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

Two men aged 48 and 35 years with severe hypertriglyceridaemia, glucose intolerance, and a secondary anaemia had more apolipoprotein C-III-2 and less apo C-III-1 on their triglyceride-rich lipoproteins (d less than 1.006) than did types IV or V lipaemic controls. Although the patients' abnormal lipoproteins seemed to produce normal activation of lipoprotein lipase, they did not serve as an efficient substrate for purified lipoprotein lipase. Adipose tissue of case 1 had considerable lipoprotein-lipase activity and the hypertriglyceridaemia responded to dietary therapy (carbohydrate 180 g, fat 80 g, protein 60 g per day, and no alcohol). The haemolytic anaemia improved, but the patient remained glucose intolerant. The abnormal content of apo C-III-2 on the triglyceride-rich lipoproteins, rendering them resistant to clearance by lipoprotein lipase, is believed to have contributed to the patients' severe hypertriglyceridaemia.
 ...
PMID:Hypertriglyceridaemia associated with an abnormal triglyceride-rich lipoprotein carrying excess apolipoprotein C-III-2. 9 Jul 60

In 13 obese children plasma triglyceride concentrations were found to be significantly elevated, while plasma cholesterol concentrations were normal. In the hypertriglyceridemic obese children, the plasma fractional triglyceride removal, measured by the intravenous fat tolerance test, was significantly reduced. These abnormalities reverted to normal in 8 patients retested after weight loss. Plasma postheparin lipoprotein lipase activity was found to be increased and significantly related to the degree of obesity. As to carbohydrate metabolism, a decreased glucose tolerance and hyperinsulinemia were found. Hyperinsulinemia reverted to normal during dietary restriction, glucose intolerance did not.
 ...
PMID:Plasma triglyceride clearing in obese children. 114 45

Data from several different studies are reviewed suggesting that a subset of hypertension is associated with metabolic abnormalities involving lipids, insulin, and often obesity, all aggregating strongly in families. Persons with 'familial dyslipidaemic hypertension (FDH)' have an especially high risk of early coronary disease. The clinical and biochemical features of FDH are compared with Reaven's Syndrome X, familial combined hyperlipidaemia, dense LDL subfractions, diabetes, impaired glucose tolerance, central and general obesity, pre-diabetes, pre-hypertension, and heterozygous lipoprotein lipase deficiency. Some contribution from major gene effects is suggested in specific subsets reported in several different genetic studies reviewed in this report. It seems likely that multiple metabolic abnormalities are genetically heterogeneous. The data also suggest significant contributions from environmental factors such as diet and physical activity.
 ...
PMID:Familial dyslipidaemic hypertension and other multiple metabolic syndromes. 148 41

Physiological actions of insulin include suppression of fat mobilization from adipose tissue and activation of adipose tissue lipoprotein lipase. Here, we report measurements of adipose tissue hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL) action in vivo in 10 normal and eight obese subjects, with the latter group having varying degrees of glucose intolerance. HSL and LPL actions (per gram of adipose tissue) were similar in the two groups, after an overnight fast. In the normal subjects, HSL action was suppressed after a meal (by 75% +/- 6% between 60 to 300 minutes, P less than .01), and the action of LPL was increased (clearance of circulating triacylglycerol [TAG] increased by 140% +/- 57% at 300 minutes, P less than .05). Despite hyperinsulinemia, these responses were blunted in the obese subjects (P less than .05 for each change being less than in normal group). The adipose tissue of the obese subjects showed continued nonesterified fatty acid (NEFA) release at a time when NEFA mobilization was completely suppressed in the normal group. Both impaired suppression of HSL and low fractional retention of fatty acids for reesterification within the adipose tissue contributed to this abnormal NEFA release. Impaired activation of LPL was associated with a greater absolute increase in plasma TAG concentration postprandially in the obese. In obese subjects, adipose tissue HSL and LPL fail to respond to immunoreactive insulin postprandially, which may be an important maladaptation in terms of lipoprotein metabolism and risk of coronary heart disease.
 ...
PMID:Adipose tissue metabolism in obesity: lipase action in vivo before and after a mixed meal. 154 65

