The main objective was to explore the relationship between the microbiota of human milk and adiposity in Mexican mothers during the first lactation stage. Methods: Seventy lactating women were included. Adiposity by anthropometric measurements and by bioelectric impedance was obtained. The donation of human milk was requested, from which bacterial DNA was extracted and qPCR of the 16S region was performed. The Mann–Whitney U test, Spearman and Pearson correlations, and multiple linear regressions models were also calculated. Results: The median percentage of Bacteroidetes had a direct and significant correlation with normal adiposity, current BMI, waist circumference, and body fat percentage. The correlation with current BMI became significantly inverse in women with BMI ≥ 25. In women with normal BMI, the percentage of Actinobacteria showed a direct and significant correlation with current BMI, waist circumference, and percentage of body fat. Multiple linear regressions showed that pre-pregnancy BMI was the variable with the highest predictive value with the Bacteroidetes phyla in normal BMI and in BMI ≥ 25. Conclusions: the adiposity of the woman before pregnancy and during lactation would have an important effect on the abundance of Bacteroidetes and Actinobacteria in human milk.

Several freeze-drying and spray-drying methods were investigated in relation to the retention of immunoglobulins (Ig) A, IgG, and IgM. Spray drying produced human milk powders with 2% humidity and a good retention of IgG (>88%) and IgM (∼70%). However, only 38% of IgA remained after spray drying. For freeze drying, only the highest heating plate temperature used in this study (40°C) brought IgA content down to 55% in powder with 1.75% residual humidity, whereas milk samples undergoing lower temperatures had higher preservation rates (75% for IgA and 80% for IgG and IgM) and higher residual moisture contents. From these results, it can be concluded that IgA is the most sensitive Ig lost during drying processing of human milk. The best method to generate human milk powders without a significant loss of Ig was thus freeze drying at 30°C heating plate temperature, which accelerated the process compared to lower processing temperatures, but still had good overall Ig retention.

The polymorphisms in leptin (LEPG-2548A) and leptin-receptor (LEPRGln223Arg) seem to influence obesity and lipid metabolism among others. The aim of this study was to investigate the effect of these polymorphisms on adiposity, leptin (sLeptin), and leptin-receptor (sLeptin-receptor) serum concentrations as well as inflammation markers. We included 382 adults originally from Western Mexico. They were genotyped by PCR-RFLP. Obese individuals showed higher sLeptin (58.2±31.35 ng/mL) but lower sLeptin-receptor (12.6±3.74 ng/mL) levels than normal weight ones (17.6±14.62 ng/mL,17.4±4.62 ng/mL, resp.),P<0.001. Obese subjects carriers of Arg/Arg genotype had more (P=0.016) sLeptin-receptor (14.7±4.96 ng/mL) and less (P=0.004) sLeptin (44.0±28.12 ng/mL) levels than Gln/Gln genotype (11.0±2.92 ng/mL,80.3±33.24 ng/mL, resp.). Body fat mass was lower (Pfrom 0.003 to 0.045) for A/A (36.5%±6.80) or Arg/Arg (36.8%±6.82) genotypes with respect to G/G (41.3%±5.52) and G/A (41.6%±5.61) or Gln/Gln (43.7%±4.74) and Gln/Arg (41.0%±5.52) genotypes carriers. Our results suggest thatLEP-2548A andLEPR223Arg could be genetic markers of less body fat mass accumulation in obese subjects from Western Mexico.

The aim of this study was to investigate the relationship between functional polymorphisms Gly482Ser inPPARGC1Aand Pro12Ala inPPARG2with the presence of obesity and metabolic risk factors. We included 375 individuals characterized as Mexican-Mestizos and classified by the body mass index (BMI). Body dimensions and distribution of body fat were measured. The HOMA-IR and adiposity indexes were calculated. Adipokines and metabolic profile quantification were performed by ELISA and routine methods. Genetic polymorphisms were determined by polymerase chain reaction restriction fragment length polymorphism analysis. A difference between obese and nonobese subjects in polymorphismPPARGC1Adistribution was observed. Among obese individuals, carriers of genotype 482Gly/Gly were observed to have decreased body fat, BMI, and body fat ratio versus 482Ser/Ser carriers and increased resistin and leptin levels in carriers Gly+ phenotype versus Gly− phenotype. Subjects withPPARG2Ala− phenotype (genotype 12Pro/Pro) showed a decreased HOMA-IR index versus individuals with Ala+ phenotype (genotypes 12Pro/Ala plus 12Ala/Ala). We propose that, in obese Mexican-Mestizos, the combination of alleles 482Ser inPPARGC1Aand 12Pro inPPARG2represents a reduced metabolic risk profile, even when the adiposity indexes are increased.

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 expressedCMKLR1receptor. The role of chemerin andCMKLR1in 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 ofCMKLR1were evaluated with qPCR and2-ΔΔCTmethod.Results. Differences (P<0.05) were observed between obesity and lean individuals in body fat storage measurements and metabolic-inflammatory markers. BothCMKLR1expression 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 ofCMKLR1expression 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 andCMKLR1have opposite expression in the context of low-grade inflammatory response manifested in the development of IR.

Genetic susceptibility has been described in insulin resistance (IR). Chemokine (C-C motif) ligand-2 (CCL2) is overexpressed in white adipose tissue and is the ligand of C-C motif receptor-2 (CCR2). TheCCL2G-2518A polymorphism is known to regulate gene expression, whereas the physiological effects of theCCR2Val64Ile polymorphism are unknown. The aim of the study is to investigate the relationship between these polymorphisms with soluble CCL2 levels (sCCL2), metabolic markers, and adiposity. In a cross-sectional study we included 380 Mexican-Mestizo individuals, classified with IR according to Stern criteria. Polymorphism was identified using PCR-RFLP/sequence-specific primers. Anthropometrics and metabolic markers were measured by routine methods and adipokines and sCCL2 by ELISA. The CCL2 polymorphism was associated with IR (polymorphicA+phenotype frequencies were 70.9%, 82.6%, in individuals with and without IR, resp.). Phenotype carriers CCL2 (A+) displayed lower body mass and fat indexes, insulin and HOMA-IR, and higher adiponectin levels. Individuals with IR presented higher sCCL2 compared to individuals without IR and was associated with CCR2 (Ile+) phenotype. The double-polymorphic phenotype carriers (A+/Ile+) exhibited higher sCCL2 than double-wild-type phenotype carriers (A−/Ile−). The present findings suggest that sCCL2 production possibly will be associated with the adiposity and polymorphic phenotypes ofCCL2andCCR2, in Mexican-Mestizos with IR.