Preheparin Serum Lipoprotein Lipase Research Articles

Twelve-Week Jogging Training Increases Pre-Heparin Serum Lipoprotein Lipase Concentrations in Overweight/Obese Middle-Aged Men

Enhancement of lipoprotein lipase (LPL) activity through drug administration has been shown to increase pre-heparin serum LPL concentrations; however, pre-heparin serum LPL responses to exercise training have not been determined. The present study was undertaken to investigate the effects of 12 weeks of supervised aerobic exercise training on pre-heparin serum LPL concentrations in overweight/obese men. Fifteen overweight/obese middle-aged men were assigned to one of two 12-week supervised exercise interventions: a walking group (eight participants gradually increasing brisk walking to 60 min/day 3 days a week) or a jogging group (seven participants gradually increasing jogging to 60 min/day 3 days a week). All participants maintained ad libitum diets. Blood samples were collected at baseline and immediately after 12 weeks. The primary outcome was pre-heparin serum LPL. Pre-heparin serum LPL concentrations were increased in the jogging group after 12 weeks compared with the baseline values (mean+/-SEM: 37.6+/-4.7 vs. 51.0+/-6.6 ng/mL, respectively, p= 0.033). In the walking group, pre-heparin serum LPL concentrations remained unchanged after 12 weeks. This study demonstrates that 12 weeks of jogging training increases pre-heparin serum LPL concentrations in overweight/obese middle-aged men.

Preheparin serum lipoprotein lipase mass interacts with gender, gene polymorphism and, positively, with smoking

Correlates of preheparin serum lipoprotein lipase (LPL) mass and its associations with the likelihood of metabolic syndrome (MS) and coronary heart disease (CHD) were investigated. A cross-sectional study was carried out in a population sample (n=352, median age 55). MS was defined according to modified Adult Treatment Panel III criteria. Age-adjusted geometric mean preheparin LPL concentrations were 58.6+/-1.04 ng/mL in men and 66.9+/-1.03 ng/mL in women (p<0.004). A positive interaction with both the LPL X447 allele (p<0.034) and age-adjusted smoking status (p=0.026 in men and p=0.11 women) was observed. LPL mass was significantly correlated in both genders with high-density lipoprotein (HDL)-cholesterol and inversely with triacylglycerol levels and HOMA index. In multiple linear regression analysis, LPL mass was significantly associated with genotype, gender, age, adiponectin, smoking status and HDL-cholesterol, and in women with C-reactive protein after adjustment for body mass index, triacylglycerol and insulin. Significantly low sex- and age-adjusted serum LPL mass was observed in cases of MS, hypertension and CHD. Logistic regression analysis after adjustment for age, sex, adiponectin and S447X polymorphism demonstrated that LPL mass was inversely associated with CHD in men and both genders (p=0.02), with hypertension confined to women (p=0.04) and with MS likelihood in both genders combined and women [odds ratio 1.51 (95% CI 1.14-2.00) for halving the likelihood]. LPL X447 genotype, female gender and smoking habit interact in increasing preheparin serum LPL mass in Turkish adults. Serum LPL mass is inversely associated with MS and CHD, independent of confounders, and probably reflects insulin sensitivity.

Relationship between the adiponectin-leptin ratio and parameters of insulin resistance in subjects without hyperglycemia

We previously reported that the adiponectin-leptin (A/L) ratio was more efficacious as a parameter of insulin resistance than adiponectin or leptin alone, and a more sensitive and reliable marker of insulin resistance than homeostasis model assessment (HOMA-R) as the fasting plasma glucose (FPG) level elevated in type 2 diabetes mellitus. In this study, we examined the usefulness of the A/L ratio as compared to HOMA-R for assessing insulin resistance in Japanese subjects without hyperglycemia. A total of 411 Japanese adults without hyperglycemia (205 men, aged 49 ± 10 years; 206 women, aged 48 ± 10 years) were enrolled. We investigated the correlation between fasting serum insulin level, FPG, leptin or adiponectin, and body mass index (BMI), fat mass (FM), triglycerides (TGs), high-density lipoprotein (HDL) cholesterol, or preheparin serum lipoprotein lipase (LPL) as parameters of insulin resistance. Next, we examined the relationships between parameters of insulin resistance and the A/L ratio or HOMA-R. By simple regression of the correlation between serum insulin level, FPG, leptin or adiponectin, and each parameter of insulin resistance, the best correlation coefficients were seen in leptin (men, r = 0.501; women, r = 0.667) as compared with BMI, in leptin (men, r = 0.658; women, r = 0.747) as compared with FM, in adiponectin ( r = −0.285) in men and leptin ( r = 0.299) in women as compared with TGs, in adiponectin (men, r = 0.405; women; r = 0.442) as compared with HDL cholesterol, and in adiponectin (men, r = 0.228; women, r = 0.452) as compared with LPL. By simple regression of the correlation between A/L ratio or HOMA-R and each parameter of insulin resistance, the highest correlation coefficients were seen with the A/L ratio except HDL cholesterol in men. Next, we carried out multiple linear regression to analyze the association between A/L ratio or HOMA-R and FM, TGs, HDL cholesterol, and LPL, excluding BMI, simultaneously. In men, the A/L ratio was significantly correlated with FM and TGs, and HOMA-R was significantly correlated with FM. This model explained 34% of the variance in the A/L ratio and 17% of the variance in HOMA-R. In women, the A/L ratio was significantly correlated with FM and LPL, and HOMA-R was significantly correlated with FM and LPL. This model explained 39% of the variance in A/L ratio and 14% of the variance in HOMA-R. In conclusion, the present study suggested that the A/L ratio might be more useful than HOMA-R to accurately assess insulin resistance in subjects without hyperglycemia.