Normal rats fed an isocaloric sucrose-rich diet (SRD) for 3 weeks developed high levels of triacylglycerol in plasma (P) (mmol triacylglycerol I-1) heart (H) and liver (L) tissues (mumol triacylglycerol mg DNA-1) as compared to control rats fed the standard chow (STD) (X +/- SEM; P: SRD 1.32 +/- 0.06 vs STD 0.49 +/- 0.05, P less than 0.001; H: SRD 2.1 +/- 0.17 vs STD 0.94 +/- 0.01, P less than 0.001; L: SRD 8.48 +/- 1.47 vs STD 1.71 +/- 0.12, P less than 0.001). A simultaneous drop in the activities (mumol glycerol ml-1 hr-1) of several plasma post heparin lipolytic enzymes was observed; total triglyceride lipase (T-TGL): SRD 5.32 +/- 0.34 vs STD 7.48 +/- 0.64, P less than 0.01; lipoprotein lipase (LPL): SRD 1.61 +/- 0.26 vs STD 2.42 +/- 0.41, P less than 0.05; hepatictriglyceride lipase (H-TGL): SRD 3.71 +/- 0.28 vs STD 5.05 +/- 0.69, P less than 0.05 and monoglyceride hydrolase (MGH) (mumol glycerol I-1 min-1): SRD 558 +/- 108 vs STD 1165 +/- 45, P less than 0.001. Rats fed the SRD presented glucose intolerance after i.v. glucose (Kg X 10(-2); 1.06 +/- 0.09 vs 2.61 +/- 0.14 of STD, P less than 0.001) in spite of the presence of hyperinsulinism (sigma plasma IRI microU/ml from 0 to 30 min: 184.6 +/- 23.6 vs 100.5 +/- 9.7 of STD, P less than 0.01) suggesting that a state of insulin resistance had developed.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of tiadenol and clofibrate on plasma post heparin lipolytic hepatic, extrahepatic and monoglyceride hydrolase activities in rats with hypertriglyceridemia induced by a sucrose rich diet. 400 66

Three patients with Menkes' disease, an inherited disorder of copper transport, were studied to determine whether the copper deficiency was associated with a lipoprotein disorder. Hypocuprinemia was documented in all three cases. Two patients had severe copper and ceruloplasmin deficiencies, whereas the third patient had a less severe deficiency. Hypertriglyceridemia was observed in the first patient, and elevations in triglyceride, cholesterol, apolipoprotein B (ApoB), and apolipoprotein C-III (ApoC-III) occurred predominantly in the very low density lipoprotein fraction (VLDL). This patient had normal lipoprotein lipase activity but mild glucose intolerance. The second patient had a borderline high cholesterol level with normal plasma triglycerides and apolipoproteins, whereas the third patient appeared to have normal total cholesterol but slightly higher triglycerides with elevated plasma apolipoprotein E (ApoE). No striking differences were observed in the chemical composition of all lipoprotein subfractions between patients and controls except that the neutral lipid content of VLDL was higher in patients than in controls. The ApoB was initially normal in molecular weight but degraded faster than the controls during storage. The appearance of the major low density lipoprotein (LDL) fraction of the first two patients was opaque white, in contrast to clear yellow in the third patient and in the age- and diet-matched controls. This abnormal appearance of LDL in these patients was associated with low plasma levels of beta-carotene and ceruloplasmin. These findings suggest that decreased serum copper levels may be associated with lipid and lipoprotein abnormalities and may enhance lipid peroxidation of LDL accounting for the color change.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Studies of lipids, lipoproteins, and apolipoproteins in Menkes' disease. 648 10

We have previously reported that normal Wistar rats fed an isocaloric, sucrose-rich (63%) diet (SRD) developed glucose intolerance and elevated triglyceride levels in plasma as well as in heart and liver tissue. This metabolic state was accompanied by hyperinsulinism both in vivo and in vitro, suggesting that a state of insulin resistance has developed. The aim of this study was to gather information on the various plasma post-heparin lipolytic activities in rats fed a SRD. Hepatic triglyceride lipase (H-TGL) was evaluated by both, protamine sulfate inhibition (PSI) of extrahepatic lipoprotein lipase (LPL) and heparin-Sepharose affinity chromatography (H-SAC). Both methods rendered comparable results. Total triglyceride lipase (T-TGL) was measured after Krauss et al. and monoglyceride hydrolase (MGH) after Vogel et al. Our results have shown a significant decline of plasma T-TGL (5.32 +/- 0.34 means +/- SEM vs. 7.48 +/- 0.64 mumol glycerol ml-1 h-1; p less than 0.01), H-TGL (3.71 +/- 0.28 vs. 5.05 +/- 0.69; p less than 0.05), LPL (1.61 +/- 0.26 vs. 2.42 +/- 0.41; p less than 0.05) and MGH (558 +/- 108 mumol glycerol l-1 min-1 vs. 1,165 +/- 45; p less than 0.001) activities. Thus, feeding a sucrose-rich diet induced a state of hyperlipemia and insulin resistance in which not only plasma T-TGL but also H-TGL and MGH activities were significantly decreased. This suggests that the latter two enzymes are also under nutritional and/or hormonal control.
 ...
PMID:Post-heparin plasma hepatic triglyceride lipase and monoglyceride hydrolase activities in hyperlipemia induced by a sucrose rich diet. 661 28

