J. Lipid Res.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nie, L.
Right arrow Articles by Cohen, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nie, L.
Right arrow Articles by Cohen, J. C.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
The Journal of Lipid Research, Vol. 39, 1127-1130, May 1998
Copyright © 1998 by Lipid Research, Inc.

Rapid Communication

Body mass index and hepatic lipase gene (LIPC) polymorphism jointly influence postheparin plasma hepatic lipase activity

Liangcai Niea, Jinping Wanga, Luther T. Clarkd, Aylmer Tangd, Gloria L. Vegaa,b, Scott M. Grundya,b,c, and Jonathan C. Cohena,b,c
a The Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9052
b Department of Clinical Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9052
c Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9052
d The State University of New York Health Science Center at Brooklyn, Brooklyn, NY 11203-2098

Correspondence to: Jonathan C. Cohen.


  ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES

The -514 polymorphism in the hepatic lipase gene (LIPC) is associated with decreased hepatic lipase activity. In the present study, the interaction between body mass index (BMI), the -514 polymorphism, and hepatic lipase activity was examined in 118 white men and in 51 African American men. BMI was significantly positively correlated with hepatic lipase activity in both populations. BMI was similar in men with genetic differences in hepatic lipase activity, indicating that high hepatic lipase activity did not cause increased BMI. The data therefore suggest that high BMI leads to increased hepatic lipase activity. The actions of BMI and the -514 polymorphism on hepatic lipase activity appear to be additive and independent, rather than synergistic.

This finding indicates that hepatic lipase activity is a multifactorial trait, determined in part by polymorphism within the LIPC gene as well as by factors that influence BMI.—Nie, L., J. Wang, L. T. Clark, A. Tang, G. L. Vega, S. M. Grundy, and J. C. Cohen. Body mass index and hepatic lipase gene (LIPC) polymorphism jointly influence postheparin plasma hepatic lipase activity. J. Lipid Res. 1998. 39: 1127–1130.

Supplementary key words: adiposity, LIPC, -514 polymorphism


  INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 REFERENCES

rapid communication

Human hepatic lipase is a 476 amino acid glycoprotein (1) (2) that exhibits phospholipase A1 and triglyceride hydrolase activities (3). The role of hepatic lipase in lipoprotein metabolism has been extensively studied (4), but much less is known about the factors that determine the activity of this enzyme in vivo. Several hormones influence hepatic lipase activity (5) (6) (7) (8) (9) but the contribution of these hormones to inter-individual variation in hepatic lipase activity is not known. Data from nuclear family (10), and twin (11) studies have suggested that inter-individual variation in hepatic lipase activity is highly heritable. Recently, we identified a common allele of the hepatic lipase gene (LIPC) that is associated with decreased hepatic lipase activity and increased plasma high density lipoprotein-cholesterol (HDL-C) concentrations in men (12). The allele, designated -514T, does not contain mutations in the coding region, or intron/exon boundaries, and is identified by four linked polymorphisms in the 5' flanking region. Postheparin plasma hepatic lipase activity is 30–50% lower in homozygotes for the -514T allele than in homozygotes for the wild type (-514C) allele (13). The -514T allele is much more common among African Americans than among white Americans, and contributes to the low hepatic lipase activities observed in African American men (13).

Even among -514T homozygotes, however, hepatic lipase activity is quite variable, indicating that other factors modulate the effects of this allele on hepatic lipase gene expression. One of these factors may be adiposity. Some (14) (15) (16) though not all (17) (18) (19) studies have suggested a correlation between hepatic lipase activity and adiposity. This inconsistency of results may be related to the relatively small sample sizes used in previous studies. In the present study, we have examined the relation between hepatic lipase activity and adiposity, as reflected by body mass index (BMI), in two large groups of men. In addition, the impact of LIPC polymorphism on the relationship between BMI and hepatic lipase activity was assessed.


  METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 REFERENCES

The study was approved by the Institutional Review Boards at the University of Texas Southwestern Medical Center and the State University of New York Health Science Center.

Subjects
African American and white men who were apparently healthy and who did not have diabetes or use lipid-lowering medication were recruited through advertisements placed on bulletin boards at the University of Texas Southwestern Medical Center and the State University of New York Health Science Center. Any man aged over 20 years who met these criteria was eligible for the study. Body mass index and hepatic lipase activity were not used as selection criteria.

