Genetic Variants Within the LPIN1 Gene, Encoding Lipin, Are Influencing Phenotypes of the Metabolic Syndrome in Humans
Genetic Variants Within the LPIN1 Gene, Encoding Lipin, Are Influencing Phenotypes of the Metabolic Syndrome in Humans Silke Wiedmann 1 , Marcus Fischer 1 , Martina Koehler 1 , Katharina Neureuther 1 , Guenter Riegger 1 , Angela Doering 2 , Heribert Schunkert 3 , Christian Hengstenberg 1 and Andrea...
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| Published in | Diabetes (New York, N.Y.) Vol. 57; no. 1; pp. 209 - 217 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Alexandria, VA
American Diabetes Association
01.01.2008
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0012-1797 1939-327X 1939-327X |
| DOI | 10.2337/db07-0083 |
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| Abstract | Genetic Variants Within the LPIN1 Gene, Encoding Lipin, Are Influencing Phenotypes of the Metabolic Syndrome in Humans
Silke Wiedmann 1 ,
Marcus Fischer 1 ,
Martina Koehler 1 ,
Katharina Neureuther 1 ,
Guenter Riegger 1 ,
Angela Doering 2 ,
Heribert Schunkert 3 ,
Christian Hengstenberg 1 and
Andrea Baessler 1
1 Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany
2 GSF-National Research Center for Environment and Health, Institute for Epidemiology, Neuherberg, Germany
3 Clinic for Internal Medicine 2, University of Schleswig-Holstein, Lübeck, Germany
Address correspondence and reprint requests to Andrea Baessler, MD, or Christian Hengstenberg, MD, Clinic for Internal Medicine
2, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany. E-mail: andrea.baessler{at}klinik.uni-regensburg.de ; or christian.hengstenberg{at}klinik.uni-regensburg.de
Abstract
OBJECTIVE— Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity,
and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome.
RESEARCH DESIGN AND METHODS— A total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants
on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication
in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of
its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used
to test the association between genetic LPIN1 variants and metabolic traits for empirical significance.
RESULTS— Linkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1 . We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the
metabolic syndrome (odds ratio 1.6 [95% CI 1.2–2.2]), while the other two, being less common (5.7 and 4.0%), are strongly
associated with lower blood pressure levels (systolic blood pressure 127 ± 18 vs. 135 ± 20 mmHg; P = 0.0001), a lower BMI (24.6 ± 3.6 vs. 26.9 ± 4.1 kg/m 2 ; P = 3.7 × 10 −7 ) and waist circumference (82 ± 12 vs. 90 ± 12 cm; P = 3.2 × 10 −8 ), lower A1C levels (5.1 ± 0.7 vs. 5.3 ± 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (−0.67 ± 1.00 vs. 0.04 ± 1.24; P = 1.4 × 10 −7 ). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were
also observed in the replication sample using the same haplotypes but with effects in the opposite direction.
CONCLUSIONS— These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic
syndrome.
LD, linkage disequilibrium
MI, myocardial infarction
MONICA, Monitoring Trends and Determinants on Cardiovascular Diseases
SNP, single nucleotide polymorphism
Footnotes
Published ahead of print at http://diabetes.diabetesjournals.org on 16 October 2007. DOI: 10.2337/db07-0083.
S.W. and M.F. contributed equally to this article.
Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db07-0083 .
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted October 10, 2007.
Received January 18, 2007.
DIABETES |
|---|---|
| AbstractList | Genetic Variants Within the LPIN1 Gene, Encoding Lipin, Are Influencing Phenotypes of the Metabolic Syndrome in Humans
Silke Wiedmann 1 ,
Marcus Fischer 1 ,
Martina Koehler 1 ,
Katharina Neureuther 1 ,
Guenter Riegger 1 ,
Angela Doering 2 ,
Heribert Schunkert 3 ,
Christian Hengstenberg 1 and
Andrea Baessler 1
1 Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany
2 GSF-National Research Center for Environment and Health, Institute for Epidemiology, Neuherberg, Germany
3 Clinic for Internal Medicine 2, University of Schleswig-Holstein, Lübeck, Germany
Address correspondence and reprint requests to Andrea Baessler, MD, or Christian Hengstenberg, MD, Clinic for Internal Medicine
2, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93053 Regensburg, Germany. E-mail: andrea.baessler{at}klinik.uni-regensburg.de ; or christian.hengstenberg{at}klinik.uni-regensburg.de
Abstract
OBJECTIVE— Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity,
and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome.