Correlation between the adiponectin-leptin ratio and parameters of insulin resistance in patients with type 2 diabetes

We studied the correlation between the adiponectin-leptin (A/L) ratio and parameters of insulin resistance in 220 Japanese patients with type 2 diabetes (138 men and 82 women). Body mass index (BMI), triglycerides (TGs), HDL cholesterol (HDL), and preheparin serum lipoprotein lipase (LPL mass) were examined as laboratory parameters of the insulin resistance. The correlations between these laboratory parameters and adiponectin, leptin, or A/L ratio were studied. Adiponectin levels correlated significantly with BMI ( r = −0.298, P = .0003), TGs ( r = −0.221, P = .0092), HDL ( r = 0.31, P = .0002), and LPL mass ( r = 0.26, P = .0021) in men, and with TGs ( r = −0.29, P = .0093), HDL ( r = 0.239, P = .0338), and LPL mass ( r = 0.499, P < .0001) in women. Leptin levels correlated significantly with only BMI ( r = 0.31, P = .0002) in men, and with BMI ( r = 0.71, P < .0001) and TGs ( r = 0.26, P = .0201) in women. Adiponectin and leptin levels tended to correlate with these parameters in an opposite manner. On the other hand, A/L ratio significantly correlated with BMI ( r = −0.4, P < .0001), TG ( r = −0.199, P = .0192), HDL ( r = 0.235, P = .0054), and LPL mass ( r = 0.244, P = .0390) in men, and with BMI ( r = −0.482, P < .0001), TG ( r = −0.402, P = .0002), HDL ( r = 0.358, P = .0011), and LPL mass ( r = 0.487, P < .0001) in women. Next, the patients were divided into 3 groups classified by their fasting plasma glucose (FPG) level, and the correlations between the parameters and A/L ratio or homeostasis model assessment (HOMA-R), and the correlation between A/L ratio and HOMA-R were investigated in each group. Significant correlations between the parameters and A/L ratio were tended to be observed as the FPG level rose; however, the significant correlations between the parameters and HOMA-R were no longer seen as FPG level elevated. The results suggested that the A/L ratio was effective in relevance as a parameter of insulin resistance to adiponectin or leptin alone, and a more sensitive and reliable marker of insulin resistance than HOMA-R as the FPG level elevated, in patients with type 2 diabetes.

グリメピリドの血糖改善効果に及ぼす患者背景要因としてのｐｒｅＬＰＬの有用性

グリメピリドの血糖改善効果に及ぼす患者背景要因としてのｐｒｅＬＰＬの有用性

The level of pre-heparin serum lipoprotein lipase mass at different stages of pregnancy

Background: Lipoprotein lipase (LPL) mass is present in pre-heparin serum, although its activity is rarely detected. To clarify the dynamics of pre-heparin LPL mass during pregnancy, we studied the relationship between pre-heparin LPL mass and lipids in normal pregnant women. Methods: Pre-heparin LPL mass and serum lipid levels were measured in 99 pregnant women during all three trimesters. Results: When compared with the first and second trimesters, a significant decrease in pre-heparin LPL mass was observed in the third trimester. Plasma triglycerides were negatively correlated with pre-heparin LPL mass ( r=−0.30; p<0.05). In contrast, LDL-C, HDL-C and total cholesterol did not exhibit a statistically significant correlation. Conclusion: The decrease in pre-heparin LPL mass is manifested only during the third trimester.