Assay of postheparin plasma hepatic lipase activity
Hepatic lipase activity was measured in postheparin plasma as described previously (20).

Assay of LIPC genotypes
LIPC genotypes were determined by polymerase chain reaction (PCR) amplification and restriction digestion (12).

Statistical analysis
The relationship between hepatic lipase activity, age, and body mass index was examined using Pearson's correlation. The potential influence of outliers was assessed by graphical inspection of the data, and by recalculating the correlation coefficients after exclusion of influential points (see Figure 1). The mean postheparin plasma hepatic lipase activities of men in the upper and lower BMI tertiles were compared using t -tests. A general linear model (implemented in the SAS program) was used to determine whether BMI and the -514 polymorphism had independent effects on hepatic lipase activity (21). The polymorphism and BMI were entered as classification and continuous variables, respectively.



View larger version (17K):
[in this window]
[in a new window]
  		Figure 1. Scatterplot of body mass index (BMI) and postheparin plasma hepatic lipase activity (PHLA) in 118 white men. The line indicates the least-squares regression line. r is the correlation coefficient calculated using all the data. When the circled point was excluded, r was 0.34.


  RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 REFERENCES

Postheparin plasma hepatic lipase activities and LIPC genotypes were determined in 118 white men aged 20 to 68 years, and in 51 African American men aged 20 to 40 years. Data from all individuals were included in the analysis. Hepatic lipase activity was not correlated with age in either group (data not shown).

Effect of BMI on hepatic lipase activity
The BMIs of the men in this study ranged from 18 to 43 kg/m2. Hepatic lipase activity was positively correlated with BMI both in white men ( Figure 1) and in African American men ( Figure 2). When white men were ranked by BMI, the lower tertile had BMIs below 24 kg/m2, while the upper tertile had BMIs greater than 27 kg/m2. Mean hepatic lipase activity was significantly higher in the upper tertile than in the middle or lower tertiles ( Table 1). Because of the smaller sample size, African Americans were divided into two groups comprising those falling above and those falling below the median BMI. Mean hepatic lipase activity was significantly higher in the group with higher BMIs than in the group with lower BMIs ( Table 2).



View larger version (14K):
[in this window]
[in a new window]
  		Figure 2. Scatterplot of body mass index (BMI) and postheparin plasma hepatic lipase activity (PHLA) in 51 African American men. The line indicates the least-squares regression line. r is the correlation coefficient.


 
View this table:
[in this window]
[in a new window]
  		Table 1. Effects of body mass index and LIPC genotype on hepatic lipase activity in white men


 
View this table:
[in this window]
[in a new window]
  		Table 2. Effects of body mass index and LIPC genotype on hepatic lipase activity in African American men

Effect of LIPC genotype on hepatic lipase activity
In both ethnic groups, hepatic lipase activity was highest in homozygotes for the -514C allele, lower in -514CT heterozygotes and lowest in -514T homozygotes (Table 1 and Table 2).

Combined effects of LIPC genotype and BMI on hepatic lipase activity
To assess the combined effect of LIPC genotype and BMI, men were grouped by genotype and then ranked by BMI. Among whites, mean hepatic lipase activity was significantly higher in the upper tertile than in the lower tertile in -514C homozygotes, and in -514CT heterozygotes ( Figure 3, Table 1). Of the seven white men who were homozygous for the -514T allele, hepatic lipase activity was lower in the three who had BMIs within the lower tertile of the whole group (i.e., less than 24 kg/m2), than in the three men who had BMIs in the upper tertile (greater than 27 kg/m2). Among African Americans, mean hepatic lipase activity was higher among men with higher BMIs than among men with lower BMIs for each genotype group. These differences in hepatic lipase activity were statistically significant for the -514C and -514T homozygotes, but not for the -514CT heterozygotes.



View larger version (11K):
[in this window]
[in a new window]
  		Figure 3. Postheparin plasma hepatic lipase activity in white men grouped by LIPC genotype and body mass index (BMI). The group CCH includes men who are -514C homozygotes and have a BMI in the upper tertile. CCL includes men who are -514C homozygotes and have a BMI in the lower tertile. The group CTH includes men who are -514CT heterozygotes and have a BMI in the upper tertile. CTL includes men who are -514CT heterozygotes and have a BMI in the lower tertile. The group TTH includes men who are -514T homozygotes and have a BMI in the upper tertile. TTL includes men who are -514T homozygotes and have a BMI in the lower tertile.

