muscle development in Ossabaw and decapitated fetuses: cellular reactions. 401 46

Adipocyte synthesis de novo and lipoprotein lipase activity have been used simultaneously to measure the lipogenic activity of adipose tissue in sheep. Acetate and glucose were used as precursors of fatty acid synthesis. The sheep were raised either outdoors or in a sheepfold. They were slaughtered by lots at mean weights of 24 and 32.5 kg. Compared to lipoprotein lipase activity, de novo synthesis of fatty acids was the main way of constituting lipid depositions. Raising the sheep outdoors favored the use of glucose as precursor of lipid synthesis at the first slaughter stage at 24 kg. Later at 32.5 kg, glucose utilization was practically zero compared to acetate, whatever the mode of rearing. The NADPH production needed for fatty acid synthesis was almost entirely due to NADP isocitrate dehydrogenase activity. Variations in both de novo synthesis and in lipoprotein lipase activity in relation with rearing method and slaughter weight were especially evident in the group raised outdoors.
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PMID:[Effect of rearing method on the storage of fats by adipose tissue in sheep]. 664 30

It is largely admitted nowadays that the early stage of the atherosclerotic lesion involves formation of oxidized (and minimally oxidized) low-density lipoprotein. Their properties are briefly reviewed. It is recalled that a lipolytic process also takes place both at the lumenal surface and in the subendothelial space of the vessels implying lipoprotein lipase (LpL) activity. Recent studies emphasize the role of LpL in accumulating LDL in the vascular tissue (Rutledge & Golberg, J. Lipid Res., 1994, 35, 1152-1160), but the role of LpL-generated unesterified fatty acids (UEFA) in these two locations and their possible implication in atherogenesis are largely neglected. Physiological and pathophysiological significance of UEFA in the human adherent monocyte modulation of the superoxide anion (O2.-) production has been examined by our group, leading to a possible mechanism of modulation of LDL oxidative modification. The O2.- production-modulating effect of a 30-min UEFA preincubation has been studied in intact human adherent monocytes (HAM) after stimulation by a direct effector of protein kinase C (PKC). It has been established that UEFA alone (in the absence of PKC effectors) were not able to modulate the O2.- production of HAM whereas they had such a capacity in the presence of PKC effectors, phorbol myristate acetate (PMA) or diacylglycerol (DAG). In this case inhibitors of PKC such as GF 109203 X suppressed the modulating effect. UEFA have also been shown to possess a bimodal action in the presence of PKC effectors: they depressed or enhanced O2.- production at micromolar or nanomolar concentrations, respectively. All these results contrasted with others obtained in neutrophils or nonadherent monocytes, suggesting an absolute requirement of PKC for the phagocyte-NADPH oxydase (PHOX) activation especially in the case of HAM. In HAM, the maximal enhancing effects were obtained with monomethyl ramified saturated (MMRS) and linear unsaturated (LU) FAs such as arachidonic, eicosapentaenoic and docosahexaenoic acids (with exception of oleic, linoleic and linolenic acids which were without effect), whereas the maximal depressing effects were obtained with MMRS-FAs and LU-FAS such as oleic, linoleic and docosahexaenoic acids. Further investigations in HAM led us to examine the UEFA capacity at modulating the translocation of PKC, on the one hand, and the endogenous phosphorylation and membrane translocation of p47phox, on the other, in the presence of PMA or DAG. Using 13-methyl myristic (iso15:0) as FA model, it has been established that i) it was able to amplify or diminish PKC translocation at nanomolar and micromolar concentrations, respectively (this was also the case with arachidonic acid) ii) it enhanced and depressed the endogenous phosphorylation and the membrane translocation of p47phox at nanomolar/micromolar concentrations and iii) it was inactive in the absence of PMA or DAG. Taken together, our results strongly suggest that the active UEFA act directly on the monocyte PKC, modifying its kinase activity through interactions with PMA/DAG binding site of the regulatory domain of the protein. This leads to modulate the phosphorylation and translocation of p47phox, which in turn allows the assembling of the active PHOX complex and triggers the O2.- production. The direct action of UEFA on the PKC regulatory-domain known to strongly interact with the membrane lipids was also supported by the fact that linear saturated FAs that have already been reported to be unable to penetrate a lipid layer were devoided of effect on monocytic O2.- production. The free form of oleic and linoleic acids and, to a lesser extent, docosahexaenoic acid (in the case of oral administration of fish oil) are present at micromolar concentrations in the plasma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Modulation by some fatty acids of protein kinase C-dependent NADPH oxidase in human adherent monocyte: mechanism of action, possible implication in atherogenesis]. 867 25

