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PURPOSE: To examine the association of the single nucleotide polymorphism A1470T in the SLC16A1 gene with blood lactate accumulation during a graded exercise test and its associated metaboreflex. METHODS: Forty-six Latin-American men (Age: 27 ± 6 years; Body fat: 17.5 ± 4.7%) performed a graded exercise test on a treadmill for the assessment of maximal oxygen uptake (VO2max), lactate threshold (LT), ventilatory threshold (VT) and the exercise intensity corresponding to maximal fat oxidation rate (FATmax), via capillary blood samples and indirect calorimetry. Genomic DNA was extracted from a peripheral blood sample. Genotyping assay was carried out by real-time polymerase chain reaction to identify the A1470T polymorphism (rs1049434). RESULTS: Genotypes distribution were in Hardy-Weinberg equilibrium (X2 = 5.6, p > 0.05), observing allele frequencies of 0.47 and 0.53 for the A and T alleles, respectively. No difference in VO2max, body composition nor FATmax were observed across genotypes, whereas carriers of the TT genotype showed a higher LT (24.5 ± 2.2 vs. 15.6 ± 1.7 mL kg-1 min-1, p < 0.01) and VT in comparison to carriers of the AA + AT genotypes (32.5 ± 3.3 vs. 21.7 ± 1.5 mL kg-1 min-1, p < 0.01). Both, VO2max and the A1470T polymorphism were positively associated to the LT (R2 = 0.50, p < 0.01) and VT (R2 = 0.55, p < 0.01). Only VO2max was associated to FATmax (R2 = 0.39, p < 0.01). CONCLUSION: Independently of cardiorespiratory fitness, the A1470T polymorphism is associated to blood lactate accumulation and its associated ventilatory response during submaximal intensity exercise. However, the A1470 polymorphism does not influence fat oxidation capacity during exercise in young men.

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Glucose and lipid metabolism regulation by the peroxisome proliferator-activated receptors (PPARs) has been extensively reported. However, the role of their polymorphisms remains unclear. OBJECTIVE: To determine the relation between PPAR-γ2 rs1801282 (Pro12Ala) and PPAR-ß/δ rs2016520 (+294T/C) polymorphisms and metabolic biomarkers in adults with type 2 diabetes (T2D). MATERIALS AND METHODS: We included 314 patients with T2D. Information on anthropometric, fasting plasma glucose (FPG), HbA1c and lipid profile measurements was taken from clinical records. Genomic DNA was obtained from peripheral blood. End-point PCR was used for PPAR-γ2 rs1801282, while for PPAR-ß/δ rs2016520 the PCR product was digested with Bsl-I enzyme. Data were compared with parametric or non-parametric tests. Multivariate models were used to adjust for covariates and interaction effects. RESULTS: minor allele frequency was 12.42% for PPAR-γ2 rs1801282-G and 13.85% for PPAR-ß/δ rs2016520-C. Both polymorphisms were related to waist circumference; they showed independent effects on HbA1c, while they interacted for FPG; carriers of both PPAR minor alleles had the highest values. Interactions between FPG and polymorphisms were identified in their relation to triglyceride level. CONCLUSIONS: PPAR-γ2 rs1801282 and PPAR-ß/δ rs2016520 polymorphisms are associated with anthropometric, glucose, and lipid metabolism biomarkers in T2D patients. Further research is required on the molecular mechanisms involved.

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The WHO identifies high BMI, high blood pressure, and high fasting plasma glucose as chronic disease risk factors, whereas physical fitness is identified as a protective behavioral factor. This study responds to the rising interest in assessing metabolic factors and physical activity within young populations of Mestizo, Tarahumara, and Mennonite from Chihuahua Mexico, due to its strong relationship with disease development and low well-being. A cross-sectional study was conducted with 201 teenagers from rural towns in Northern Mexico, and relationships between physical fitness and cardio-metabolic risk related to anthropometric, glycolipid, and vascular function factors were assessed. ANOVA-tested differences among ethnic groups using physical fitness as a grouping variable and measures of cardio-metabolic risks were used as dependent variables. A stepwise regression analysis allowed us to identify the best predictors for physical fitness. Clinical risk factors were analyzed by ethnic group and sex. No differences were found among ethnic groups in physical fitness and cardio-metabolic health risks; sex differentiated higher health risks related to behavioral factors, since young women showed lower physical fitness across ethnicities. Clinically, the Mestizo sample showed higher numbers of individuals with one risk factor. Mennonites showed a high frequency of anthropometric and fitness health risks with low glycolipid and vascular risks. Tarahumara had fewer risk factors as compared with both Mestizo and Mennonite. Rural populations are harder to reach, both for health assessment and intervention; health professionals must work close to local community organizations to gain access.

