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Clustering of insulin resistance, total and central abdominal fat: same genes or same environment?

Published online by Cambridge University Press:  21 February 2012

Katherine Samaras ,
Tuan V Nguyen ,
Arthur B Jenkins ,
John A Eisman ,
Gabrielle M Howard ,
Paul J Kelly  and
Lesley V Campbell
Katherine Samaras
Affiliation:
Metabolism, Garvan Institute of Medical Research, Sydney.
Tuan V Nguyen
Affiliation:
Bone and Mineral Research, Garvan Institute of Medical Research, Sydney.
Arthur B Jenkins
Affiliation:
Department of Biomedical Science, University of Wollongong, NSW.
John A Eisman
Affiliation:
Bone and Mineral Research, Garvan Institute of Medical Research, Sydney.
Gabrielle M Howard
Affiliation:
Bone and Mineral Research, Garvan Institute of Medical Research, Sydney.
Paul J Kelly
Affiliation:
Department of Endocrinology, St Vincent' Hospital, Sydney, Australia.
Lesley V Campbell*
Affiliation:
Metabolism, Garvan Institute of Medical Research, Sydney. [email protected]
*
*Correspondence: Professor LV Campbell, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney, 384 Victoria St, Darlinghurst, NSW, 2010 Australia. Tel: 9361 2622; Fax: 9331 6626;

Abstract

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Obesity, insulin resistance and disturbed glucose metabolism cluster within the Insulin Resistance Syndrome (IRS). Whether this reflects shared genetic or environmental factors detectable in ‘normal’ populations (not selected for IRS features) is unknown. This study estimated (i) genetic influences on IRS traits and (ii) shared and specific genetic and environmental factors on the relationships between these traits in healthy female twins. Fasting insulin, glucose, total and central fat were measured in 59 monozygotic (MZ) and 51 dizygotic (DZ) female twin pairs aged ( ± SD) 52 ± 13 years. Body fat was measured by dual-energy X-ray absorptiometry, insulin resistance and secretion by a modified homeostasis model assessment. Using intraclass correlation coefficients and univariate model-fitting analyses, genetic influences were found in total fat, central fat, insulin resistance, fasting glucose and insulin secretion, with genetic factors explaining 64, 57, 59, 75 and 68% of their variance, respectively, using the latter technique. In matched analysis intra-pair differences in total and central fat related to intra-pair differences in insulin resistance (r2 = 0.19, P < 0.001). Multivariate model-fitting showed a close genetic relationship between total and central fat (r = 0.88). The genetic correlation between IR and central fat (0.41) was significantly greater than that for total fat (0.24), suggesting that central fat is not only a predictor of, but shares considerable genetic influence with, insulin resistance. In Cholesky analysis, these genetic influences were separate from those shared between central and total fat. In conclusion, both shared and specific genetic factors regulate components of the IRS in healthy females. However, there were discrete genetic influences on -cell insulin secretion, not shared with other IRS components, suggesting that a separate genetic propensity exists for Type2 diabetes. These findings suggest we may understand the genetic and environmental influences on IRS from the study of the normal population.

Keywords

twinsinsulininsulin resistanceglucosegenetic epidemiologyfatvisceral fatabdominal fatDXA
Type
Articles
Information
Twin Research and Human Genetics , Volume 2 , Issue 3 , 01 June 1999 , pp. 218 - 225
Copyright
Copyright © Cambridge University Press 1999