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Perilipin polymorphism interacts with saturated fat and carbohydrates to modulate insulin resistance.

ABSTRACT: Macronutrient intakes and genetic variants have been shown to interact to alter insulin resistance, but replications of gene-nutrient interactions across independent populations are rare, despite their critical importance in establishing credibility. We aimed to investigate a previously demonstrated saturated fat and carbohydrate interaction for insulin resistance for perilipin (PLIN1), a regulator of adipocyte metabolism.We investigated the previously shown interaction for PLIN1 11482G > A (rs894160) on insulin resistance in US men (n = 462) and women (n = 508) (mean ± SD, 49 ± 16 years). In multivariable linear regression models, we found an interaction (P < 0.05) between the ratio of saturated fat to carbohydrate intake as a continuous variable and PLIN1 11482G > A for HOMA-IR (homeostasis model assessment of insulin resistance) in women. For carriers of the minor allele but not for non-carriers, as the ratio of saturated fat to carbohydrate intake increased, predicted HOMA-IR increased (P = 0.002). By dichotomizing the ratio of saturated fat to carbohydrate intake into high and low, we found significant interaction terms for insulin and HOMA-IR (P < 0.05). When the ratio of saturated fat to carbohydrate was high, insulin and HOMA-IR were higher in minor allele carriers (P = 0.004 and P = 0.003, respectively), but did not differ when the ratio was low. Similar patterns or trends were observed when saturated fat and carbohydrate were dichotomized into high and low as individual macronutrients.Replication of the previously reported interaction between macronutrient intakes and PLIN1 genotype for insulin resistance reinforces the potential usefulness of applying genotype information in the dietary management of insulin resistance.

SUBMITTER: Smith CE

PROVIDER: S-EPMC3117106 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature

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Perilipin polymorphism interacts with saturated fat and carbohydrates to modulate insulin resistance.

Smith C E CE Arnett D K DK Corella D D Tsai M Y MY Lai C Q CQ Parnell L D LD Lee Y C YC Ordovás J M JM

Nutrition, metabolism, and cardiovascular diseases : NMCD 20101230 5

<h4>Background and aims</h4>Macronutrient intakes and genetic variants have been shown to interact to alter insulin resistance, but replications of gene-nutrient interactions across independent populations are rare, despite their critical importance in establishing credibility. We aimed to investigate a previously demonstrated saturated fat and carbohydrate interaction for insulin resistance for perilipin (PLIN1), a regulator of adipocyte metabolism.<h4>Methods and results</h4>We investigated th ...[more]

PMID: 21193293

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Project description:S100 calcium-binding protein A9 (S100A9) has previously been identified as a type 2 diabetes (T2D) gene. However, this finding requires independent validation and more in-depth analyses in other populations and ancestries.We aimed to replicate the associations between an S100A9 variant and insulin resistance and T2D and to initiate an investigation of potential interactions with the habitual diet in several independent populations.We investigated the association of the S100A9 variant rs3014866 with insulin resistance and T2D risk and its interactions with diet in 3 diverse populations as follows: the CORDIOPREV (Coronary Diet Intervention with Olive Oil and Cardiovascular Prevention; n = 711), which consisted of Spanish white adults; the GOLDN (Genetics of Lipids Lowering Drugs and Diet Network; n = 818), which involved North American non-Hispanic white adults; and Hispanic adults who participated in the BPRHS (Boston Puerto Rican Health Study; n = 1155).Meta-analysis indicated that T carriers presented a lower risk of T2D than CC carriers (pooled OR: 0.714; 95% CI: 0.584, 0.845; P = 0.002). In all 3 populations (CORDIOPREV, GOLDN, and BPRHS), we showed a significant interaction between the rs3014866 single nucleotide polymorphism and dietary SFA:carbohydrate ratio intake for the homeostasis model assessment of insulin resistance (HOMA-IR) (P = 0.028, P = 0.017, and P = 0.026, respectively). CC carriers had a significantly higher HOMA-IR only when SFA:carbohydrate intake was high (P = 0.045 for the CORDIOPREV, P = 0.033 for the GOLDN, and P = 0.046 for the BPRHS) but not when SFA:carbohydrate ratio intake was low.The minor allele (T) of the S100A9 variant rs3014866 is associated with lower T2D risk in 3 populations of different ancestries. Note that individuals with the high-risk CC genotype may be more likely to benefit from a low SFA:carbohydrate ratio intake to improve insulin resistance as evaluated with the use of the HOMA-IR. These trials were registered at clinicaltrials.gov as NCT00924937 (CORDIOPREV), NCT00083369 (GOLDN), and NCT01231958 (BPRHS).

Dataset Information

Perilipin polymorphism interacts with saturated fat and carbohydrates to modulate insulin resistance.

Publications

Perilipin polymorphism interacts with saturated fat and carbohydrates to modulate insulin resistance.

Similar Datasets

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