Familiality of quantitative metabolic traits in Finnish families with non-insulin-dependent diabetes mellitus. Finland-United States Investigation of NIDDM Genetics (FUSION) Study investigators - PubMed (original) (raw)
Multicenter Study
doi: 10.1159/000022865.
Affiliations
- PMID: 10364681
- DOI: 10.1159/000022865
Multicenter Study
Familiality of quantitative metabolic traits in Finnish families with non-insulin-dependent diabetes mellitus. Finland-United States Investigation of NIDDM Genetics (FUSION) Study investigators
R M Watanabe et al. Hum Hered. 1999 Jun.
Abstract
Type 2 diabetes mellitus (NIDDM) is a complex disorder encompassing multiple metabolic defects. There exists strong evidence for a genetic component to NIDDM; however, to date there have been few reports of linkage between genetic markers along the genome and NIDDM or NIDDM-related quantitative traits. We sought to determine whether individual quantitative traits which determine glucose tolerance exhibit familiality in Finnish families with at least one NIDDM-affected sibling pair. Tolbutamide-modified frequently sampled intravenous glucose tolerance tests (FSIGT) were performed on unaffected offspring (n = 431) and spouses (n = 154) of affected sibling pairs sampled for the Finland-United States Investigation of NIDDM Genetics (FUSION) study. FSIGT data were analyzed using the Minimal Model to obtain quantitative measures of insulin sensitivity (SI), glucose effectiveness (SG), and insulin secretion assessed as the acute insulin response to glucose (AIR). The disposition index (DI), a measure of insulin resistance-corrected beta-cell function, was also derived as the product of SI and AIR. Variance components analysis was used to determine for each trait, the heritability (h2), the proportion of the total trait variance accounted for by additive genes. After adjustment for age, gender, and body mass index, h2 estimates were: SG: 18 +/- 9%, SI: 28 +/- 8%, AIR: 35 +/- 8%, and DI: 23 +/- 8%. We conclude that there is strong evidence for modest heritability of Minimal-Model-derived NIDDM-related quantitative traits in unaffected spouses and offspring of Finnish affected sibling pairs.
Similar articles
- Mapping genes for NIDDM. Design of the Finland-United States Investigation of NIDDM Genetics (FUSION) Study.
Valle T, Tuomilehto J, Bergman RN, Ghosh S, Hauser ER, Eriksson J, Nylund SJ, Kohtamäki K, Toivanen L, Vidgren G, Tuomilehto-Wolf E, Ehnholm C, Blaschak J, Langefeld CD, Watanabe RM, Magnuson V, Ally DS, Hagopian WA, Ross E, Buchanan TA, Collins F, Boehnke M. Valle T, et al. Diabetes Care. 1998 Jun;21(6):949-58. doi: 10.2337/diacare.21.6.949. Diabetes Care. 1998. PMID: 9614613 - The Finland-United States investigation of non-insulin-dependent diabetes mellitus genetics (FUSION) study. II. An autosomal genome scan for diabetes-related quantitative-trait loci.
Watanabe RM, Ghosh S, Langefeld CD, Valle TT, Hauser ER, Magnuson VL, Mohlke KL, Silander K, Ally DS, Chines P, Blaschak-Harvan J, Douglas JA, Duren WL, Epstein MP, Fingerlin TE, Kaleta HS, Lange EM, Li C, McEachin RC, Stringham HM, Trager E, White PP, Balow J Jr, Birznieks G, Chang J, Eldridge W. Watanabe RM, et al. Am J Hum Genet. 2000 Nov;67(5):1186-200. Epub 2000 Oct 13. Am J Hum Genet. 2000. PMID: 11032784 Free PMC article. - High heritability and genetic correlation of intravenous glucose- and tolbutamide-induced insulin secretion among non-diabetic family members of type 2 diabetic patients.
Gjesing AP, Hornbak M, Allin KH, Ekstrøm CT, Urhammer SA, Eiberg H, Pedersen O, Hansen T. Gjesing AP, et al. Diabetologia. 2014 Jun;57(6):1173-81. doi: 10.1007/s00125-014-3207-y. Epub 2014 Mar 7. Diabetologia. 2014. PMID: 24604100 - Toward an integrated phenotype in pre-NIDDM.
Bergman RN, Watanabe R, Rebrin K, Ader M, Steil G. Bergman RN, et al. Diabet Med. 1996 Sep;13(9 Suppl 6):S67-77. Diabet Med. 1996. PMID: 8894486 Review. - Molecular physiology and genetics of NIDDM. Importance of metabolic staging.
Granner DK, O'Brien RM. Granner DK, et al. Diabetes Care. 1992 Mar;15(3):369-95. doi: 10.2337/diacare.15.3.369. Diabetes Care. 1992. PMID: 1559407 Review.
Cited by
- Insulin secretion and action and the response of endogenous glucose production to a lack of glucagon suppression in nondiabetic subjects.
Adams JD, Egan AM, Laurenti MC, Schembri Wismayer D, Bailey KR, Cobelli C, Dalla Man C, Vella A. Adams JD, et al. Am J Physiol Endocrinol Metab. 2021 Nov 1;321(5):E728-E736. doi: 10.1152/ajpendo.00284.2021. Epub 2021 Oct 18. Am J Physiol Endocrinol Metab. 2021. PMID: 34658253 Free PMC article. Clinical Trial. - Are caveolin-1 minor alleles more likely to be risk alleles in insulin resistance mechanisms in metabolic diseases?
Abaj F, Saeedy SAG, Mirzaei K. Abaj F, et al. BMC Res Notes. 2021 May 17;14(1):185. doi: 10.1186/s13104-021-05597-6. BMC Res Notes. 2021. PMID: 34001235 Free PMC article. - The Variant rs1784042 of the SIDT2 Gene is Associated with Metabolic Syndrome through Low HDL-c Levels in a Mexican Population.
León-Reyes G, Rivera-Paredez B, López JCF, Ramírez-Salazar EG, Aquino-Gálvez A, Gallegos-Carrillo K, Denova-Gutiérrez E, Salmerón J, Velázquez-Cruz R. León-Reyes G, et al. Genes (Basel). 2020 Oct 14;11(10):1192. doi: 10.3390/genes11101192. Genes (Basel). 2020. PMID: 33066450 Free PMC article. - Genetics Insights in the Relationship Between Type 2 Diabetes and Coronary Heart Disease.
Goodarzi MO, Rotter JI. Goodarzi MO, et al. Circ Res. 2020 May 22;126(11):1526-1548. doi: 10.1161/CIRCRESAHA.119.316065. Epub 2020 May 21. Circ Res. 2020. PMID: 32437307 Free PMC article. Review. - Genome-Wide Association Study of Metabolic Syndrome Reveals Primary Genetic Variants at CETP Locus in Indians.
Prasad G, Bandesh K, Giri AK, Kauser Y, Chanda P, Parekatt V, Mathur S, Madhu SV, Venkatesh P, Bhansali A, Marwaha RK, Basu A, Tandon N, Bharadwaj D; INDICO. Prasad G, et al. Biomolecules. 2019 Jul 30;9(8):321. doi: 10.3390/biom9080321. Biomolecules. 2019. PMID: 31366177 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical