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      Adiponectin gene variant rs266729 interacts with different macronutrient distributions of two different hypocaloric diets during nine months Translated title: La variante del gen de la adiponectina rs266729 interactúa con diferentes distribuciones de macronutrientes de dos dietas hipocalóricas durante nueve meses

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          Abstract

          Abstract Background: the role of ADIPOQ gene variants on metabolic changes after weight loss secondary to different hypocaloric diets remains unclear and poorly investigated. Objective: we evaluated the effect of polymorphism rs266729 of ADIPOQ gene on biochemical changes and weight loss after a high-protein/low-carbohydrate diet vs a standard severe hypocaloric diet during 9 months. Material and methods: a population of 269 obese patients was enrolled in a randomized intervention trial for 9 months with two diets. Diet HP (high protein) was 33 % of carbohydrates (86.1 g/day), 33 % of fat (39.0 g/day), and 34 % of proteins (88.6 g/day). Diet S (standard) was 1093 cal/day, 53 % carbohydrates (144.3 g/day), 27 % fats (32.6 g), and 20 % proteins (55.6 g/day). Before and after the intervention an anthropometric evaluation, an assessment of nutritional intake, and a biochemical analysis were carried out. Results: all patients lost weight regardless of genotype and diet. After the intervention with a high protein hypocaloric diet (diet HP) only subjects with CC genotype showed significant improvement in cholesterol (14.4 ± 1.8 md/dL vs -5.0 ± 1.9 mg/dL; p = 0.02), LDL-cholesterol (14.4 ± 1.9 mg/dL vs -5.1 ± 1.8 mg/dL; p = 0.01), insulin (-4.1 ± 0.3 mU/L vs -2.0 ± 0.6 mU/L; p = 0.02), HOMA-IR (-1.4 ± 0.2 units vs -0.5 ± 0.3 units; p = 0.02) and adiponectin (10.2 ± 1.4 ng/dL vs 3.1 ± 1.1 ng/dL; p = 0.01) levels. After the second dietary strategy with a standard hypocaloric diet (diet S) only subjects with CC genotype showed significant improvement in total cholesterol (CC vs CG + GG) (-17.1 ± 1.9 md/dL vs -5.3 ± 1.3 mg/dL; p = 0.02), LDL-cholesterol (-12.3 ± 1.9 mg/dL vs -8.0 ± 1.2 mg/dL; p = 0.01), insulin (-4.0 ± 0.9 mU/L vs -1.3 ± 0.5 mU/L; p = 0.02), HOMA-IR (-1.2 ± 0.1 units vs -0.6 ± 0.2 units; p = 0.02), and adiponectin (11.1 ± 2.7 ng/dL vs 3.3 ± 1.2 ng/dL; p = 0.02) levels. Conclusion: non G-allele carriers showed a better response of LDL-cholesterol, HOMA-IR, insulin, and adiponectin levels than G-allele carriers before weight loss with both diets.