The effects of BMI and the -514 polymorphism were both highly significant (P < 0.001) in the general linear model, indicating that both parameters were significantly and independently related to hepatic lipase activity.

Effect of LIPC genotype on BMI
No effect of LIPC genotype on BMI was detected in either ethnic group. In white men, mean BMI was 26 ± 4, 25 ± 3, and 26 ± 3 for CC, CT, and TT genotypes, respectively (P = 0.2). The corresponding mean values in African American men were 26 ± 6, 27 ± 5, and 26 ± 5 for C, CT, and TT genotypes, respectively (P = 0.7).


  DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
REFERENCES

A common LIPC allele (-514T) is associated with low hepatic lipase activity in white and in African American men (13). In the present study, we investigated the relationship between the -514 LIPC polymorphism, BMI, and hepatic lipase activity in these two populations. Two primary observations were established. First, our data provide strong evidence that increased BMI is associated with increased hepatic lipase activity in men. Second, a striking additive effect of BMI and the -514 polymorphism on hepatic lipase activity was observed. The joint effects of BMI and LIPC genotype strongly influenced hepatic lipase activity and were significantly greater than the effects of either factor considered alone.

To accurately assess the correlation between BMI and hepatic lipase, the present study design included three sequential steps: i) a large sample size was used to ensure ample statistical power, ii) the potential influence of "outliers" in the data was carefully assessed, and iii) the findings were corroborated by analysis of an independent population. In both white men and African American men, a significant positive correlation was observed between BMI and hepatic lipase activity. This correlation was not an artifact of "outliers" in either population. Therefore these data provide strong evidence for a positive correlation between BMI and hepatic lipase activity in men.

To determine whether hepatic lipase activity is a determinant of BMI, we measured BMI in men with genetically defined differences in hepatic lipase activity. In both ethnic groups, mean BMI was similar in men with the CC, CT, and TT genotypes, indicating that genetic variation in hepatic lipase activity does not influence BMI. Therefore the correlation between BMI and hepatic lipase activity almost certainly is not due to an effect of hepatic lipase activity on adiposity.

A second possible explanation for the correlation observed is that an unidentified common factor(s) exerts independent effects on BMI and hepatic lipase activity. While we cannot formally exclude this possibility, we suggest that a third explanation is more likely, namely that one or more factors associated with high BMI leads to increased hepatic lipase activity. Increased BMI is associated with changes in circulating hormone levels including decreased circulating testosterone levels (22) and increased plasma insulin concentrations (23) that potentially affect hepatic lipase activity. Androgens stimulate hepatic lipase activity (5), therefore the reduced androgen levels associated with obesity are unlikely to account for the effects of BMI on the activity of the enzyme. Some studies have reported positive correlations between hepatic lipase activity and the plasma insulin response to oral glucose, an index of insulin resistance (14) (16) (18). Consequently, the association between BMI and hepatic lipase activity may reflect insulin resistance in the liver secondary to obesity.

Finally, the effects of BMI on hepatic lipase activity were observed in each of the three LIPC genotypes in this study. These data indicate that BMI and the sequence polymorphisms in the -514T allele influence hepatic lipase activity by different mechanisms. Their action appears to be additive, and independent rather than synergistic. This finding indicates that hepatic lipase activity is a multifactorial trait, determined in part by polymorphism within the LIPC gene as well as by factors that influence BMI.


  ACKNOWLEDGMENTS

We thank Hanh Nguyen, Sijing Niu, Sharon Haynes R.N., and Han Tron for excellent technical assistance, Dick Verstraete for subject recruitment, and Ann White for helpful discussion. This work was supported by National Institutes of Health grants HL-53917 and M-01-RR-00633, the Department of Veterans Affairs, the Southwestern Medical Foundation, and the Moss Heart Foundation, Dallas, TX.

Manuscript received December 4, 1997; and in revised form February 9, 1998; and in revised form February 18, 1998.

