Association between nutritional risk markers and polymorphisms rs2291166 in TJP1 and VNTR (CAG)n in ATXN2 in an obese adolescent Mexican population. / Asociación entre marcadores de riesgo nutricionales con los polimorfismos rs2291166 de TJP1 y el VNTR (CAG)n de ATXN2 en población mexicana adolescente con obesidad.

OBJECTIVE: To estimate the correlation between indices of diet quality (DQIs), insulin sensitivity (QUICKI) and resistance (HOMA-IR), waist circumference (WHR) and body mass (BMI) and the alleles and genotypes of the TJP1 SNP rs2291166 and the VNTR of ATXN2 in adolescent patients. SUBJECTS AND METHOD: The study enrolled 85 subjects aged 10-20years, from the city of Tuxtepec, Oaxaca, Mexico, recruited in the period 2017-2018. DQIs, BMI, WHR, HOMA-IR, QUICKI, and diet quality index were measured. The rs2291166 polymorphism in TJP1 was determined by allele-specific PCR and the (CAG)n expansion in ATXN2 was determined by hot start PCR. PCR products were analyzed using 8% PAGE electrophoresis and silver nitrate staining. RESULTS: A correlation was found of indices DQIs, HOMA-IR, WHR and BMI with the heterozygous genotype of the TJP1 SNP rs2291166 and the long and short repeats of the ATXN2 CAG repeat in obese adolescent patients. A very strong positive correlation was seen between the TJP1 SNP and the HOMA-IR index (P<.05). A positive correlation was also found between the ATXN2 CAG repeat and the QUICKI index (P=.000) (P<.05), while the DQIs index correlated more closely with BMI and WHR. CONCLUSIONS: DQIs, TJP1 SNP rs2291166, and ATXN2 CAG repeat are determinants of obesity-related risk parameters such as BMI, WHR, QUICKI, and HOMA-IR in the adolescent population analyzed.

Inverse Relationship of the CMKLR1 Relative Expression and Chemerin Serum Levels in Obesity with Dysmetabolic Phenotype and Insulin Resistance.

BACKGROUND: In obesity there is a subclinical chronic low-grade inflammatory response where insulin resistance (IR) may develop. Chemerin is secreted in white adipose tissue and promotes low-grade inflammatory process, where it expressed CMKLR1 receptor. The role of chemerin and CMKLR1 in inflammatory process secondary to obesity is not defined yet. METHODS: Cross-sectional study with 134 individuals classified as with and without obesity by body mass index (BMI) and IR. Body fat storage measurements and metabolic and inflammatory markers were measured by routine methods. Soluble chemerin and basal levels of insulin by ELISA and relative expression of CMKLR1 were evaluated with qPCR and 2(-ΔΔCT) method. RESULTS: Differences (P < 0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. Both CMKLR1 expression and chemerin levels were increased in obesity without IR. Soluble chemerin levels correlate with adiposity and metabolic markers (r = 8.8% to 38.5%), P < 0.05. CONCLUSION: The increment of CMKLR1 expression was associated with insulin production. Increased serum levels of chemerin in obesity were observed, favoring a dysmetabolic response. The results observed in this study suggest that both chemerin and CMKLR1 have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.

Asociación del polimorfismo 3’UTR+62G>A en resistina con resistencia a la insulina, adiposidad y el índice adiponectina-resistina en población mexicana / Association of resistin gene 3’utr +62g>a polymorphism with insulin resistance, adiposity and the adiponectin-resistin index in Mexican population

