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Topical Area: Precision Nutrition/Nutrient-Gene Interactions

Precision Nutrition/Nutrient-Gene Interactions (Poster Session)

(P10-021-23) The SLC16A11 Risk Haplotype for Type 2 Diabetes (T2D) Is Associated With Differentiated Responses in HbA1c and Weight Loss After Treatments To Prevent T2D

Saturday, July 22, 2023
12:00 PM – 1:00 PM ET
Location: Poster Board 527
Disclosure(s):
Magdalena Sevilla-Gonzalez, PhD: No relevant financial relationship(s) with ineligible companies to disclose.


Objectives: Dietary modification and/or metformin remain the most cost-effective treatment to prevent type 2 diabetes (T2D). Yet, there is an important variation to receive the benefit among individuals. A haplotype in SLC16A11 is associated with decreased insulin action, and risk for type 2 diabetes (T2D) in Mexicans. We aim to determine the impact of the risk haplotype on SLC16A11 on early therapeutic responses in treatments to prevent T2D.

Methods: We recruited individuals with at least one prediabetes criteria according to the American Diabetes Association with a body mass index (BMI) between 25 and 45 kg/m2. Participants were randomized into two groups: lifestyle intervention (LSI): hypocaloric diet, 25 kcal/kg of ideal weight, 45% of the total intake of carbohydrates, 30% lipids, and 15% protein sources + physical activity ( >150 min medium intensity per week), or LSI + 750 mg metformin twice a day. Standardized dietitians delivered the LSI. The treatment goal was to achieve >3% weight loss during the 12-week follow-up. Participants were genotyped for the risk allele rs13342232. The effects of the risk haplotype were evaluated with linear and logistic regressions adjusted by age, sex, five genetic principal components, BMI, and prediabetes criteria at baseline. Primary outcome was a significant interaction between the treatment arm and genotype in fold change (FC) HbA1c.

Results: Among 301 participants screened, 109 were randomized (mean age, 51 [42-56] years; 62% women; mean BMI, 29.7 (25.6-32.7); 60 [55%] had a T2D-risk genotype). The baseline HbA1c% was 5.9 [5.7 - 6.1]. Weight change at 12 weeks was -3.24kg in the overall sample and 58% (n=51) reached the < 3% weight loss goal. There was a significant treatment-genotype interaction (P = .032) in FC HbA1c and weight loss goal (P = .024). These results suggest that carriers with prediabetes with LSI + metformin treatment have higher probabilities to reduce HbA1c and reach their weight loss goal.

Conclusions: In individuals with prediabetes the risk haplotype on SLC16A11 carriers might benefit more from LSI + metformin to reduce HbA1c and reach a 3% weight loss after 12 weeks of treatment. Our findings can serve to inform and design future tailored T2D prevention strategies in high-risk populations.

Funding Sources: Miguel Aleman Foundation Award