Germán D Carrasquilla1, Hermina Jakupović1, Tuomas O Kilpeläinen2. 1. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, Mærsk Building (8. floor), Copenhagen, Denmark. 2. Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, Mærsk Building (8. floor), Copenhagen, Denmark. tuomas.kilpelainen@sund.ku.dk.
Abstract
PURPOSE OF REVIEW: We review recent evidence of the relationship between dietary fat intake and risk of type 2 diabetes (T2D), the role of epigenetic alterations as a mediator of this relationship, and the impact of gene-dietary fat interactions in the development of the disease. Based on the observations made, we will discuss whether there is evidence to support genetic personalization of fat intake recommendations in T2D prevention. RECENT FINDINGS: Strong evidence suggests that polyunsaturated fatty acids (PUFA) have a protective effect on T2D risk, whereas the roles of saturated and monounsaturated fatty acids (SFA and MUFA) remain unclear. Diets enriched with PUFA vs SFA lead to distinct epigenetic alterations that may mediate their effects on T2D risk by changing gene function. However, it is not currently known which of the epigenetic alterations, if any, are causal for T2D. The current literature shows no replicated evidence of genetic variants modifying the effect of dietary fat intake on T2D risk. There is consistent evidence of a protective role of PUFA in T2D prevention. No evidence supports genetic personalization of dietary recommendations in T2D prevention.
PURPOSE OF REVIEW: We review recent evidence of the relationship between dietary fat intake and risk of type 2 diabetes (T2D), the role of epigenetic alterations as a mediator of this relationship, and the impact of gene-dietary fat interactions in the development of the disease. Based on the observations made, we will discuss whether there is evidence to support genetic personalization of fat intake recommendations in T2D prevention. RECENT FINDINGS: Strong evidence suggests that polyunsaturated fatty acids (PUFA) have a protective effect on T2D risk, whereas the roles of saturated and monounsaturated fatty acids (SFA and MUFA) remain unclear. Diets enriched with PUFA vs SFA lead to distinct epigenetic alterations that may mediate their effects on T2D risk by changing gene function. However, it is not currently known which of the epigenetic alterations, if any, are causal for T2D. The current literature shows no replicated evidence of genetic variants modifying the effect of dietary fat intake on T2D risk. There is consistent evidence of a protective role of PUFA in T2D prevention. No evidence supports genetic personalization of dietary recommendations in T2D prevention.
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