Introduction: Insulin resistance (IR) is a disease with genetic susceptibility characterized by the increase in storage and irregular body fat distribution, and impaired production of adipokines. Objective: The objective was to investigate the relationship between 3'UTR+62G>A RETN gene polymorphism, with adiponectin-resistin index (ARindex), adiposity, and inmuno-metabolic markers. Methods: In this cross-sectional study, 260 individuals characterized as Mexican-Mestizo and classified in lean and overweight, and IR and without-IR, were included. Anthropometrics, body composition, body fat distribution and inflammation and metabolic markers were measured by routine methods, RETN 3'UTR+62G>A alleles were identified by PCR-RFLP and soluble insulin, total adiponectin and resistin were measured by ELISA methods. Results: The +62G allele frequencies for lean and overweight individuals were different P=0.0343 (95.4% and 98.4%, respectively). The lean GA genotype carriers showed significant low measures of ARindex, adiposity, and inmuno-metabolic markers, than the GG genotype carriers. We found differences between individuals with IR and without-IR: in ARindex (P=0.002), adiponectin (P=0.002) and resistin levels (P=0.033): 1.102 ± 0.03, 5.167 ± 0.36ug/mL and 8.827 ± 0.42ng/mL versus 1.336 ± 0.07, 3.577 ± 0.34ug/mL and 10.480 ± 0.65ng/mL. Showed correlations with inflammation markers, distribution and body fat storage (r=0.262 to 0.414), PA polymorphism is associated with overweight. The presence of the +62A allele was associated with increase of total adiponectin, ARindex, resistin levels, metabolic markers and body fat storage. ARindex can be an early indicator of insulin resistance (AU)

Introducción: La resistencia a la insulina (RI) se caracteriza por susceptibilidad genética, incremento en la adiposidad y distribución irregular de grasa corporal, con alteración en la producción de adipocinas. Objetivo: Investigar la asociación del polimorfismo 3’UTR+62G>A en resistina con RI, índice adiponectina-resistina (ARindex), adiposidad y marcadores inmuno-metabólicos. Métodos: En un estudio transversal a 260 mestizos-mexicanos, clasificados con peso normal, exceso de peso, sin y con RI, se les evaluó: composición corporal, distribución de masa grasa y marcadores inmuno-metabólicos. Los alelos del polimorfismo 3’UTR+62G>A en resistina se identificaron por PCR-RFLP. La concentración sérica de insulina, adiponectina total y resistina se midieron por la técnica de ELISA. Resultados: Las frecuencias del alelo +62G para los individuos con peso normal y exceso de peso, fueron (95.4% y 98.4%, respectivamente) P=0.0343. Los portadores del genotipo GA con peso normal mostraron valores menores del ARindex, adiposidad y marcadores inmuno-metabólicos comparados con los portadores del genotipo GG. Se observó diferencia entre los individuos sin y con RI en el ARindex (P=0.002), concentración sérica de adiponectina (P=0.002) y resistina (P=0.033): 1.102±0.03, 5.167±0.36ug/mL y 8.827±0.42ng/mL versus 1.336±0.07, 3.577±0.34ug/mL y 10.480±0.65ng/mL, respectivamente. Los marcadores inmuno-metabólicos, reserva y distribución de grasa corporal correlacionan con ARindex (r=0.262 a 0.414), PA en los individuos mestizos-mexicanos con exceso de peso. El alelo +62A se asoció con incremento de adiponectina total, valores menores del ARindex, concentración de resistina, marcadores metabólicos y reserva de grasa corporal. El ARindex puede ser un indicador temprano de RI (AU)

[Association of resistin gene 3'UTR+62G>A polymorphism with insulin resistance, adiposity and the adiponectin-resistin index in Mexican population]. / Asociación del polimorfismo 3'UTR+62G>A en resistina con resistencia a la insulina, adiposidad y el índice adiponectina-resistina en población mexicana.

INTRODUCTION: Insulin resistance (IR) is a disease with genetic susceptibility characterized by the increase in storage and irregular body fat distribution, and impaired production of adipokines. OBJECTIVE: The objective was to investigate the relationship between 3'UTR+62G>A RETN gene polymorphism, with adiponectin-resistin index (ARindex), adiposity, and inmuno-metabolic markers. METHODS: In this cross-sectional study, 260 individuals characterized as Mexican-Mestizo and classified in lean and overweight, and IR and without-IR, were included. Anthropometrics, body composition, body fat distribution and inflammation and metabolic markers were measured by routine methods, RETN 3'UTR+62G>A alleles were identified by PCR-RFLP and soluble insulin, total adiponectin and resistin were measured by ELISA methods. RESULTS: The +62G allele frequencies for lean and overweight individuals were different P=0.0343 (95.4% and 98.4%, respectively). The lean GA genotype carriers showed significant low measures of ARindex, adiposity, and inmuno-metabolic markers, than the GG genotype carriers. We found differences between individuals with IR and without-IR: in ARindex (P=0.002), adiponectin (P=0.002) and resistin levels (P=0.033): 1.102 ± 0.03, 5.167 ± 0.36 ug/mL and 8.827 ± 0.42 ng/mL versus 1.336 ± 0.07, 3.577 ± 0.34 ug/mL and 10.480 ± 0.65 ng/mL. Showed correlations with inflammation markers, distribution and body fat storage (r=0.262 to 0.414), P< 0.05. CONCLUSIONS: The present data suggest that in a Mexican-mestizo population the RETN +62G>A polymorphism is associated with overweight. The presence of the +62A allele was associated with increase of total adiponectin, ARindex, resistin levels, metabolic markers and body fat storage. ARindex can be an early indicator of insulin resistance.