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The maximal fat oxidation rate (MFO) assessed during a graded exercise test is a remarkable physiological indicator associated with metabolic flexibility, body weight loss and endurance performance. The present review considers existing biomarkers related to MFO, highlighting the validity of maximal oxygen uptake and free fatty acid availability for predicting MFO in athletes and healthy individuals. Moreover, we emphasize the role of different key enzymes and structural proteins that regulate adipose tissue lipolysis (i.e., triacylglycerol lipase, hormone sensitive lipase, perilipin 1), fatty acid trafficking (i.e., fatty acid translocase cluster of differentiation 36) and skeletal muscle oxidative capacity (i.e., citrate synthase and mitochondrial respiratory chain complexes II-V) on MFO variation. Likewise, we discuss the association of MFO with different polymorphism on the ACE, ADRB3, AR and CD36 genes, identifying prospective studies that will help to elucidate the mechanisms behind such associations. In addition, we highlight existing evidence that contradict the paradigm of a higher MFO in women due to ovarian hormones activity and highlight current gaps regarding endocrine function and MFO relationship.

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Fatty acid translocase/cluster of differentiation 36 (FAT/CD36) is a multifunctional membrane protein activated by a high-fat diet, physical exercise, fatty acids (FAs), leptin, and insulin. The principal function of FAT/CD36 is to facilitate the transport of long-chain fatty acids through cell membranes such as myocytes, adipocytes, heart, and liver. Under high-energy expenditure, the different isoforms of FAT/CD36 in the plasma membrane and mitochondria bind to the mobilization and oxidation of FAs. Furthermore, FAT/CD36 is released in its soluble form and becomes a marker of metabolic dysfunction. Studies with healthy animals and humans show that physical exercise and a high-lipid diet increase FAT/CD36 expression and caloric expenditure. However, several aspects such as obesity, diabetes, Single Nucleotide polymorphisms (SNPs), and oxidative stress affect the normal FAs metabolism and function of FAT/CD36, inducing metabolic disease. Through a comprehensive systematic review of primary studies, this work aimed to document molecular mechanisms related to FAT/CD36 in FAs oxidation and trafficking in skeletal muscle under basal conditions, physical exercise, and diet in healthy individuals.

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Obesity is thought to be associated with a reduced capacity to increase fat oxidation in response to physical exercise; however, scientific evidence supporting this paradigm remains scarce. This study aimed to determine the interrelationship of different submaximal exercise metabolic flexibility (Metflex) markers and define its association with body fatness on subjects with obesity. Twenty-one male subjects with obesity performed a graded-intensity exercise protocol (Test 1) during which cardiorespiratory fitness (CRF), maximal fat oxidation (MFO) and its corresponding exercise intensity (FATmax) were recorded. A week afterward, each subject performed a 60-min walk (treadmill) at FATmax (Test 2), and the resulting fat oxidation area under the curve (TFO) and maximum respiratory exchange ratio (RERpeak) were recorded. Blood lactate (LAb) levels was measured during both exercise protocols. Linear regression analysis was used to study the interrelationship of exercise Metflex markers. Pearson's correlation was used to evaluate all possible linear relationships between Metflex and anthropometric measurement, controlling for CRF). The MFO explained 38% and 46% of RERpeak and TFO's associated variance (p < 0.01) while TFO and RERpeak were inversely related (R2 = 0.54, p < 0.01). Body fatness positively correlated with MFO (r = 0.64, p < 0.01) and TFO (r = 0.63, p < 0.01) but inversely related with RERpeak (r = -0.67, p < 0.01). This study shows that MFO and RERpeak are valid indicators of TFO during steady-state exercise at FATmax. The fat oxidation capacity is directly associated with body fatness in males with obesity.

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Exercise training performed at the maximal fat oxidation intensity (FMT) stands out as a potential treatment of overweight and obesity. This work is a meta-analysis of randomized clinical trials of studies about the effect of FMT on fat mass and maximal oxygen consumption using PubMed, SCOPUS, EBSCOhost, and ScienceDirect as databases. Two independent reviewers selected 11 trials from 356 publications identified by the following keywords: fatmax, lipoxmax, maximal fat oxidation, peak of fat oxidation, physical training, physical exercise, body fat (BF), fat mass, overweight, and obesity. The risk of bias was assessed following the Cochrane Guidelines. The pooled mean difference was computed for each outcome with the random-effects model and the inverse-variance method. The meta-analysis was performed with the RevMan software v 5.3, and the heterogeneity across studies by the I2. The statistical significance was accepted at p < 0.05. Results showed that the FMT reduced body weight (MD = -4.30 kg, p < 0.01, I2 = 0%), fat mass (MD = -4.03 kg, p < 0.01, I2 = 0%), and waist circumference (MD = -3.34 cm, p < 0.01). Fat-free mass remains unchanged (MD = 0.08 kg, p = 0.85), but maximal oxygen consumption increased (MD = 2.96 mL∙kg-1∙min-1, p < 0.01, I2 = 0%). We conclude that FMT at short and medium-term (eight to twenty weeks) reduces body weight and BF, increasing cardiovascular fitness in low physical fitness people with obesity.

