SORCS1: A Novel Human Type 2 Diabetes Susceptibility Gene Suggested by the Mouse

SORCS1: A Novel Human Type 2 Diabetes Susceptibility Gene Suggested by the Mouse Mark O. Goodarzi 1 2 , Donna M. Lehman 3 , Kent D. Taylor 2 , Xiuqing Guo 2 , Jinrui Cui 2 , Manuel J. Quiñones 4 , Susanne M. Clee 5 , Brian S. Yandell 5 , John Blangero 6 , Willa A. Hsueh 4 , Alan D. Attie 5 , Michael...

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Published inDiabetes (New York, N.Y.) Vol. 56; no. 7; pp. 1922 - 1929
Main Authors Goodarzi, Mark O., Lehman, Donna M., Taylor, Kent D., Guo, Xiuqing, Cui, Jinrui, Quiñones, Manuel J., Clee, Susanne M., Yandell, Brian S., Blangero, John, Hsueh, Willa A., Attie, Alan D., Stern, Michael P., Rotter, Jerome I.
Format Journal Article
LanguageEnglish
Published Alexandria, VA American Diabetes Association 01.07.2007
Subjects
Animals
Biological and medical sciences
Cardiovascular disease
Chromosomes
Coronary vessels
Diabetes
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - genetics
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Female
Gene loci
Genetic aspects
Genetic Predisposition to Disease
Genetic susceptibility
Genomes
Glucose
Haplotypes
Hispanic Americans
Humans
Insulin - blood
Insulin - metabolism
Insulin resistance
Male
Medical sciences
Mexican Americans
Mice
Middle Aged
Obesity
Overweight
Polymorphism, Single Nucleotide
Receptors, Cell Surface - genetics
Research design
Risk factors
Type 2 diabetes
Vein & artery diseases
United States
Endocrinopathy
Type 2 diabetes
Human
Vertebrata
Sensitivity
Mammalia
Gene
Mouse
Animal
Rodentia
Metabolic diseases
Online AccessGet full text
ISSN0012-1797
1939-327X
1939-327X
DOI10.2337/db06-1677