          Translated abstract

          Resumen Antecedentes: el papel de las variantes del gen ADIPOQ en los cambios metabólicos después de la pérdida de peso secundaria a diferentes dietas hipocalóricas sigue sin estar claro y es un área poco investigada. Objetivo: evaluamos el efecto del polimorfismo rs266729 del gen ADIPOQ sobre los cambios bioquímicos y la pérdida de peso después de una dieta con alto contenido en proteínas y baja en carbohidratos frente a una dieta hipocalórica severa estándar durante 9 meses. Material y métodos: se reclutó una muestra de 269 pacientes obesos en un ensayo de intervención aleatorizado de 9 meses con dos dietas. La dieta HP (alta en proteínas) tenía la siguiente composicion: 33 % de carbohidratos (86,1 g/día), 33 % de grasas (39,0 g/día) y 34 % de proteínas (88,6 g/día). La dieta S (estándar), de 1093 cal/día, tenía 53 % de carbohidratos (144,3 g/día), 27 % de grasas (32,6 g) y 20 % de proteínas (55,6 g/día). Antes y después de la intervención se realizaron una evaluación antropométrica, una valoración de la ingesta nutricional y un análisis bioquímico. Resultados: todos los pacientes bajaron de peso independientemente del genotipo y la dieta utilizada. Después de la intervención con la dieta HP, solo los sujetos con genotipo CC mostraron una mejoría significativa de los niveles de colesterol (14,4 ± 1,8 mg/dl vs. -5,0 ± 1,9 mg/dl; p = 0,02), colesterol-LDL (14,4 ± 1,9 mg/dl frente a -5,1 ± 1,8 mg/dl; p = 0,01), insulina (-4,1 ± 0,3 mU/L frente a -2,0 ± 0,6 mU/L; p = 0,02), HOMA-IR (-1,4 ± 0,2 unidades frente a -0,5 ± 0,3 unidades; p = 0,02) y adiponectina (10,2±1,4 ng/dl frente a 3,1 ± 1,1 ng/dl; p = 0,01). Después de la segunda estrategia dietética con una dieta hipocalórica estándar (dieta S), solo los sujetos con genotipo CC mostraron una mejora significativa de los niveles de colesterol total (CC vs. CG + GG) (-17,1 ± 1,9 mg/dl vs. -5,3 ± 1,3 mg/dl; p = 0,02), colesterol-LDL (-12,3 ± 1,9 mg/dl frente a -8,0 ± 1,2 mg/dl; p = 0,01), insulina (-4,0 ± 0,9 mU/L frente a -1,3 ± 0,5 mU/L; p = 0,02), HOMA-IR (-1,2 ± 0,1 unidades frente a -0,6 ± 0,2 unidades; p = 0,02) y adiponectina (11,1 ± 2,7 ng/dl frente a 3,3 ± 1,2 ng/dl; p = 0,02). Conclusión: los no portadores del alelo G mostraron una mejor respuesta de los niveles de colesterol-LDL, HOMA-IR, insulina y adiponectina que los portadores del alelo G antes de la pérdida de peso con ambas dietas.

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          Multiplex bead array assays for detection of soluble cytokines: comparisons of sensitivity and quantitative values among kits from multiple manufacturers.

          Multiplex bead array assays permit simultaneous cytometric quantitation of multiple cytokines in solution by capturing these to spectrally distinct beads. Because several manufacturers offer reagents to quantitate the same cytokines on a single instrument, a comparison should be made to determine whether these kits yield similar data and whether these data are comparable to enzyme-linked immunosorbent assay (ELISA). This study compared cytokine detection kits by using Luminex 100. Twenty-six serum samples from seven subjects were analyzed for interferon-gamma, interleukins 1beta, 6, and 8, and tumor necrosis factor-alpha by using multiplex kits from LINCO Research, Bio-Rad Laboratories, R&D Systems, and BioSource International. Each assay was performed according to the manufacturers' specifications. Standard curves were generated by using reference concentrations supplied by each manufacturer. ELISAs for interleukin-8 were performed by using kits from R&D and BioSource. Cytokine levels followed similar patterns, although absolute concentrations differed among kits. ELISA and Luminex values for interleukin-8 were similar in kits from the same manufacturer. Because relative cytokine measurements are often valuable when performed serially, it may be possible to make interlaboratory comparisons by using different kits. When comparison of absolute values is crucial, kits from the same supplier should be used. Within-vendor, bead array, and ELISA values appear comparable.
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            Genomic structure and mutations in adipose-specific gene, adiponectin.