Introducción: La resistencia a la insulina (RI) se caracteriza por susceptibilidad genética, incremento en la adiposidad y distribución irregular de grasa corporal, con alteración en la producción de adipocinas. Objetivo: Investigar la asociación del polimorfismo 3'UTR+62G>A en resistina con RI, índice adiponectina-resistina (ARindex), adiposidad y marcadores inmuno-metabólicos. Métodos: En un estudio transversal a 260 mestizos-mexicanos, clasificados con peso normal, exceso de peso, sin y con RI, se les evaluó: composición corporal, distribución de masa grasa y marcadores inmuno-metabólicos. Los alelos del polimorfismo 3'UTR+62G>A en resistina se identificaron por PCR-RFLP. La concentración sérica de insulina, adiponectina total y resistina se midieron por la técnica de ELISA. Resultados: Las frecuencias del alelo +62G para los individuos con peso normal y exceso de peso, fueron (95.4% y 98.4%, respectivamente) P=0.0343. Los portadores del genotipo GA con peso normal mostraron valores menores del ARindex, adiposidad y marcadores inmuno-metabólicos comparados con los portadores del genotipo GG. Se observó diferencia entre los individuos sin y con RI en el ARindex (P=0.002), concentración sérica de adiponectina (P=0.002) y resistina (P=0.033): 1.102±0.03, 5.167±0.36ug/mL y 8.827±0.42ng/mL versus 1.336±0.07, 3.577±0.34ug/mL y 10.480±0.65ng/mL, respectivamente. Los marcadores inmuno-metabólicos, reserva y distribución de grasa corporal correlacionan con ARindex (r=0.262 a 0.414), PA en los individuos mestizos-mexicanos con exceso de peso. El alelo +62A se asoció con incremento de adiponectina total, valores menores del ARindex, concentración de resistina, marcadores metabólicos y reserva de grasa corporal. El ARindex puede ser un indicador temprano de RI.

Association of ADIPOQ +45T>G polymorphism with body fat mass and blood levels of soluble adiponectin and inflammation markers in a Mexican-Mestizo population.

PURPOSE: Obesity is a disease with genetic susceptibility characterized by an increase in storage and irregular distribution of body fat. In obese patients, the decrease in the Adiponectin gene (ADIPOQ) expression has been associated with a systemic low-grade inflammatory state. Our aim was to investigate the relationship between ADIPOQ +45T>G gene simple nucleotide polymorphism (SNP rs2241766) with serum adiponectin (sAdiponectin), distribution of body fat storage, and inflammation markers. SUBJECTS AND METHODS: In this cross-sectional study, 242 individuals from Western Mexico characterized as Mexican-Mestizo and classified by body mass index (BMI), were included. Anthropometrics, body composition, body fat distribution, and inflammation markers were measured by routine methods. Genotypes were characterized using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique and sAdiponectin by the ELISA method. A P-value <0.05 was considered the statistically significant threshold. RESULTS: sAdiponectin is associated with BMI (P < 0.001) and the genotypes (P < 0.001 to 0.0046) GG (8169 ± 1162 ng/mL), TG (5189 ± 501 ng/mL), and TT (3741 ± 323 ng/mL), but the SNP ADIPOQ +45T>G is not associated with BMI. However, the detailed analysis showed association of this SNP with a pattern of fat distribution and correlations (P < 0.05) with inflammation markers and distribution of body fat storage (Pearson's r = -0.169 to -0.465) were found. CONCLUSION: In this study, we have suggested that the ADIPOQ +45G allele could be associated with distribution of body fat storage in obesity. On the other hand, as no association was observed between ADIPOQ +45T>G gene polymorphism and obesity, it cannot be concluded that the ADIPOQ +45G allele is responsible for the increase of adiponectin levels.