Hormony tarczycy (thyroid hormones, TH) są zaangażowane w wiele różnych procesów biologicznych, wliczając rozwój układu nerwowego, regulację metabolizmu pośredniego oraz zużycie energii. Aktywnie uczestniczą w podstawowym zużyciu energii i termogenezie adaptacyjnej i z tego względu mogą mieć wpływ na masę ciała w przebiegu chorób tarczycy. Otyłość to niezakaźna, przewlekła, zapalna choroba metaboliczna, która implikuje dodatni bilans energetyczny. Tkanka tłuszczowa produkuje szereg hormonów i adipocytokin, takich jak leptyna, które mogą wpływać na stan tarczycy na różnych poziomach. Istnieją dowody na to, że dysfunkcja tarczycy może predysponować do otyłości i odwrotnie, istnieją dowody sugerujące, że otyłość powoduje zmiany dotyczące tarczycy. Celem tej pracy było opisanie związku między układem tarczycy a otyłością. Ponadto w pracy zaprezentowano hipotetyczny model podkreślający znaczenie obwodowej dejodynacji hormonów tarczycy i jego rolę w ustanowieniu dodatniego bilansu energetycznego. Podsumowując, możemy stwierdzić, że relacja między układem tarczycy a otyłością i nadwagą jest złożona i obejmuje wiele poziomów interakcji. Ponadto, poddając ocenie otyłego pacjenta, powinno się rozważyć ocenę funkcji tarczycy, aby uzyskać lepsze i spersonalizowane efekty leczenia. Hormony tarczycy (thyroid hormones, TH) są zaangażowane w wiele różnych procesów biologicznych, wliczając rozwój układu nerwowego, regulację metabolizmu pośredniego oraz zużycie energii. Aktywnie uczestniczą w podstawowym zużyciu energii i termogenezie adaptacyjnej i z tego względu mogą mieć wpływ na masę ciała w przebiegu chorób tarczycy. Otyłość to niezakaźna, przewlekła, zapalna choroba metaboliczna, która implikuje dodatni bilans energetyczny. Tkanka tłuszczowa produkuje szereg hormonów i adipocytokin, takich jak leptyna, które mogą wpływać na stan tarczycy na różnych poziomach. Istnieją dowody na to, że dysfunkcja tarczycy może predysponować do otyłości i odwrotnie, istnieją dowody sugerujące, że otyłość powoduje zmiany dotyczące tarczycy. Celem tej pracy było opisanie związku między układem tarczycy a otyłością. Ponadto w pracy zaprezentowano hipotetyczny model podkreślający znaczenie obwodowej dejodynacji hormonów tarczycy i jego rolę w ustanowieniu dodatniego bilansu energetycznego. Podsumowując, możemy stwierdzić, że relacja między układem tarczycy a otyłością i nadwagą jest złożona i obejmuje wiele poziomów interakcji. Ponadto, poddając ocenie otyłego pacjenta, powinno się rozważyć ocenę funkcji tarczycy, aby uzyskać lepsze i spersonalizowane efekty leczenia.

Childhood overweight and obesity are worldwide public health problems and risk factors for chronic diseases. The presence of SNP in several genes has been associated with the presence of obesity. A total of 580 children (8–13 years old) from Queretaro, Mexico, participated in this cross-sectional study, which evaluated the associations of rs9939609 (fat mass obesity-associated (FTO)), rs17782313 (melanocortin 4 receptor (MC4R)) and rs6548238 (transmembrane protein 18 (TMEM18)) SNP with obesity and metabolic risk factors. Overweight and obesity prevalence was 19·8 and 19·1 %, respectively. FTO, MC4R and TMEM18 risk allele frequency was 17, 9·8 and 89·5 %, respectively. A significant association between FTO homozygous and MC4R heterozygous risk alleles and obesity was found (OR 3·9; 95 % CI 1·46, 10·22, and OR 2·1; 95 % CI 1·22, 3·71; respectively). The FTO heterozygous subjects showed higher systolic and diastolic blood pressures, compared with the homozygous for the ancestral allele subjects. These results remain significant after considering adiposity as a covariate. The FTO and MC4R genotypes were not significantly associated with total cholesterol, HDL-cholesterol and insulin concentration. No association was found between TMEM18 risk allele and obesity and/or metabolic alterations. Our results show that, in addition to a higher BMI, there is also an association of the risk genotype with blood pressure in the presence of the FTO risk genotype. The possible presence of a risk genotype in obese children must be considered to offer a more comprehensive therapeutic approach in order to delay and/or prevent the development of chronic diseases.