The effect of 10 wk of treadmill training on glucose tolerance, serum lipids, tissue lipoprotein lipase (LPL) activities, and triglyceride secretion rates (TGSR) were studied in normal and diabetic rats. Training had little effect on the glucose tolerance of the normal rats but ameliorated the deterioration of glucose intolerance seen in the sedentary diabetic rats. Trained diabetic and normal rats had lower serum triglycerides than their sedentary counterparts [diabetic 34 +/- 5 vs. 61 +/- 4 (means +/- SE); normal 34 +/- 3 vs. 50 +/- 3 mg/dl]. This hypotriglyceridemic effect was associated with a reduction in the TGSR in the trained rats (diabetics 0.34 +/- 0.05 vs. 0.51 +/- 0.02; normal 0.48 +/- 0.05 vs. 0.53 +/- 0.04 mg/min). There were no differences in the tissue LPL activities (soleus, gastrocnemius, epididymal fat, and heart) between the trained and sedentary rats in both groups. Training also did not affect the serum cholesterol and the high-density lipoprotein cholesterol levels in both groups of rats.
 ...
PMID:Physical training in diabetic rats: effect on glucose tolerance and serum lipids. 710 60

In 10 patients with acute pancreatitis the lipid- and lipoprotein-metabolism was studied. In all patients blood samples were drawn for estimation of the fasting concentration of the lipoproteins. In 7 patients the postheparinlipasesystem was testet by an intravenous heparintest. Afterwards, 0.2 g fat/kg bodyweight were injected intravenously in 2 min. Before, 5, 10, 30 and 40 min after injection blood was drawn. Lipids were estimated by means of full encymatic methods, lipoproteins were determined according to the lipid research clinics method, NIH, using a combination of ultracentrifuge and polyanion precipitation. In comparison with healthy people the cholesterol, specially the LDL fraction was low. Additionally the triglycerides were elevated in 3 patients, caused by elevation of the VLDL fraction. After injection of heparin in all patients the triglyceride concentrations fell. That shows a functionating lipoprotein lipase system. Intravenously injected fat was eliminated in all patients with an elimination rate between 1 and 2 %/min. From these results it is concluded that exogenous fat is eliminated sufficiently from serum in acute pancreatitis. There is no sign for disturbed fat metabolism in these patients. Therefore the contraindication for fat emulsions in acute pancreatitis does not seem to be justified. Due to the fact of glucose intolerance in these patients fat emulsions could be used for an adequate supply of energy. Patients with a hyperlipoproteinemia should be excluded from this therapy by daily detection of triglycerides.
 ...
PMID:[Lipid and lipoprotein metabolism in acute pancreatitis]. 719 62

In male spontaneously hypertensive rats (SHR) and normotensive Wistar rats at 4, 8 and 20 weeks of age the postheparin lipolytic activity (PHLA) has been estimated. PHLA was significantly higher in all SHR than in age- and weight-matched controls, although it decreased with advancing age in both groups. The data are discussed with regard to hyperinsulinemia and hypotriglyceridemia in SHR ascertained by a previous study. It is assumed that in young SHR catecholamine-induced lipolysis provokes impaired glucose tolerance and higher insulin response after glucose load. Insulin enhancement can stimulate PHLA via increased synthesis of lipoprotein lipase. The resulting augmented uptake of triglycerides by adipose tissue is suggested to be a beneficial (adaptive?) mechanism to compensate a primary increase of lipolysis. The well-known lower adipose cell size and body weight in SHR in comparison to age-related normotensive control rats might indicate that this mechanism is insufficient to balance the triglyceride supply in these animals.
 ...
PMID:High postheparin lipolytic activity as a possible cause of hypotriglyceridemia in spontaneously hypertensive rats. 721 Oct 69


1 2 3 4 5 6 Next >>