Abbreviations: BMI, body mass index; HDL-C, high density lipoprotein-cholesterol; PCR, polymerase chain reaction


  REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES

  1. Stahnke, G., Sprengel, R., Augustin, J., Will, H. 1987. Human hepatic triglyceride lipase: cDNA cloning, amino acid sequence and expression in a cultured cell line. Differentiation. 35:45-52[Medline].

  2. Datta, S., Luo, C. C., Li, W. H., VanTuinen, P., Ledbetter, D. H., Brown, M. A., Chen, S. H., Liu, S. W., Chan, L. 1988. Human hepatic lipase. Cloned cDNA sequence, restriction fragment length polymorphisms, chromosomal localization, and evolutionary relationships with lipoprotein lipase and pancreatic lipase. J. Biol. Chem. 263:1107-1110[Abstract/Free Full Text].

  3. Shirai, K., Barnhart, R. L., Jackson, R. L. 1981. Hydrolysis of human plasma high density lipoprotein 2-phospholipids and triglycerides by hepatic lipase. Biochem. Biophys. Res. Commun. 100:591-599[Medline].

  4. Jansen, H., Hulsmann, W. C. 1985. Enzymology and physiological role of hepatic lipase. Biochem. Soc. Trans. 13:24-26[Medline].

  5. Tikkanen, M. J., Nikkila, E. A. 1987. Regulation of hepatic lipase and serum lipoproteins by sex steroids. [Review]. Am. Heart J. 113:562-567[Medline].

  6. Packard, C. J., Shepherd, J., Lindsay, G. M., Gaw, A., Taskinen, M. R. 1993. Thyroid replacement therapy and its influence on postheparin plasma lipases and apolipoprotein-B metabolism in hypothyroidism. J. Clin. Endocrinol. Metab. 76:1209-1216[Abstract].

  7. Baynes, C., Henderson, A. D., Richmond, W., Johnston, D. G., Elkeles, R. S. 1992. The response of hepatic lipase and serum lipoproteins to acute hyperinsulinaemia in type 2 diabetes. Eur. J. Clin. Invest. 22:341-346[Medline].

  8. Beshyah, S. A., Henderson, A., Baynes, C., Copping, D., Richmond, W., Johnston, D. G. 1995. Post-heparin plasma lipase activity in hypopituitary adults. Horm. Res. 44:69-74[Medline].

  9. Taskinen, M. R., Nikkila, E. A., Pelkonen, R., Sane, T. 1983. Plasma lipoproteins, lipolytic enzymes, and very low density lipoprotein triglyceride turnover in Cushing's syndrome. J. Clin. Endocrinol. Metab. 57:619-626[Abstract].

  10. Perusse, L., Rice, T., Despres, J-P., Bergeron, J., Province, M. A., Gagnon, J., Leon, A. S., Rao, D. C., Skinner, J. S., Wilmore, J. H., Bouchard, C. 1997. Familial resemblance of plasma lipids, lipoproteins and postheparin lipoprotein and hepatic lipases in the HERITAGE family study. Arterioscler. Thromb. Vasc. Biol. 17:3263-3269[Abstract/Free Full Text].

  11. Kuusi, T., Kesaniemi, Y. A., Vuoristo, M., Miettinen, T. A., Koskenvuo, M. 1987. Inheritance of high density lipoprotein and lipoprotein lipase and hepatic lipase activity. Arteriosclerosis. 7:421-425[Abstract/Free Full Text].

  12. Guerra, R., Wang, J. P., Grundy, S. M., Cohen, J. C. 1997. A hepatic lipase (LIPC) allele associated with high plasma concentrations of high density lipoprotein cholesterol. Proc. Natl. Acad. Sci. USA. 94:4532-4537[Abstract/Free Full Text].

  13. Vega, G. L., Clark, L. T., Tang, A., Marcovina, S., Grundy, S. M., Cohen, J. C. 1998. Hepatic lipase activity is lower in African American than in white American men: effects of 5' flanking polymorphism in the hepatic lipase gene. J. Lipid. Res. 39:228-232[Abstract/Free Full Text].

  14. Katzel, L. I., Coon, P. J., Busby, M. J., Gottlieb, S. O., Krauss, R.M., Goldberg, A.P. 1992. Reduced HDL2 cholesterol subspecies and elevated postheparin hepatic lipase activity in older men with abdominal obesity and asymptomatic myocardial ischemia. Arterioscler. Thromb. 12:814-823[Abstract/Free Full Text].