Four lactating dairy cows were arranged in a 4 x 4 Latin square design to study the effect of intestinal glucose supply on milk fat synthesis. Glucose (0, 443, 963, and 2398 g/d) was continuously infused in the duodenum over 14-d periods. Grass silage-based diets were formulated to be isoenergetic and isonitrogenous and met 100 and 110% of energy and protein requirements according to INRA (1989). Mammary uptake of nutrients was estimated through assay of arteriovenous differences and blood flow measurements. Glucose infusions decreased arterial concentrations of acetate, beta-hydroxybutyrate, and nonesterified fatty acids linearly and total glycerides curvilinearly. Milk fat yield was slightly decreased (- 52 g/d) between 0 and 963 g/d of glucose and milk fatty acid composition was modified by a marked decrease in long-chain fatty acids and an increase in de novo synthesis. The decrease in long-chain fatty acids, related to the decreased mammary uptake of plasma total glycerides, was likely due to a decrease in lipoprotein lipase and esterification activities. In regards to the evolution of metabolite concentrations in milk, the enhanced de novo synthesis and chain elongation was probably allowed by a greater availability of NADPH synthesized through pentose phosphate pathway. The greatest dose of glucose clearly decreased milk fat yield (-234 g/d). A mammary cell mediated intracellular reaction likely caused a homothetic decrease in milk fatty acids. However, reduced synthesis was not due to a shortage of glycerol-3-phosphate because its milk concentration remained unchanged. In conclusion, changes in exogenous glucose supply, in cows fed a grass silage-based diet, decreased milk fat production and modified milk fatty acid composition.
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PMID:Duodenal infusion of glucose decreases milk fat production in grass silage-fed dairy cows. 1241 6

The metabolic functions of NADP(+)-specific isocitrate dehydrogenase (ID2), which may participate in the production of NADPH and biosynthesis of fatty acids, are not yet clearly understood. Accordingly, the current study investigated the effect of oxalomalate, known as a competitive inhibitor of ID2 in vitro, on lipid metabolism and the cellular defense system in vivo. Male Sprague Dawley rats (3 weeks old) were divided into two groups, fed a pelletized AIN-76 semisynthetic diet for 8 weeks, and injected intraperioneally with either saline or oxalomalate (25 mg/kg BW) dissolved in saline every 2 days. Oxalomalate did not lower the body weight and adipose tissue weight significantly; however, it significantly lower the plasma leptin concentration (p < 0.000), plasma and hepatic triglyceride levels (p < 0.01, p < 0.05), and adipocyte lipoprotein lipase activity (p < 0.01) compared to the control group. Meanwhile, hepatic antioxidant enzyme activities, except for superoxide dismutase activity (p < 0.01), glutathione content, and thiobarbituric acid reactive substances levels were not significantly different between the groups. Therefore, the current data suggests that oxalomalate produces a triglyceride-lowering activity and play a possible inhibitory role in fat accumulation. Furthermore, it was not found to affect the most antioxidative enzyme activities, glutathione content, and thiobarbituric acid reactive substances levels in rats fed normal diet.
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PMID:Effect of oxalomalate on lipid metabolism and antioxidant defense system in rats. 1459 52

