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)

High circulating fasting and prandial triglyceride levels are associated with both insulin resistance and the development of cardiovascular disease. The aim of this investigation was to study the effects of NO-1886, a novel lipoprotein lipase (LPL) activator, on triglyceride levels, fat oxidation, and glucose tolerance in fructose-fed rats, a hypertriglyceridemic model of insulin resistance. Adult male Wistar rats were fed for 4 weeks with a high-starch diet or a high-fructose diet without and with NO-1886 (50 mg x kg[-1] x d[-1] orally). Fructose feeding increased plasma triglyceride levels, an effect that was ameliorated by NO-1886 treatment (week 1/week 4: starch-fed, 2.4 +/- 0.1/2.8 +/- 0.2 mmol/L; fructose-fed, 3.6 +/- 0.5/5.5 +/- 0.5; fructose + NO-1886, 2.7 +/- 0.2/3.6 +/- 0.3). The mean 24-hour respiratory quotient (RQ) was significantly lower in the fructose + NO-1886 group compared with fructose-fed rats, indicating increased oxidation of fat. Fructose feeding elevated liver triglyceride levels by 74% (P < .01), an effect not altered by NO-1886. Red and white quadriceps hindlimb muscle triglyceride levels were not different between groups. Glucose tolerance (intravenous test in long-term cannulated rats) was mildly deteriorated and fasting insulin and glucose levels were elevated in fructose-fed rats, effects which were ameliorated by NO-1886. In conclusion, in the fructose-fed rat model of hypertriglyceridemia and insulin resistance, addition of a LPL activator reduced circulating triglyceride levels without causing increased muscle triglyceride accumulation or deterioration in glucose tolerance. LPL activators may prove to be a fruitful avenue to explore in the search for new therapeutic agents in the treatment of dyslipidemias and insulin resistance.
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PMID:The actions of a novel lipoprotein lipase activator, NO-1886, in hypertriglyceridemic fructose-fed rats. 947 61

Offspring of dams exposed to excess folic acid during the perigestational period have been shown by us to be predisposed to metabolic dysfunction revealed by hyperglycemia, glucose intolerance, increased insulin and decreased adiponectin in late adulthood. This work aims to characterize adipocyte phenotype and expression profile of genes in the regulation of lipid and glucose metabolism in visceral adipose tissue and in skeletal muscle. From mating until weaning, a recommended dose of folic acid for pregnancy (C, 2 mg of folic acid per kg of diet) or a high folic acid dose (HFA, 40 mg of folic acid per kg of diet) was administered to Sprague-Dawley females. At 10 months of age progeny were divided into groups fed the standard chow (C/STD and HFA/STD) and groups fed the standard chow plus drinking water with 10% fructose (C/FRU and HFA/FRU), as an additional metabolic challenge. Adipocyte morphology and quantification of key genes involved in lipid and glucose metabolism were studied in visceral adipose tissue and skeletal muscle of 13 months old offspring. HFA exposure led to an enlargement of visceral adipose cells most likely mediated by an upregulation of lipoprotein lipase, and it tended to downregulate Glut4 in visceral adipose tissue and skeletal muscle. Fructose exposure in a background of perigestational excess folic acid, but not in controls, induced an upregulation of lipogenesis pathway genes and it decreased jejunal expression of the proton-coupled folate transporter (Pcft1). In addition, fructose exposure led to a downregulation of jejunal Sglt1 in control animals. Our data suggest that high folic acid exposure during the perigestational period caused morphologic and genic alterations related to insulin resistant states indicating that this intervention may act as an effective programmer of long-term metabolic dysfunction.
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PMID:Perigestational high folic acid: impact on offspring's peripheral metabolic response. 3161 77

A high fructose intake exacerbates postprandial plasma triacylglycerol (TAG) concentration, an independent risk factor for cardiovascular disease, although it is unclear whether this is due to increased production or impaired clearance of triacylglycerol (TAG)-rich lipoproteins. We determined the in vivo acute effect of fructose on postprandial intestinal and hepatic lipoprotein TAG kinetics and de novo lipogenesis (DNL). Five overweight men were studied twice, 4 weeks apart. They consumed hourly mixed-nutrient drinks that were high-fructose (30% energy) or low-fructose (<2% energy) for 11 h. Oral 2H2O was administered to measure fasting and postprandial DNL. Postprandial chylomicron (CM)-TAG and very low-density lipoprotein (VLDL)-TAG kinetics were measured with an intravenous bolus of [2H5]-glycerol. CM and VLDL were separated by their apolipoprotein B content using antibodies. Plasma TAG (p < 0.005) and VLDL-TAG (p = 0.003) were greater, and CM-TAG production rate (PR, p = 0.046) and CM-TAG fractional catabolic rate (FCR, p = 0.073) lower when high-fructose was consumed, with no differences in VLDL-TAG kinetics. Insulin was lower (p = 0.005) and apoB48 (p = 0.039), apoB100 (p = 0.013) and non-esterified fatty acids (NEFA) (p = 0.013) were higher after high-fructose. Postprandial hepatic fractional DNL was higher than intestinal fractional DNL with high-fructose (p = 0.043) and low-fructose (p = 0.043). Fructose consumption had no effect on the rate of intestinal or hepatic DNL. We provide the first measurement of the rate of intestinal DNL in humans. Lower CM-TAG PR and CM-TAG FCR with high-fructose consumption suggests lower clearance of CM, rather than elevated production, may contribute to elevated plasma TAG, possibly due to lower insulin-mediated stimulation of lipoprotein lipase.
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PMID:The Effect of Fructose Feeding on Intestinal Triacylglycerol Production and De Novo Fatty Acid Synthesis in Humans. 3254 14