  15. Despres, J-P., Ferland, M., Moorjani, S., Nadeau, A., Tremblay, A., Lupien, P. J., Theriault, G., Bouchard, C. 1989. Role of hepatic-triglyceride lipase activity in the association between intra-abdominal fat and plasma HDL cholesterol in obese women. Arteriosclerosis. 9:485-492[Abstract/Free Full Text].

  16. Cominacini, L., Garbin, U., Davoli, A., Campagnola, M., De, S. A., Pasini, A. M., Pastorino,, Bosello, O. 1993. High-density lipoprotein cholesterol concentrations and postheparin hepatic and lipoprotein lipases in obesity: relationships with plasma insulin levels. Ann. Nutr. Metab. 37:175-184[Medline].

  17. Sorbris, R., Petersson, B. G., Nilsson-Ehle, P. 1981. Effects of weight reduction on plasma lipoproteins and adipose tissue metabolism in obese subjects. Eur. J. Clin. Invest. 11:491-498[Medline].

  18. Pollare, T., Vessby, B., Lithell, H. 1991. Lipoprotein lipase activity in skeletal muscle is related to insulin sensitivity. Arterioscler. Thromb. 11:1192-1203[Abstract/Free Full Text].

  19. Reitman, J. S., Kosmakos, F. C., Howard, B. V., Taskinen, M. R., Kuusi, T., Nikkila, E. A. 1982. Characterization of lipase activities in obese Pima indians. Decreases with weight reduction. J. Clin. Invest. 70:791-797.

  20. Blades, B., Vega, G. L., Grundy, S. M. 1993. Activities of lipoprotein lipase and hepatic triglyceride lipase in postheparin plasma of patients with low concentrations of HDL cholesterol. Arterioscler. Thromb. 13:1227-1235[Abstract/Free Full Text].

  21. SAS Institutes Inc. 1989. SAS/STAT® User's Guide. Version 6, Fourth Edition, Volume 2. SAS Institute Inc., Cary, NC. 891–993.

  22. Vermeulen, A. 1996. Decreased androgen levels and obesity in men. Ann. Med. 28:13-15[Medline].

  23. Cooney, G. J., Storlien, L. H. 1994. Insulin action, thermogenesis and obesity. Baillieres. Clin. Endocrinol. Metab. 8:481-507[Medline].
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 J. Clin. Endocrinol. Metab.Home page
N. Grarup, C. H. Andreasen, M. K. Andersen, A. Albrechtsen, A. Sandbaek, T. Lauritzen, K. Borch-Johnsen, T. Jorgensen, O. Schmitz, T. Hansen, et al.
The -250G>A Promoter Variant in Hepatic Lipase Associates with Elevated Fasting Serum High-Density Lipoprotein Cholesterol Modulated by Interaction with Physical Activity in a Study of 16,156 Danish Subjects
J. Clin. Endocrinol. Metab., June 1, 2008; 93(6): 2294 - 2299.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
G. F. Lewis and D. J. Rader
New Insights Into the Regulation of HDL Metabolism and Reverse Cholesterol Transport
Circ. Res., June 24, 2005; 96(12): 1221 - 1232.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
C. Zhang, R. Lopez-Ridaura, E. B Rimm, N. Rifai, D. J Hunter, and F. B Hu
Interactions between the -514C->T polymorphism of the hepatic lipase gene and lifestyle factors in relation to HDL concentrations among US diabetic men
Am. J. Clinical Nutrition, June 1, 2005; 81(6): 1429 - 1435.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
A. Isaacs, F. A. Sayed-Tabatabaei, O. T. Njajou, J. C. M. Witteman, and C. M. van Duijn
The -514 C->T Hepatic Lipase Promoter Region Polymorphism and Plasma Lipids: A Meta-Analysis
J. Clin. Endocrinol. Metab., August 1, 2004; 89(8): 3858 - 3863.
[Abstract] [Full Text] [PDF]

Home page
 J. Lipid Res.Home page
M. C. Carr, J. D. Brunzell, and S. S. Deeb
Ethnic differences in hepatic lipase and HDL in Japanese, black, and white Americans: role of central obesity and LIPC polymorphisms
J. Lipid Res., March 1, 2004; 45(3): 466 - 473.
[Abstract] [Full Text] [PDF]