RESEARCH DESIGN AND METHODS— A total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants
on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication
in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of
its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used
to test the association between genetic LPIN1 variants and metabolic traits for empirical significance.
RESULTS— Linkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1 . We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the
metabolic syndrome (odds ratio 1.6 [95% CI 1.2–2.2]), while the other two, being less common (5.7 and 4.0%), are strongly
associated with lower blood pressure levels (systolic blood pressure 127 ± 18 vs. 135 ± 20 mmHg; P = 0.0001), a lower BMI (24.6 ± 3.6 vs. 26.9 ± 4.1 kg/m 2 ; P = 3.7 × 10 −7 ) and waist circumference (82 ± 12 vs. 90 ± 12 cm; P = 3.2 × 10 −8 ), lower A1C levels (5.1 ± 0.7 vs. 5.3 ± 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (−0.67 ± 1.00 vs. 0.04 ± 1.24; P = 1.4 × 10 −7 ). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were
also observed in the replication sample using the same haplotypes but with effects in the opposite direction.
CONCLUSIONS— These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic
syndrome.
LD, linkage disequilibrium
MI, myocardial infarction
MONICA, Monitoring Trends and Determinants on Cardiovascular Diseases
SNP, single nucleotide polymorphism
Footnotes
Published ahead of print at http://diabetes.diabetesjournals.org on 16 October 2007. DOI: 10.2337/db07-0083.
S.W. and M.F. contributed equally to this article.
Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db07-0083 .
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted October 10, 2007.
Received January 18, 2007.
DIABETES OBJECTIVE:- Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome. RESEARCH DESIGN AND METHODS- A total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used to test the association between genetic LPIN1 variants and metabolic traits for empirical significance. RESULTS:- Linkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1. We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the metabolic syndrome (odds ratio 1.6 [95% CI 1.2-2.2]), while the other two, being less common (5.7 and 4.0%), are strongly associated with lower blood pressure levels (systolic blood pressure 127 plus or minus 18 vs. 135 plus or minus 20 mmHg; P = 0.0001), a lower BMI (24.6 plus or minus 3.6 vs. 26.9 plus or minus 4.1 kg/m super(2); P = 3.7 x 10 super(-7)) and waist circumference (82 plus or minus 12 vs. 90 plus or minus 12 cm; P = 3.2 x 10 super(-8)), lower A1C levels (5.1 plus or minus 0.7 vs. 5.3 plus or minus 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (-0.67 plus or minus 1.00 vs. 0.04 plus or minus 1.24; P = 1.4 x 10 super(-7)). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were also observed in the replication sample using the same haplotypes but with effects in the opposite direction. CONCLUSIONS:- These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic syndrome. OBJECTIVE— Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome. RESEARCH DESIGN AND METHODS— A total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used to test the association between genetic LPIN1 variants and metabolic traits for empirical significance. RESULTS— Linkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1. We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the metabolic syndrome (odds ratio 1.6 [95% CI 1.2–2.2]), while the other two, being less common (5.7 and 4.0%), are strongly associated with lower blood pressure levels (systolic blood pressure 127 ± 18 vs. 135 ± 20 mmHg; P = 0.0001), a lower BMI (24.6 ± 3.6 vs. 26.9 ± 4.1 kg/m2; P = 3.7 × 10−7) and waist circumference (82 ± 12 vs. 90 ± 12 cm; P = 3.2 × 10−8), lower A1C levels (5.1 ± 0.7 vs. 5.3 ± 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (−0.67 ± 1.00 vs. 0.04 ± 1.24; P = 1.4 × 10−7). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were also observed in the replication sample using the same haplotypes but with effects in the opposite direction. CONCLUSIONS— These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic syndrome. Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome.OBJECTIVELipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome.A total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used to test the association between genetic LPIN1 variants and metabolic traits for empirical significance.RESEARCH DESIGN AND METHODSA total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used to test the association between genetic LPIN1 variants and metabolic traits for empirical significance.Linkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1. We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the metabolic syndrome (odds ratio 1.6 [95% CI 1.2-2.2]), while the other two, being less common (5.7 and 4.0%), are strongly associated with lower blood pressure levels (systolic blood pressure 127 +/- 18 vs. 135 +/- 20 mmHg; P = 0.0001), a lower BMI (24.6 +/- 3.6 vs. 26.9 +/- 4.1 kg/m(2); P = 3.7 x 10(-7)) and waist circumference (82 +/- 12 vs. 90 +/- 12 cm; P = 3.2 x 10(-8)), lower A1C levels (5.1 +/- 0.7 vs. 5.3 +/- 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (-0.67 +/- 1.00 vs. 0.04 +/- 1.24; P = 1.4 x 10(-7)). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were also observed in the replication sample using the same haplotypes but with effects in the opposite direction. CONCLUSIONS These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic syndrome.RESULTSLinkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1. We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the metabolic syndrome (odds ratio 1.6 [95% CI 1.2-2.2]), while the other two, being less common (5.7 and 4.0%), are strongly associated with lower blood pressure levels (systolic blood pressure 127 +/- 18 vs. 135 +/- 20 mmHg; P = 0.0001), a lower BMI (24.6 +/- 3.6 vs. 26.9 +/- 4.1 kg/m(2); P = 3.7 x 10(-7)) and waist circumference (82 +/- 12 vs. 90 +/- 12 cm; P = 3.2 x 10(-8)), lower A1C levels (5.1 +/- 0.7 vs. 5.3 +/- 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (-0.67 +/- 1.00 vs. 0.04 +/- 1.24; P = 1.4 x 10(-7)). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were also observed in the replication sample using the same haplotypes but with effects in the opposite direction. CONCLUSIONS These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic syndrome. Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome. A total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used to test the association between genetic LPIN1 variants and metabolic traits for empirical significance. Linkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1. We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the metabolic syndrome (odds ratio 1.6 [95% CI 1.2-2.2]), while the other two, being less common (5.7 and 4.0%), are strongly associated with lower blood pressure levels (systolic blood pressure 127 +/- 18 vs. 135 +/- 20 mmHg; P = 0.0001), a lower BMI (24.6 +/- 3.6 vs. 26.9 +/- 4.1 kg/m(2); P = 3.7 x 10(-7)) and waist circumference (82 +/- 12 vs. 90 +/- 12 cm; P = 3.2 x 10(-8)), lower A1C levels (5.1 +/- 0.7 vs. 5.3 +/- 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (-0.67 +/- 1.00 vs. 0.04 +/- 1.24; P = 1.4 x 10(-7)). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were also observed in the replication sample using the same haplotypes but with effects in the opposite direction. CONCLUSIONS These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic syndrome. Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis. Thus, we hypothesized that genetic variants within LPIN1 are associated with traits of the metabolic syndrome. A total of 15 single nucleotide polymorphisms (SNPs) covering the LPIN1 gene region were genotyped in an age- and sex-stratified sample of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Study Augsburg; DNA and phenotypes of 1,416 Caucasians). Ten SNPs were also genotyped for replication in an independent sample of 1,030 subjects recruited throughout Germany. The metabolic syndrome was defined via the sum of its core components and, additionally, by a factor score derived from factor analysis. Permutation-based methods were used to test the association between genetic LPIN1 variants and metabolic traits for empirical significance. Linkage disequilibrium (LD) analysis revealed three LD blocks encompassing LPIN1. We identified three associated three-marker haplotypes: one common haplotype (26.8% frequency) increases the risk for the metabolic syndrome (odds ratio 1.6 [95% CI 1.2-2.2]), while the other two, being less common (5.7 and 4.0%), are strongly associated with lower blood pressure levels (systolic