Cardiovascular disease is common in patients with chronic kidney disease (CKD). As renal function fails, many patients become progressively malnourished, as evidenced by reduced levels of albumin, prealbumin, and transferrin. Malnourished patients have increased levels of C reactive protein (CRP), interleukin-6 (IL-6), and concomitant cardiovascular disease when they reach end stage. Many diseases that cause CKD, diabetes, and hypertension are also associated with cardiovascular disease. Thus the direct effect of renal failure per se directly contributing to the inflammation-malnutrition-atherosclerosis paradigm is not completely established in early stages of CKD. Some aspects of progressive renal failure, however, cause changes in plasma composition and endothelial structure and function that favor vascular injury. As renal function fails, hepatic apo A-I synthesis decreases and HDL levels fall. HDL is an important antioxidant and defends the endothelium from the effects of cytokines. Inflammation causes further structural and functional abnormalities in HDL. Apolipoprotein C III (apo C III), a competitive inhibitor of lipoprotein lipase is increased in CKD. Serum triglyceride levels increase as a result of accumulation of intermediate-density lipoprotein (IDL) comprising VLDL and chylomicron remnants. These impede vascular relaxation and are associated with cardiovascular disease. Activation of the renin angiotensin axis is a component of many renal diseases and adaptation to loss of renal mass. Angiotensin II (AngII) activates NADPH oxidases, leading to production of the superoxide anion and decreased availability of nitric oxide (NO), further impairing vascular function. H(2)O(2), produced as a consequence of superoxide dismutation, stimulates vascular cell proliferation and hypertrophy. Leukocyte-derived myeloperoxidase functions as an "NO Oxidase" in the inflamed vasculature and contributes to decreased NO bioavailability and compromised vascular reactivity. The changes in lipoprotein composition and structure as well as AngII-mediated alterations in endothelial function amplify the effect of subsequent inflammatory events.
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PMID:The role of oxidative stress-altered lipoprotein structure and function and microinflammation on cardiovascular risk in patients with minor renal dysfunction. 1497 55

Chronic and excessive consumption of alcohol is an important factor responsible for the onset of pancreatitis. However, the incidence of chronic pancreatitis in heavy drinkers differs in individuals, suggesting that these individual differences may involve various genetic and environmental factors. In the present study, we investigated an association of alcoholic pancreatitis with polymorphisms of the various genes related to metabolism of the oxidative compounds. We analyzed polymorphisms of NADPH-quinone oxidoreductase 2 (NQO2), multidrug resistance 1 (MDR1), alcohol dehydrogenase 1B (ADH1B) and lipoprotein lipase (LPL). The subjects consisted of 53 patients with chronic alcoholic pancreatitis (AlCP), 54 alcoholic patients without pancreatic dysfunction (Alc), and 42 healthy individuals. DNA samples were prepared from the peripheral blood of all subjects, and the genetic mutations were analyzed by polymerase chain reaction and restriction fragment length polymorphism methods. The ADH1B gene frequencies were significantly different between healthy controls and Alc patients (P < 0.001), and also between AlCP and Alc patients (P < 0.05). However, no significant difference was found between healthy controls and AlCP patients. The gene frequencies of MDR1 (3435C > T) and MDR1 (2677G > A/T) of patients with AlCP or Alc were different when compared with healthy controls, although the difference was not significant. The NQO2 and LPL genes showed no relation with Alc and AlCP patients. The ADH1B*1 gene frequency in AlCP was significantly lower compared with Alc. We speculate that the ADH1B*1 gene may function by reducing vulnerability to the onset of alcoholic pancreatitis. Other genes analyzed in the present study lacked association with AlCP.
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PMID:Association analysis among polymorphisms of the various genes and chronic alcoholic pancreatitis. 1833 68

In environment, birds often fast in connection with breeding, migration or drastic climatic conditions and need to mobilize lipid reserves during these periods. The impairment of lipid metabolism by cadmium (Cd; 1 mg kg(-1) added in diet) was investigated on palmiped Cairina moschata. Expression levels of genes involved in lipid metabolism, mitochondrial metabolism and detoxification were investigated in liver and muscle of ducks. Lipid content in muscle and liver were analysed and plasma triglycerides were quantified. After 20 days, ducks exposed to Cd displayed a lower body weight and lower lipid content in liver than controls. In muscle, the increase of lipid content was only significant for control ducks but not for exposed ducks. Exposed ducks appeared unable to sufficiently transport and store lipids into peripheral tissues. Cd impairs lipid metabolism by several ways. First, Cd triggered the down-regulation of fatty acids synthesis in liver even if the NADPH production and the mitochondrial metabolism are enhanced, suggesting a stronger energy needs. Secondly, the associated decrease of plasma triglycerides and lipoprotein lipase activity with Cd are consistent with impairment of lipids storage in peripheral tissues.
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PMID:Effect of dietary cadmium on lipid metabolism and storage of aquatic bird Cairina moschata. 1968 83


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