Home page
 Am J EpidemiolHome page
J. E. Hokanson, M. I. Kamboh, S. Scarboro, R. H. Eckel, and R. F. Hamman
Effects of the Hepatic Lipase Gene and Physical Activity on Coronary Heart Disease Risk
Am. J. Epidemiol., November 1, 2003; 158(9): 836 - 843.
[Abstract] [Full Text] [PDF]

Home page
 Diabetes CareHome page
I. I.L. Berk-Planken, N. Hoogerbrugge, R. P. Stolk, A. H. Bootsma, and H. Jansen
Atorvastatin Dose-Dependently Decreases Hepatic Lipase Activity in Type 2 Diabetes: Effect of sex and the LIPC promoter variant
Diabetes Care, February 1, 2003; 26(2): 427 - 432.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
References
Circulation, December 17, 2002; 106(25): 3373 - 3421.
[Full Text]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
J. Pihlajamaki, L. Karjalainen, P. Karhapaa, I. Vauhkonen, M.-R. Taskinen, S. S. Deeb, and M. Laakso
G-250A Substitution in Promoter of Hepatic Lipase Gene Is Associated With Dyslipidemia and Insulin Resistance in Healthy Control Subjects and in Members of Families With Familial Combined Hyperlipidemia
Arterioscler. Thromb. Vasc. Biol., July 1, 2000; 20(7): 1789 - 1795.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
J. Q. Purnell, S. E. Kahn, J. J. Albers, D. N. Nevin, J. D. Brunzell, and R. S. Schwartz
Effect of Weight Loss with Reduction of Intra-Abdominal Fat on Lipid Metabolism in Older Men
J. Clin. Endocrinol. Metab., March 1, 2000; 85(3): 977 - 982.
[Abstract] [Full Text]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
M. C. Carr, J. E. Hokanson, S. S. Deeb, J. Q. Purnell, E. S. Mitchell, and J. D. Brunzell
A Hepatic Lipase Gene Promoter Polymorphism Attenuates the Increase in Hepatic Lipase Activity With Increasing Intra-abdominal Fat in Women
Arterioscler. Thromb. Vasc. Biol., November 1, 1999; 19(11): 2701 - 2707.
[Abstract] [Full Text] [PDF]

Home page
 Arterioscler. Thromb. Vasc. Bio.Home page
R. V. Shohet, G. L. Vega, A. Anwar, J. E. Cigarroa, S. M. Grundy, and J. C. Cohen
Hepatic Lipase (LIPC) Promoter Polymorphism in Men With Coronary Artery Disease : Allele Frequency and Effects on Hepatic Lipase Activity and Plasma HDL-C Concentrations
Arterioscler. Thromb. Vasc. Biol., August 1, 1999; 19(8): 1975 - 1978.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
M. Chandalia, N. Abate, A. Garg, J. Stray-Gundersen, and S. M. Grundy
Relationship between Generalized and Upper Body Obesity to Insulin Resistance in Asian Indian Men
J. Clin. Endocrinol. Metab., July 1, 1999; 84(7): 2329 - 2335.
[Abstract] [Full Text]

Home page
 J. Lipid Res.Home page
T. P. Bersot, G. L. Vega, S. M. Grundy, K. E. Palaoglu, P. Atagündüz, S. Özbayrakçi, O. Gökdemir, and R. W. Mahley
Elevated hepatic lipase activity and low levels of high density lipoprotein in a normotriglyceridemic, nonobese Turkish population
J. Lipid Res., March 1, 1999; 40(3): 432 - 438.
[Abstract] [Full Text]

Home page
 J. Lipid Res.Home page
G. L. Vega, J. Gao, T. P. Bersot, R. W. Mahley, R. Verstraete, S. M. Grundy, A. White, and J. C. Cohen
The -514 polymorphism in the hepatic lipase gene (LIPC) does not influence androgen-mediated stimulation of hepatic lipase activity
J. Lipid Res., July 1, 1998; 39(7): 1520 - 1524.
[Abstract] [Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nie, L.
Right arrow Articles by Cohen, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nie, L.
Right arrow Articles by Cohen, J. C.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today