            Adiponectin is a collagen-like plasma protein specifically synthesized in adipose tissue. Plasma adiponectin concentrations are decreased in obesity whereas it is adipose-specific. To clarify the significance of the genetic variations in adiponectin gene on its plasma concentrations and obesity. Two hundred and nineteen unrelated adult Japanese subjects (123 men and 96 women, age: 20-83 y, BMI: 16-43 kg/m2) including 77 obese subjects (BMI>26.4 kg/m2). Human adiponectin gene was isolated from PAC DNA pools. Mutations in the adiponectin gene were screened by direct sequencing or restriction-fragment polymorphism. The levels of plasma adiponectin were determined by the enzyme-linked immunosorbent assay (ELISA). Adiponectin gene spanned 17 kb on chromosome 3q27, consisting of three exons and two introns. Within 2.1 kb of the 5'-flanking region, there were two octamer elements present in the promoter of adipsin. Two nucleotide changes were identified. One was a polymorphism (G/T) occurring in exon 2, and the other was a missense mutation (R112C) in exon 3. The mean plasma adiponectin levels of the subjects carrying G allele were low (G/G: 4.5 microg/ml; G/T: 5.9 microg/ml; and T/T: 6.3 microg/ml), but were not statistically significant. The allelic frequency between the obese and the non-obese showed no significant difference. The subject carrying R112C mutation showed markedly low concentration of plasma adiponectin. Two nucleotide changes have been identified in the adiponectin gene. G/T polymorphism in exon 2 was associated with neither plasma adiponectin concentrations nor the presence of obesity. A subject carrying missense mutation (R112C) showed markedly low plasma adiponectin concentration.
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              Association of ADIPOQ gene variants with body weight, type 2 diabetes and serum adiponectin concentrations: the Finnish Diabetes Prevention Study

              Background Adiponectin, secreted mainly by mature adipocytes, is a protein with insulin-sensitising and anti-atherogenic effects. Human adiponectin is encoded by the ADIPOQ gene on the chromosomal locus 3q27. Variations in ADIPOQ are associated with obesity, type 2 diabetes (T2DM) and related phenotypes in several populations. Our aim was to study the association of the ADIPOQ variations with body weight, serum adiponectin concentrations and conversion to T2DM in overweight subjects with impaired glucose tolerance. Moreover, we investigated whether ADIPOQ gene variants modify the effect of lifestyle changes on these traits. Methods Participants in the Finnish Diabetes Prevention Study were randomly assigned to a lifestyle intervention group or a control group. Those whose DNA was available (n = 507) were genotyped for ten ADIPOQ single nucleotide polymorphisms (SNPs). Associations between SNPs and baseline body weight and serum adiponectin concentrations were analysed using the univariate analysis of variance. The 4-year longitudinal weight data were analysed using linear mixed models analysis and the change in serum adiponectin from baseline to year four was analysed using Kruskal-Wallis test. In addition, the association of SNPs with the risk of developing T2DM during the follow-up of 0-11 (mean 6.34) years was analysed by Cox regression analysis. Results rs266729, rs16861205, rs1501299, rs3821799 and rs6773957 associated significantly (p < 0.05) with body weight at baseline and in the longitudinal analyses. The rs266729 C allele and the rare minor alleles of rs2241766 and rs2082940 were associated with an increased adjusted hazard ratio of developing T2DM. The differences in baseline serum adiponectin concentrations were seen according to rs16861210, rs17366568, rs2241766, rs6773957 and rs2082940 and differences in the change of serum adiponectin levels from baseline to the four year examination were seen according to rs16861205, especially in subjects who were able to lose weight during the first year of intervention. Conclusions These results from the Finnish Diabetes Prevention Study support the concept that genetic variation in ADIPOQ locus contributes to variation in body size and serum adiponectin concentrations and may also modify the risk of developing T2DM. Trial registration number ClinicalTrials.gov NCT00518167
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                Author and article information

                Journal
                nh
                Nutrición Hospitalaria
                Nutr. Hosp.
                Grupo Arán (Madrid, Madrid, Spain )
                0212-1611
                1699-5198
                April 2021
                : 38
                : 2
                : 274-280
                Affiliations
                [1] Valladolid orgnameHospital Clinico Universitario-Universidad de Valladolid orgdiv1School of Medicine. Department of Endocrinology and Nutrition orgdiv2Centro de Investigación de Endocrinología y Nutrición Spain
                Article
                S0212-16112021000200274 S0212-1611(21)03800200274
                10.20960/nh.03423
                68aa415b-318e-426f-8090-6bc6529d8e41

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 05 November 2020
                : 26 January 2021
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 30, Pages: 7
                Product

                SciELO Spain

                Categories
                Original Papers

                Adiponectin,Dietary intervention,Insulin resistance,Obesity,rs266729,Adiponectina,Intervención dietética,Resistencia a la insulina,Obesidad

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