Iodide is a trace element and a key component of thyroid hormones (TH). The availability of this halogen is the rate-limiting step for TH synthesis; therefore, thyroidal iodide uptake and recycling during TH synthesis are of major importance in maintaining an adequate supply. In the rat, the thyroid gland co-expresses a distinctive pair of intrathyroidal deiodinating enzymes: the thyroid iodotyrosine dehalogenase (tDh) and the iodothyronine deiodinase type 1 (ID1). In the present work, we studied the activity of these two dehalogenases in conditions of hypo- and hyperthyroidism as well as during acute and chronic iodide administration in both intact and hypophysectomized (HPX) rats. In order to confirm our observations, we also measured the mRNA levels for both dehalogenases and for the sodium/iodide symporter, the protein responsible for thyroidal iodide uptake. Our results show that triiodothyronine differentially regulates tDh and ID1 enzymatic activities, and that both acute and chronic iodide administration significantly decreases rat tDh and ID1 activities and mRNA levels. Conversely, both enzymatic activities increase when intrathyroidal iodide is pharmacologically depleted in TSH-replaced HPX rats. These results show a regulatory effect by iodide on the intrathyroidal dehalogenating enzymes and suggest that they contribute to the iodide-induced autoregulatory processes involved in the Wolff–Chaikoff effect.

This investigation aimed to detect coincidences in the antimicrobial resistance genes (ARG) profiles between members of a group living in a household and to compare them between other groups in order to establish if an exchange of ARG occurs and if dental plaque microbiota can be considered as a source and reservoir of ARG that can be shared between humans and pets. One hundred sixty dental plaque samples were obtained from four groups. Shelter Dogs group (n = 20), Adult pet owners and Dogs group (AD group, n = 40), Adult pet owners, Children and Dogs group (ACD group, n = 60), and Adult non-pet owners and Children group (AC group, n = 40). DNA was obtained, and specific primers with polymerase chain reaction for ARG detection were used. The AD group exhibited the most coincidences in their ARG profiles, 14(70%) of the 20 profiles coincided in 100% followed by the ACD group with 9(45%) coincidences. While the AC group was the less coincident group, only 7(35%) of the 20 profiles coincided. tetM was the most prevalent with 53.1%, followed by tetQ with 52.5% and cfxA with 51.2%. While the less prevalent were tetW with 31.8%, blaTEM-1 with 27.5%, and ermC with 18.7%. Dental plaque microbiota can be considered as a source and reservoir of ARG that can be shared between humans and dogs living in a household. The dogs seems to play an important role in the transference of ARG, and the children appear to be the most affected by carrying the most significant number of ARG.

The estrogenic receptor beta (ERβ) protects against carcinogenesis by stimulating apoptosis. Bisphenol A (BPA) is related to promoting cancer, and naringenin has chemoprotective activities both can bind to ERβ. Naringenin in the colon is metabolized by the microbiota. Cancer involves genetic and epigenetic mechanisms, including miRNAs. The objective of the present study was to evaluate the co-exposure effect of colonic in vitro fermented extract of naringenin (FEN) and BPA, to elucidate molecular effects in HT-29 colon cancer cell line. For this, we quantified genes related to the p53 signaling pathway as well as ERβ, miR-200c, and miR-141. As an important result, naringenin (IC50 250 µM) and FEN (IC50 37%) promoted intrinsic pathways of apoptosis through phosphatase and tensin homolog (PTEN) (+2.70, +1.72-fold, respectively) and CASP9 (+3.99, +2.03-fold, respectively) expression. BPA decreased the expression of PTEN (−3.46-fold) gene regulated by miR-200. We suggest that once co-exposed, cells undergo a greater stress forcing them to mediate other extrinsic apoptosis mechanisms associated with death domain FASL. In turn, these findings are related to the increase of ERβ (5.3-fold with naringenin and 13.67-fold with FEN) gene expression, important in the inhibition of carcinogenic development.

Antimicrobial resistance is a global public health problem. Root canal microbiota associated with apical periodontitis represents a well-known reservoir of antimicrobial resistance genes (ARGs). However, the effect of type 2 diabetes mellitus (T2DM) in this reservoir is unknown. This study aimed to establish if root canal microbiota associated with apical periodontitis in T2DM patients is an augmented reservoir by identifying the prevalence of nine common ARGs and comparing it with the prevalence in nondiabetic patients. This cross-sectional study included two groups: A T2DM group conformed of 20 patients with at least ten years of living with T2DM and a control group of 30 nondiabetic participants. Premolar or molar teeth with pulp necrosis and apical periodontitis were included. A sample was collected from each root canal before endodontic treatment. DNA was extracted, and ARGs were identified by polymerase chain reaction. tetW and tetM genes were the most frequent (93.3 and 91.6%, respectively), while ermA was the least frequent (8.3%) in the total population. The distribution of the ARGs was similar in both groups, but a significant difference (p<0.005) was present in ermB, ermC, cfxA, and tetQ genes, being more frequent in the T2DM group. A total of eighty percent of the T2DM patients presented a minimum of four ARGs, while 76.6% of the control group presented a maximum of three. Root canal microbiota associated with apical periodontitis in T2DM patients carries more ARGs. Therefore, this pathological niche could be considered an augmented reservoir.