Background: A high adherence (adh.) to a MedDiet pattern was associated with a reduced GDM risk. Studies have shown associations between MTNR1B rs10830963, TCF7L2 rs7903146, MC4R rs17782313 SNPs and GDM risk. The conferring risk could be modified by a MedDiet. This study’s aim was to investigate if the association between the degree of adh. to a MedDiet and GDM incidence is modulated by MTNR1B rs10830963 C>G, TCF7L2 rs7903146 C>T and MC4R rs17782313 T>C polymorphisms.

Methods and Findings: 874 women were stratified into 3 groups defined as high, moderate or low adh. according to late first-trimester (>12 gestational weeks) compliance with 6 food targets: vegetables >12 s/w, fruits >12 s/w, juice <2 s/w, nuts> 3 s/w, consumption of extra virgin olive oil (EVOO) >6 d/w and 40 mL/d EVOO. High adh. was defined as complying with 5-6 targets; moderate 2-4 targets and low 0-1 targets. Patients were genotyped for rs10830963, rs7903146 and rs17782313. Logistic regression analysis was adjusted for ethnicity, age, parity and BMI.

Results: There was a significant association between rs10830963 risk allele G and GDM risk (OR) 1.87(1.29-2.73); and fasting 1.77(0.88-2.66) and 1 h glycaemia 6.27 (1.72-10.83) during 75g OGTT (all p<0.0001). Subjects with rs10830963 G allele who had low adh. had higher fasting glucose (mg/dL) compared to carriers with high adh. (88.24±0.93 vs. 84.59±0.85, p inter< 0.05). For T carriers of rs7903146 and C carriers of rs17782313 the genetic risk for GDM was significantly lower in women with high adh. 0.43 (0.23-0.80) compared to low adh. 0.2 (0.14-0.99), p-inter <0.01. The genetic risk score confirmed a significant gene-MedDiet interaction (p=0,05) for GDM. There was no effect in non-risk genotype carriers for the 3 SNPs.

Conclusions: MTNR1B, TCF7L2, MC4R genes modulate the effect of a DietMed on the development of impaired glucose metabolism and GDM.


A. Barabash: None. J. Valerio Deogracia: None. C. Assaf-Balut: None. L. Del Valle: None. N. Garcia de la Torre: None. E. Bordiu: None. A. Duran: None. M. Fuentes: None. J. Ines: None. M. Cuesta: None. M.A. Rubio: None. A.L. Calle: None.


Instituto de Salud Carlos III of Spain; Fondo Europeo de Desarrollo Regional; Sociedad de Endocrinolog?a Nutrici?n y Diabetes de la Comunidad de Madrid (IPI/2017/NR2)

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