Journal ArticleDOI
Partitioning the variability of fasting plasma glucose levels in pedigrees. Genetic and environmental factors.
Reads0
Chats0
TLDR
Fasting plasma glucose measurements made in 1972-1977 on normoglycemic individuals in three-generation Caucasian pedigrees from Rochester, Minnesota were analyzed and found that familial factors provide an explanation for at least half the variability in normalized fasting plasma glucose which remains after regression on known concomitants.Abstract:
Fasting plasma glucose measurements made in 1972-1977 on normoglycemic individuals in three-generation Caucasian pedigrees from Rochester, Minnesota were analyzed. The authors determined the contributions of polygenic loci and environmental factors to fasting plasma glucose variability in these pedigrees. To that end, fasting plasma glucose measurements were normalized by an inverse normal scores transformation and then regressed separately for males and females on measured concomitants including age, body mass index (weight/height2), season of measurement, sex hormone use, and diuretic use. The authors found that 27.7% of the variability in normalized fasting plasma glucose in these pedigrees is explained by these measured concomitants. Subsequent variance components analysis suggested that unmeasured polygenic loci and unmeasured shared environmental factors together account for at least an additional 36.7% of the variability in normalized fasting plasma glucose, with genes alone accounting for at least 27.3%. These results are consistent with the known familiality of diabetes, for which fasting plasma glucose level is an important predictor. Further, these familial factors provide an explanation for at least half the variability in normalized fasting plasma glucose which remains after regression on known concomitants.read more
Citations
More filters
Journal ArticleDOI
Genetic and environmental contributions to cardiovascular risk factors in Mexican Americans: The San Antonio Family Heart Study
Braxton D. Mitchell,Candace M. Kammerer,John Blangero,Michael C. Mahaney,David L. Rainwater,Bennett Dyke,James E. Hixson,Richard D. Henkel,R. Mark Sharp,Anthony G. Comuzzie,John L. VandeBerg,Michael P. Stern,Jean W. MacCluer +12 more
TL;DR: Among Mexican Americans from San Antonio (Tex), the relative contributions of both genetic and environmental influences to a large panel of cardiovascular risk factors, including serum levels of lipids, lipoproteins, glucose, hormones, adiposity, and blood pressure are quantified.
Journal ArticleDOI
The genetic basis of plasma variation in adiponectin, a global endophenotype for obesity and the metabolic syndrome.
Anthony G. Comuzzie,Tohru Funahashi,Gabriele E. Sonnenberg,Lisa J. Martin,Howard J. Jacob,Anne E. Kwitek Black,Diana Maas,Masahiko Takahashi,Shinji Kihara,Sachiyo Tanaka,Yuji Matsuzawa,John Blangero,Daniel A. Cohen,Ahmed H. Kissebah +13 more
TL;DR: These results identify quantitative trait loci with significant effects on a newly described, and potentially very important, adipocyte-derived protein and reveal the emergence of a consistent pattern of linkage results for obesity-related traits across a number of human populations.
Journal ArticleDOI
Genetic Analysis of the IRS Pleiotropic Effects of Genes Influencing Insulin Levels on Lipoprotein and Obesity Measures
Braxton D. Mitchell,Candace M. Kammerer,Michael C. Mahaney,John Blangero,Anthony G. Comuzzie,Larry D. Atwood,Steven M. Haffner,Michael P. Stern,Jean W. MacCluer +8 more
TL;DR: Results suggest that a common set of genes influencing insulin levels also influences other insulin resistance syndrome-related traits, although for the most part this pleiotropic effects are not attributable to the 2-hour insulin level major locus.
Journal ArticleDOI
Variations in the G6PC2/ABCB11 genomic region are associated with fasting glucose levels.
Wei-Min Chen,Michael R. Erdos,Anne U. Jackson,Richa Saxena,Serena Sanna,Serena Sanna,Kristi D. Silver,Nicholas J. Timpson,Torben Hansen,Marco Orrù,Maria Grazia Piras,Lori L. Bonnycastle,Cristen J. Willer,Valeriya Lyssenko,Haiqing Shen,Johanna Kuusisto,Shah Ebrahim,Natascia Sestu,William L. Duren,Maria Cristina Spada,Heather M. Stringham,Laura J. Scott,Nazario Olla,Amy J. Swift,Samer S. Najjar,Braxton D. Mitchell,Debbie A Lawlor,George Davey Smith,Yoav Ben-Shlomo,Gitte Andersen,Knut Borch-Johnsen,Torben Jørgensen,Jouko Saramies,Timo T. Valle,Timo T. Valle,Thomas A. Buchanan,Alan R. Shuldiner,Edward G. Lakatta,Richard N. Bergman,Manuela Uda,Jaakko Tuomilehto,Jaakko Tuomilehto,Oluf Pedersen,Oluf Pedersen,Antonio Cao,Leif Groop,Karen L. Mohlke,Markku Laakso,David Schlessinger,Francis S. Collins,David Altshuler,Gonçalo R. Abecasis,Michael Boehnke,Angelo Scuteri,Richard M. Watanabe +54 more
TL;DR: The results in combination with data reported in the literature suggest that G6PC2, a glucose-6-phosphatase almost exclusively expressed in pancreatic islet cells, may underlie variation in fasting glucose, though it is possible that ABCB11, which is expressed primarily in liver, may also contribute to such variation.
Journal ArticleDOI
Genetic Epidemiology of Insulin Resistance and Visceral Adiposity ☆: The IRAS Family Study Design and Methods
Leora Henkin,Richard N. Bergman,Donald W. Bowden,Darrell L. Ellsworth,Steven M. Haffner,Carl D. Langefeld,Braxton D. Mitchell,Jill M. Norris,Marian Rewers,Mohammed F. Saad,Elizabeth R. Stamm,Lynne E. Wagenknecht,Stephen S. Rich +12 more
TL;DR: Results are consistent with the expectation that intermediate measures of insulin resistance and visceral adiposity are heritable, and that the IRAS Family Study has statistical power to detect these intermediate phenotypes of type 2 diabetes and atherosclerosis.