Using genetic variants to assess the relationship between circulating lipids and type 2 diabetes.

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Fall, Tove (author): Uppsala universitet,Lund University,Lunds universitet,Genomik, diabetes och endokrinologi,Forskargrupper vid Lunds universitet,Genomics, Diabetes and Endocrinology,Lund University Research Groups,Science for Life Laboratory, SciLifeLab,Molekylär epidemiologi

Xie, Weijia (author)

Poon, Wenny (author): Lund University,Lunds universitet,Genomik, diabetes och endokrinologi,Forskargrupper vid Lunds universitet,Genomics, Diabetes and Endocrinology,Lund University Research Groups

Yaghootkar, Hanieh (author)

Mägi, Reedik (author)

Knowles, Joshua W (author)

Lyssenko, Valeriya (author): Lund University,Lunds universitet,Genomik, diabetes och endokrinologi,Forskargrupper vid Lunds universitet,Genomics, Diabetes and Endocrinology,Lund University Research Groups

Weedon, Michael (author)

Frayling, Timothy M (author)

Ingelsson, Erik (author): Uppsala universitet,Molekylär epidemiologi,Science for Life Laboratory, SciLifeLab

(creator_code:org_t)

2015-05-06
2015
English.
In: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 64:7, s. 2676-2684

Related links:: http://www.ncbi.nlm....; show more...; http://dx.doi.org/10...; https://diabetes.dia...; https://lup.lub.lu.s...; https://doi.org/10.2...; https://urn.kb.se/re...; show less...

Abstract Subject headings

The effects of dyslipidemia on the risk of type 2 diabetes (T2D) and related traits are not clear. We used regression models and 140 lipid-associated genetic variants to estimate associations between circulating HDL-cholesterol, LDL-cholesterol and triglycerides, and T2D and related traits. Each genetic test was corrected for effects of variants on the other two lipid types and surrogates of adiposity. We used the largest datasets available - 34,840 T2D cases and 114,981 controls from the DIAGRAM consortium and up to 133,010 non-diabetic individuals for insulin secretion and sensitivity, from the MAGIC and GENESIS studies.Eight out of 21 associations between groups of variants and diabetes traits were significant at the nominal level, including those between genetically determined lower HDL-C (β=-0.12, P=0.03) and T2D, and genetically determined lower LDL-C (β =-0.21, P=5x10(-6)) and T2D. While some of these may represent causal associations, we discuss why caution must be used when using Mendelian randomization in the context of circulating lipid levels and diabetes traits. In conclusion, we found evidence of links between genetic variants associated with lipids and T2D, but deepened knowledge of the underlying genetic mechanisms of specific lipid variants is needed before drawing definite conclusions about causality using Mendelian randomization methodology.

By the author/editor: Fall, Tove; Xie, Weijia; Poon, Wenny; Yaghootkar, Hani ...; Mägi, Reedik; Knowles, Joshua ...; show more...; Lyssenko, Valeri ...; Weedon, Michael; Frayling, Timoth ...; Ingelsson, Erik; show less...

About the subject

MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Clinical Medicin ...; and Endocrinology an ...

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