1P-0019 Low preheparin serum lipoprotein lipase mass is an important coronary risk factor for various types of coronary artery disease

1P-0019 Low preheparin serum lipoprotein lipase mass is an important coronary risk factor for various types of coronary artery disease

2P-0398 Low preheparin serum lipoprotein lipase mass is visceral fat accumulation related coronary risk factor

An Arabidopsis thaliana partial cDNA was previously identified with a sequence similar to the lauroyl-acyl carrier protein (ACP) thioesterase from Umbellularia californica (Grellet et al., 1993, Plant Physiol. Biochem. 31, 599-602). Using this DNA fragment, we isolated a 1.8-kb cDNA coding for a 412-amino-acid preprotein. The deduced amino acid sequence is 51% identical to the lauroyl-ACP thioesterase but only 39% identical to safflower oleoyl-ACP thioesterase. The cDNA was expressed in Escherichia coli and the gene product showed thioesterase activity for long-chain acyl-ACPs (14:0, 16:0, 18:0, 18:1Δ9cis). When expressed in beta-oxidation mutants of E. coli, lipid analysis revealed that cells transformed with the thioesterase produced high amounts of free fatty acids that mostly consisted of 16:0 and some 14: 0, 16:1Δ9cis and 18:1Δ11cis. Antibodies were raised to the recombinant protein and used to determine tissue-specific and developmental expression in A. thaliana and Brassica napus. A 40-kDa protein was detected by immunoblots in A. thaliana siliques, leaves, and roots. A maximal expression of the B. napus protein between 18 and 31 days after flowering was found, which correlates with the rapid accumulation of triacylglycerols in the seeds. Based upon these results, we suggest that this long-chain acyl-ACP thioesterase may be a ubiquitous enzyme in plants which is involved in the synthesis of long-chain fatty acids.

Low lipoprotein lipase mass in preheparin serum of type 2 diabetes mellitus patients and its recovery with insulin therapy

There exists lipoprotein lipase mass in preheparin serum, even though the activity is scarcely found. We studied the preheparin serum lipoprotein lipase mass levels (prehaparin LPL mass) in type 2 diabetes mellitus patients and the effect of insulin therapy on the levels of preheparin LPL mass. In 40 type 2 diabetes mellitus patients, preheparin LPL mass were measured by the sandwich enzyme-linked immunosorbent assay (ELISA), and were compared with those of non-diabetic healthy control. The correlation between preheparin LPL mass and Hemoglobin A 1c (HbA 1c), serum lipids were studied. Preheparin LPL mass were measured before and after insulin therapy. Preheparin LPL mass of type 2 diabetes mellitus patients was significantly lower than that of non-diabetic healthy control. In diabetic patients, preheparin LPL mass were negatively correlated with HbA 1c. Fifteen patients started to take insulin therapy. Preheparin LPL mass increased significanaly at 4th week, when fasting blood glucose decreased. These results suggested that preheparin LPL mass was greatly regulated by insulin action.

Association between preheparin serum lipoprotein lipase mass and acute myocardial infarction in Japanese men.

A sensitive immunoassay system using a specific monoclonal antibody against lipoprotein lipase (LPL) recently demonstrated the presence of an LPL mass in preheparin serum. We reported that a preheparin serum LPL mass (pre-LPL mass) reflected the level of functioning LPL activity in the whole body and could be deeply involved in the progression of coronary atherosclerosis of stable organic angina pectoris. We examined the relation between the pre-LPL mass and acute myocardial infarction (AMI). We studied 44 males with AMI (AMI group) and 16 males with a normal coronary artery (NCA group), and measured the pre-LPL mass by enzyme-linked immunosorbent assay. Coronary risk factors including the pre-LPL mass were compared between the two groups and multiple regression analysis was performed for AMI. There were no significant differences in the lipid data, but the pre-LPL mass level was significantly low in the AMI group (52 +/- 16 vs 41 +/- 14 ng/ml, p = 0.01), and a low pre-LPL mass concentration was observed in the small sized LDL group and/or the Midband positive group. Multiple regression analysis revealed that a low pre-LPL mass and hypertriglyceridemia were independent risk factors for AMI (t value = 2.1, 2.4). The result indicates that a low pre-LPL mass may be an important risk factor for AMI and stable organic angina pectoris.

Preheparin serum lipoprotein lipase mass is negatively related to coronary atherosclerosis

In preheparin serum, there exists lipoprotein lipase (LPL) mass with little activity. The clinical significance of this preheparin serum LPL mass (preheparin LPL mass) is unclear. We studied the levels of preheparin LPL mass in patients with coronary atherosclerosis, comparing the results with those in healthy men. We also evaluated the correlation between preheparin LPL mass and the severity of coronary atherosclerosis by comparing with other risk factors such as age, smoking, family history, hypertension, hyperuricemia, diabetes mellitus, total cholesterol, triglyceride, high density lipoprotein-cholesterol and body mass index. The subjects, 70 men presenting with symptoms of coronary artery disease, underwent coronary angiographic examination. Significant narrowness was defined as≥75%. Control group comprised 77 men who had annual health checks and showed no abnormal findings. Preheparin LPL mass in the stenosis group was lower than normal coronary group and also than the control group. Multivariate analysis showed that preheparin LPL mass had the highest t-value (−2.53) for the number of lesions among the risk factors listed above. These results suggest that low preheparin LPL mass may be deeply involved in the progression of coronary atherosclerosis.

Enhancement of preheparin serum lipoprotein lipase mass by bezafbirate administration

To clarify the clinical implication of preheparin serum lipoprotein lipase mass (preheparin LpL mass), we studied the relationships between preheparin LpL mass and serum lipids, including midband lipoproteins, which migrate between very low density lipoproteins and low density lipoproteins on polyacrylamide gel disc electrophoresis, in hyperlipidemias. And we also studied the changes of preheparin LpL mass in hypertriglyceridemic patients during bezafibrate administration, which is known to enhance LpL activity in postheparin plasma. Preheparin LpL mass correlated positively with high-density lipoprotein-cholesterol (HDL-C) ( r=0.418, P<0.01) and negatively with triglyceride (TG) ( r=−0.256, P<0.01), but did not correlate with total cholesterol (TC) in 64 hyperlipidemic (type IIa, IIb and IV) patients. The midband lipoproteins were observed in 80% of hypertriglyceridemic patients (32/40). Preheparin LpL mass in midband lipoprotein-positive subjects was lower significantly than that in midband-negative subjects. When bezafibrate (400 mg/day) was administrated to 40 hypertriglyceridemic patients for 4 months, TG level significantly decreased (−49±7%, P<0.01), TC levels decreased (−11±4%, not significant), and HDL-C levels increased (+27±4%, P<0.01). The midband lipoproteins disappeared in 95% of patients. Preheparin LpL mass significantly increased (+25±6%, P<0.0005). In nine patients who stopped bezafibrate, TG levels significantly increased (+49±7%, P<0.01) and HDL-C levels decreased (−27±4%, P<0.01). Preheparin LPL mass significantly decreased (−25±6%, P<0.0005). These results suggested that bezafibrate administration enhanced preheparin LpL mass. And it might be implicated that enhanced LpL production by bezafibrate could reflect an increase of preheparin LpL mass.

The effect of insulin sensitizer, troglitazone, on lipoprotein lipase mass in preheparin serum

Lipoprotein lipase mass exists in preheparin serum, even though the activity is scarcely found. The implication of this is unclear. We studied the effect of an insulin sensitizer, troglitazone, on this preheparin serum lipoprotein lipase mass (preheparin LPL mass) in non-insulin-dependent diabetes mellitus (NIDDM) patients as well as on serum lipid levels and low density lipoproteins (LDL) particle size. Thirty-one NIDDM patients with poor control were administered troglitazone 400 mg/day. Hemoglobin A1c had significantly decreased (13%, P<0.001) 2 months later. Preheparin LPL mass had gradually increased and a 69% increase ( P<0.01) was observed 4 months later. Triglyceride significantly decreased (23%, P<0.01) and high density lipoprotein-cholesterol increased (10%, P<0.0l), whereas total cholesterol and LDL levels did not change 4 months later. The size of LDL increased significantly ( P<0.01). These results were consistent with the idea that preheparin LPL mass might be relating to the insulin sensitivity enhanced by troglitazone, as well as LDL particle size.

Preheparin serum lipoprotein lipase mass level: the effects of age, gender, and types of hyperlipidemias

To clarify the factors regulating preheparin serum lipoprotein lipase mass (preheparin LPL mass), the correlations between preheparin LPL mass and age, gender and types of hyperlipidemias were investigated in 377 persons who underwent annual health examinations. Preheparin LPL mass level did not significantly differ in individuals from 19 to 70 years old, for both men and women. Preheparin LPL mass level correlated negatively with triglyceride (TG), positively with high density lipoprotein-cholesterol (HDL-C), and not at all with total cholesterol (TC) or low density lipoprotein-cholesterol (LDL-C). Preheparin LPL mass levels were apparently higher in women than in men, but when serum lipid levels were adjusted, preheparin LPL mass levels were identical. In type IV and IIb hyperlipidemia, preheparin LPL mass levels were lower than in type IIa patients and in normals. Remnant positive individuals had lower levels of preheparin LPL mass than the negative individuals. In conclusion, preheparin LPL mass levels were not affected by aging and gender, but were lower in the conditions in which TG catabolism was disturbed, indicating that preheparin LPL mass might reflect somewhat the amount of LPL working in the body.