Froylan D Martínez-Sánchez1, Valerie Paola Vargas-Abonce2, Anna Paula Guerrero-Castillo3, Manuel De Los Santos-Villavicencio4, Jocelyn Eseiza-Acevedo5, Clara Elena Meza-Arana6, Alfonso Gulias-Herrero7, Miguel Ángel Gómez-Sámano8. 1. Department of Endocrinology and Metabolism, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Vasco de Quiroga # 15, Belisario Domínguez Sección XVI, Tlalpan, 14080 Mexico City, Mexico; Facultad de Ciencias de la Salud, Universidad Anáhuac México Norte, Av. Universidad Anáhuac #46. Lomas Anáhuac, 52786 Huixquilucan, Estado de Mexico, Mexico. Electronic address: froylan.martinez@anahuac.mx. 2. Department of Endocrinology and Metabolism, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Vasco de Quiroga # 15, Belisario Domínguez Sección XVI, Tlalpan, 14080 Mexico City, Mexico. Electronic address: valerie.vargas.abonce@gmail.com. 3. Department of Endocrinology and Metabolism, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Vasco de Quiroga # 15, Belisario Domínguez Sección XVI, Tlalpan, 14080 Mexico City, Mexico. Electronic address: annapaulaguerrero@gmail.com. 4. Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, 239, Mexico City, Mexico City, Mexico. Electronic address: manuelle.s.v@gmail.com. 5. Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, 239, Mexico City, Mexico City, Mexico. Electronic address: 97ea.joss@gmail.com. 6. Department of Endocrinology and Metabolism, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Vasco de Quiroga # 15, Belisario Domínguez Sección XVI, Tlalpan, 14080 Mexico City, Mexico. Electronic address: claraelena88@hotmail.com. 7. Department of Endocrinology and Metabolism, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Vasco de Quiroga # 15, Belisario Domínguez Sección XVI, Tlalpan, 14080 Mexico City, Mexico. Electronic address: alfonso.guliash@innsz.mx. 8. Department of Endocrinology and Metabolism, Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran, Vasco de Quiroga # 15, Belisario Domínguez Sección XVI, Tlalpan, 14080 Mexico City, Mexico. Electronic address: miguel.gomezs@incmnsz.mx.
Abstract
AIMS: Insulin resistance (IR) predisposes to type 2 diabetes mellitus (T2DM). Although previous studies have associated serum uric acid concentration with IR in T2DM, its association with impaired insulin secretion and beta-cell dysfunction in subjects at risk for developing T2DM remains uncertain. Thus, we aimed to analyze the association of serum uric acid concentration with IR using surrogate insulin resistance/secretion and beta-cell function indices in subjects at risk for developing T2DM. METHODS: This is a cross-sectional study that included 354 subjects who underwent an oral glucose tolerance test who had at least two risk factors for T2DM without any chronic disease. RESULTS: Participants were 51±8 years old, 72.2% were women, had a mean body mass index of 29.9±6.5kg/m2 and mean serum uric acid concentration of 5.7±1.3mg/dL. HOMA-IR, first-phase insulin secretion (S1PhOGTT), second-phase insulin secretion (S2PhOGTT), Matsuda and disposition indices were significantly correlated with serum uric acid concentrations (r=0.239, r=0.225, r=0.201, r=-0.287, r=-0.208; respectively). After multiple linear regression analysis, serum uric acid concentration was independently associated with HOMA-IR (β=0.283), HOMA-B (β=0.185), S1PhOGTT (β=0.203), S2PhOGTT (β=0.186), and Matsuda Index (β=-0.322). A serum uric acid concentration of 5.5mg/dL had the best sensitivity/sensibility to identify subjects with IR (HOMA-IR ≥2.5). CONCLUSIONS: Serum uric acid concentration is significantly associated with IR and impaired insulin secretion, but not with beta-cell dysfunction, in subjects at risk for developing T2DM.
AIMS: Insulin resistance (IR) predisposes to type 2 diabetes mellitus (T2DM). Although previous studies have associated serum uric acid concentration with IR in T2DM, its association with impaired insulin secretion and beta-cell dysfunction in subjects at risk for developing T2DM remains uncertain. Thus, we aimed to analyze the association of serum uric acid concentration with IR using surrogate insulin resistance/secretion and beta-cell function indices in subjects at risk for developing T2DM. METHODS: This is a cross-sectional study that included 354 subjects who underwent an oral glucose tolerance test who had at least two risk factors for T2DM without any chronic disease. RESULTS:Participants were 51±8 years old, 72.2% were women, had a mean body mass index of 29.9±6.5kg/m2 and mean serum uric acid concentration of 5.7±1.3mg/dL. HOMA-IR, first-phase insulin secretion (S1PhOGTT), second-phase insulin secretion (S2PhOGTT), Matsuda and disposition indices were significantly correlated with serum uric acid concentrations (r=0.239, r=0.225, r=0.201, r=-0.287, r=-0.208; respectively). After multiple linear regression analysis, serum uric acid concentration was independently associated with HOMA-IR (β=0.283), HOMA-B (β=0.185), S1PhOGTT (β=0.203), S2PhOGTT (β=0.186), and Matsuda Index (β=-0.322). A serum uric acid concentration of 5.5mg/dL had the best sensitivity/sensibility to identify subjects with IR (HOMA-IR ≥2.5). CONCLUSIONS: Serum uric acid concentration is significantly associated with IR and impaired insulin secretion, but not with beta-cell dysfunction, in subjects at risk for developing T2DM.