blood pressure 127 +/- 18 vs. 135 +/- 20 mmHg; P = 0.0001), a lower BMI (24.6 +/- 3.6 vs. 26.9 +/- 4.1 kg/m(2); P = 3.7 x 10(-7)) and waist circumference (82 +/- 12 vs. 90 +/- 12 cm; P = 3.2 x 10(-8)), lower A1C levels (5.1 +/- 0.7 vs. 5.3 +/- 0.9%; P = 0.0002), as well as a lower metabolic syndrome factor score (-0.67 +/- 1.00 vs. 0.04 +/- 1.24; P = 1.4 x 10(-7)). Furthermore, the frequencies of arterial hypertension (23.7 vs. 46.4%; P = 0.00001), obesity (12.9 vs. 30.8%; P = 0.0003), diabetes (2.2 vs. 8.2%; P = 0.041), and the presence of three or more metabolic syndrome components (3.3 vs. 13.7%; P = 0.002) were significantly lower than in subjects not carrying one of these protective haplotypes. Strong associations were also observed in the replication sample using the same haplotypes but with effects in the opposite direction. CONCLUSIONS These data suggest that allelic variants of the LPIN1 gene have significant effects in human metabolic traits and thus implicate lipin in the pathophysiology of the metabolic syndrome. |
| Audience | Professional |
| Author | Heribert Schunkert Marcus Fischer Martina Koehler Guenter Riegger Christian Hengstenberg Andrea Baessler Angela Doering Silke Wiedmann Katharina Neureuther |
| Author_xml | – sequence: 1 givenname: Silke surname: Wiedmann fullname: Wiedmann, Silke organization: Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany – sequence: 2 givenname: Marcus surname: Fischer fullname: Fischer, Marcus organization: Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany – sequence: 3 givenname: Martina surname: Koehler fullname: Koehler, Martina organization: Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany – sequence: 4 givenname: Katharina surname: Neureuther fullname: Neureuther, Katharina organization: Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany – sequence: 5 givenname: Guenter surname: Riegger fullname: Riegger, Guenter organization: Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany – sequence: 6 givenname: Angela surname: Doering fullname: Doering, Angela organization: GSF-National Research Center for Environment and Health, Institute for Epidemiology, Neuherberg, Germany – sequence: 7 givenname: Heribert surname: Schunkert fullname: Schunkert, Heribert organization: Clinic for Internal Medicine 2, University of Schleswig-Holstein, Lübeck, Germany – sequence: 8 givenname: Christian surname: Hengstenberg fullname: Hengstenberg, Christian organization: Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany – sequence: 9 givenname: Andrea surname: Baessler fullname: Baessler, Andrea organization: Clinic for Internal Medicine II, University of Regensburg, Regensburg, Germany |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19980804$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17940119$$D View this record in MEDLINE/PubMed |
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| Snippet | Genetic Variants Within the LPIN1 Gene, Encoding Lipin, Are Influencing Phenotypes of the Metabolic Syndrome in Humans
Silke Wiedmann 1 ,
Marcus Fischer 1 ,... OBJECTIVE— Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis.... Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis. Thus, we... OBJECTIVE:- Lipin, a novel molecular protein expressed by adipocytes, has marked effects on adipose tissue mass, insulin sensitivity, and glucose homeostasis.... |
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| SubjectTerms | Adipocytes Adult Aged Angioplasty Biological and medical sciences Blood pressure Body fat Body Mass Index Cardiovascular disease Complications and side effects Development and progression Diabetes Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Genetic aspects Genetic Markers Genetic Variation Genotype Glucose Haplotypes Health Surveys Heart attacks Homeostasis Humans Hypertension Insulin resistance Linkage Disequilibrium Male Medical sciences Metabolic diseases Metabolic syndrome Metabolic Syndrome - genetics Metabolic syndrome X Middle Aged Miscellaneous Nuclear Proteins - genetics Obesity Other metabolic disorders Phenotype Phosphatidate Phosphatase Polymorphism, Single Nucleotide Population Research design Risk factors Trends Type 2 diabetes |
| Title | Genetic Variants Within the LPIN1 Gene, Encoding Lipin, Are Influencing Phenotypes of the Metabolic Syndrome in Humans |
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