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Abstract SORCS1: A Novel Human Type 2 Diabetes Susceptibility Gene Suggested by the Mouse Mark O. Goodarzi 1 2 , Donna M. Lehman 3 , Kent D. Taylor 2 , Xiuqing Guo 2 , Jinrui Cui 2 , Manuel J. Quiñones 4 , Susanne M. Clee 5 , Brian S. Yandell 5 , John Blangero 6 , Willa A. Hsueh 4 , Alan D. Attie 5 , Michael P. Stern 3 and Jerome I. Rotter 2 1 Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 2 Departments of Pediatrics and Medicine, Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California 3 Department of Medicine/Clinical Epidemiology, University of Texas Health Science Center, San Antonio, Texas 4 Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 5 Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 6 Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas Address correspondence and reprint requests to Mark O. Goodarzi, MD, PhD, Cedars-Sinai Medical Center, Division of Endocrinology, Diabetes, and Metabolism, 8700 Beverly Blvd., Becker B-131, Los Angeles, CA 90048. E-mail: mark.goodarzi{at}cshs.org Abstract OBJECTIVE —A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits. RESEARCH DESIGN AND METHODS —We assessed the contribution of variation in SORCS1 to human insulin–related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease. RESULTS —We first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort. CONCLUSIONS —Identification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes. CAD, coronary artery disease LD, linkage disequilibrium MACAD, Mexican-American Coronary Artery Disease QTL, quantitative trait locus SAFADS, San Antonio Family Diabetes Study SNP, single nucleotide polymorphism Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 10 April 2007. DOI: 10.2337/db06-1677. Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db06-1677 . 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 April 3, 2007. Received November 30, 2006. DIABETES
AbstractList A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits. We assessed the contribution of variation in SORCS1 to human insulin-related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease. We first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort. Identification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes.
OBJECTIVE—A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits. RESEARCH DESIGN AND METHODS—We assessed the contribution of variation in SORCS1 to human insulin–related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease. RESULTS—We first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort. CONCLUSIONS—Identification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes.
SORCS1: A Novel Human Type 2 Diabetes Susceptibility Gene Suggested by the Mouse Mark O. Goodarzi 1 2 , Donna M. Lehman 3 , Kent D. Taylor 2 , Xiuqing Guo 2 , Jinrui Cui 2 , Manuel J. Quiñones 4 , Susanne M. Clee 5 , Brian S. Yandell 5 , John Blangero 6 , Willa A. Hsueh 4 , Alan D. Attie 5 , Michael P. Stern 3 and Jerome I. Rotter 2 1 Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 2 Departments of Pediatrics and Medicine, Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California 3 Department of Medicine/Clinical Epidemiology, University of Texas Health Science Center, San Antonio, Texas 4 Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 5 Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 6 Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas Address correspondence and reprint requests to Mark O. Goodarzi, MD, PhD, Cedars-Sinai Medical Center, Division of Endocrinology, Diabetes, and Metabolism, 8700 Beverly Blvd., Becker B-131, Los Angeles, CA 90048. E-mail: mark.goodarzi{at}cshs.org Abstract OBJECTIVE —A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits. RESEARCH DESIGN AND METHODS —We assessed the contribution of variation in SORCS1 to human insulin–related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease. RESULTS —We first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort. CONCLUSIONS —Identification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes. CAD, coronary artery disease LD, linkage disequilibrium MACAD, Mexican-American Coronary Artery Disease QTL, quantitative trait locus SAFADS, San Antonio Family Diabetes Study SNP, single nucleotide polymorphism Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 10 April 2007. DOI: 10.2337/db06-1677. Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db06-1677 . 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 April 3, 2007. Received November 30, 2006. DIABETES
A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits.OBJECTIVEA small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits.We assessed the contribution of variation in SORCS1 to human insulin-related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease.RESEARCH DESIGN AND METHODSWe assessed the contribution of variation in SORCS1 to human insulin-related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease.We first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort.RESULTSWe first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort.Identification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes.CONCLUSIONSIdentification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes.
OBJECTIVE:-A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits. RESEARCH DESIGN AND METHODS-We assessed the contribution of variation in SORCS1 to human insulin-related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease. RESULTS:-We first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort. CONCLUSIONS:-Identification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes.
A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to influence diabetes or related traits in mice are likely to be susceptibility genes in humans. SorCS1 is the gene identified as responsible for the mouse chromosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secretion and increased islet disruption in obese females. Genes that impair compensatory insulin secretion in response to obesity-induced insulin resistance may be particularly relevant to human diabetes. Thus, we sought to determine whether variation in the human SORCS1 gene was associated with diabetes-related traits. We assessed the contribution of variation in SORCS1 to human insulin-related traits in two distinct Mexican-American cohorts. One cohort (the Mexican-American Coronary Artery Disease [MACAD] cohort) consisted of nondiabetic individuals, allowing assessment of genetic association with subclinical intermediate insulin-related traits; the second cohort (the San Antonio Family Diabetes Study [SAFADS]) contained individuals with diabetes, allowing association analyses with overt disease. We first found association of SORCS1 single nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACAD cohort. Similar to our results in the mice, the genetic association was strongest in overweight women. We then observed association with diabetes risk and age at diagnosis in women of the SAFADS cohort. Identification of SORCS1 as a novel gene affecting insulin secretion and diabetes risk is likely to provide important insight into the biology of obesity-induced type 2 diabetes.
Audience Professional
Author Alan D. Attie
Michael P. Stern
Donna M. Lehman
Jerome I. Rotter
Xiuqing Guo
Brian S. Yandell
Willa A. Hsueh
Kent D. Taylor
Mark O. Goodarzi
John Blangero
Susanne M. Clee
Jinrui Cui
Manuel J. Quiñones
Author_xml – sequence: 1
  givenname: Mark O.
  surname: Goodarzi
  fullname: Goodarzi, Mark O.
  organization: Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, Departments of Pediatrics and Medicine, Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California
– sequence: 2
  givenname: Donna M.
  surname: Lehman
  fullname: Lehman, Donna M.
  organization: Department of Medicine/Clinical Epidemiology, University of Texas Health Science Center, San Antonio, Texas
– sequence: 3
  givenname: Kent D.
  surname: Taylor
  fullname: Taylor, Kent D.
  organization: Departments of Pediatrics and Medicine, Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California
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  givenname: Xiuqing
  surname: Guo
  fullname: Guo, Xiuqing
  organization: Departments of Pediatrics and Medicine, Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California
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  surname: Cui
  fullname: Cui, Jinrui
  organization: Departments of Pediatrics and Medicine, Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California
– sequence: 6
  givenname: Manuel J.
  surname: Quiñones
  fullname: Quiñones, Manuel J.
  organization: Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California
– sequence: 7
  givenname: Susanne M.
  surname: Clee
  fullname: Clee, Susanne M.
  organization: Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin
– sequence: 8
  givenname: Brian S.
  surname: Yandell
  fullname: Yandell, Brian S.
  organization: Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin
– sequence: 9
  givenname: John
  surname: Blangero
  fullname: Blangero, John
  organization: Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas
– sequence: 10
  givenname: Willa A.
  surname: Hsueh
  fullname: Hsueh, Willa A.
  organization: Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California
– sequence: 11
  givenname: Alan D.
  surname: Attie
  fullname: Attie, Alan D.
  organization: Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin
– sequence: 12
  givenname: Michael P.
  surname: Stern
  fullname: Stern, Michael P.
  organization: Department of Medicine/Clinical Epidemiology, University of Texas Health Science Center, San Antonio, Texas
– sequence: 13
  givenname: Jerome I.
  surname: Rotter
  fullname: Rotter, Jerome I.
  organization: Departments of Pediatrics and Medicine, Medical Genetics Institute, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, Los Angeles, California
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ContentType Journal Article
Copyright 2007 INIST-CNRS
COPYRIGHT 2007 American Diabetes Association
Copyright American Diabetes Association Jul 2007
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Keywords Endocrinopathy
Type 2 diabetes
Human
Vertebrata
Sensitivity
Mammalia
Gene
Mouse
Animal
Rodentia
Metabolic diseases
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Snippet SORCS1: A Novel Human Type 2 Diabetes Susceptibility Gene Suggested by the Mouse Mark O. Goodarzi 1 2 , Donna M. Lehman 3 , Kent D. Taylor 2 , Xiuqing Guo 2 ,...
OBJECTIVE—A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found...
A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found to...
OBJECTIVE:-A small number of susceptibility genes for human type 2 diabetes have been identified by candidate gene analysis or positional cloning. Genes found...
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StartPage 1922
SubjectTerms Animals
Biological and medical sciences
Cardiovascular disease
Chromosomes
Coronary vessels
Diabetes
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - genetics
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Female
Gene loci
Genetic aspects
Genetic Predisposition to Disease
Genetic susceptibility
Genomes
Glucose
Haplotypes
Hispanic Americans
Humans
Insulin - blood
Insulin - metabolism
Insulin resistance
Male
Medical sciences
Mexican Americans
Mice
Middle Aged
Obesity
Overweight
Polymorphism, Single Nucleotide
Receptors, Cell Surface - genetics
Research design
Risk factors
Type 2 diabetes
Vein & artery diseases
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