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Peroxisome proliferator-activated receptors (PPARs) play roles in glucose and lipid metabolism regulation. Pro12Ala PPAR-γ2 and +294T/C PPAR-δ have been associated with dyslipidemia, hyperglycemia and high body mass index (BMI). We compared metabolic traits and determined associations with Pro12Ala PPAR-γ2 or +294T/C PPAR-δ polymorphism among teenagers from different ethnicity. Four hundred and twelve samples with previous biochemical and biometric measurements were used. Genomic DNA from peripheral blood was extracted and analyzed by end-point PCR for Pro12Ala PPAR-γ2. The +294T/C PPAR-δ PCR product was also digested with Bsl I. Two genotype groups were formed: major allele homozygous and minor allele carriers. Pro12Ala PPAR-γ2 G minor allele frequencies were: 10% in Mestizo-1, 19% in Mestizo-2, 23% in Tarahumara, 12% in Mennonite, and 17% in the total studied population. The +294T/C PPAR-δ C minor allele frequencies were: 18% in Mestizo-1, 20% in Mestizo-2, 6% in Tarahumara, 13% in Mennonite, and 12% in the total studied population. Teenagers with PPAR-γ2 G allele showed a greater risk for either high waist/height ratio or low high-density lipoprotein; and, also had lower total cholesterol. Whereas, PPAR-γ2 G allele showed lower overweight/obesity phenotype (BMI Z-score) frequency, PPAR-δ C allele was a risk factor for it. Metabolic traits were associated with both PPAR polymorphisms.

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Abstract The GSTT1 and GSTM1 genes are key molecules in cellular detoxification. Null variants in these genes are associated with increase susceptibility to developing different types of cancers. The aim of this study was to determine the prevalence of GSTT1 and GSTM1 null genotypes in Mestizo and Amerindian individuals from the Northwestern region of Mexico, and to compare them with those reported worldwide. GSTT1 and GSTM1 null variants were genotyped by multiplex PCR in 211 Mestizos and 211 Amerindian individuals. Studies reporting on frequency of GSTT1 and GSTM1 null variants worldwide were identified by a PubMed search and their geographic distribution were analyzed. We found no significant differences in the frequency of the null genotype for GSTT1 and GSM1 genes between Mestizo and Amerindian individuals. Worldwide frequencies of the GSTT1 and GSTM1 null genotypes ranges from 0.10 to 0.51, and from 0.11 to 0.67, respectively. Interestingly, in most countries the frequency of the GSTT1 null genotype is common or frequent (76%), whereas the frequency of the GSMT1 null genotype is very frequent or extremely frequent (86%). Thus, ethnic-dependent differences in the prevalence of GSTT1 and GSTM1 null variants may influence the effect of environmental carcinogens in cancer risk.

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The GSTT1 and GSTM1 genes are key molecules in cellular detoxification. Null variants in these genes are associated with increase susceptibility to developing different types of cancers. The aim of this study was to determine the prevalence of GSTT1 and GSTM1 null genotypes in Mestizo and Amerindian individuals from the Northwestern region of Mexico, and to compare them with those reported worldwide. GSTT1 and GSTM1 null variants were genotyped by multiplex PCR in 211 Mestizos and 211 Amerindian individuals. Studies reporting on frequency of GSTT1 and GSTM1 null variants worldwide were identified by a PubMed search and their geographic distribution were analyzed. We found no significant differences in the frequency of the null genotype for GSTT1 and GSM1 genes between Mestizo and Amerindian individuals. Worldwide frequencies of the GSTT1 and GSTM1 null genotypes ranges from 0.10 to 0.51, and from 0.11 to 0.67, respectively. Interestingly, in most countries the frequency of the GSTT1 null genotype is common or frequent (76%), whereas the frequency of the GSMT1 null genotype is very frequent or extremely frequent (86%). Thus, ethnic-dependent differences in the prevalence of GSTT1 and GSTM1 null variants may influence the effect of environmental carcinogens in cancer risk.