Background: This cross-sectional observational study aimed to describe the position-specific kinanthropometric characteristics of Mexican professional American football players competing in the 2019–2020 seasons of the Liga de Fútbol Americano. Methods: A total of 189 athletes were assessed following International Society for the Advancement of Kinanthropometry standards. Twenty-six anthropometric variables were measured to estimate body composition (five-way fractionation), somatotype, proportionality indices, and tissue-specific masses. Positional differences were examined using ANOVA or Kruskal–Wallis tests with corresponding effect sizes (η² or ε²). An exploratory stepwise discriminant analysis identified the anthropometric dimensions contributing most to positional differentiation, and classification accuracy was calculated. Results: Offensive and defensive linemen showed the greatest absolute size and higher adipose, muscle, and bone mass compared with other positions. The overall somatotype corresponded to a balanced endomorphic mesomorph (3.8–7.0–0.8), with wide receivers and defensive backs presenting lower endomorphy. The discriminant model identified arm relaxed girth, biiliocristal breadth, and sitting height as the variables contributing most to positional differentiation, achieving a classification accuracy of 57.7%. Given its exploratory nature and the absence of cross-validation, the discriminatory capacity of the model should be interpreted with caution. Somatotype Attitudinal Mean indicated greater interpositional heterogeneity among linemen. Conclusions: This study provides population-specific reference data for Mexican professional American football players, highlighting clear positional morphological characteristics. These findings may support talent identification and positional profiling; however, the exploratory discriminant model and league-specific sample limit generalization to other populations.

Background/Objectives: High-fat diet (HFD) feeding disrupts systemic metabolism and hypothalamic mechanisms that coordinate energy balance. Whether quercetin modifies coordinated hypothalamic transcription linking m6A-related regulation with leptin–insulin- and melanocortin-associated biology remains unclear. We examined the metabolic and hypothalamic transcriptional response to quercetin during chronic HFD exposure. Methods: Male Wistar rats were studied for 16 weeks in a 2 × 2 factorial design: Control (n = 8), Control + quercetin (n = 5), HFD (n = 5), and HFD + quercetin (n = 6). Quercetin was administered orally at 100 mg/kg/day. Body weight, fasting glucose, food/fluid intake, calculated energy intake, oral glucose tolerance, terminal adiposity, lipids, and a 21-transcript hypothalamic RT-qPCR panel were evaluated. Analyses included factorial models with HC3 inference and FDR control, PCA/PERMANOVA, predefined transcriptional modules, bootstrap and leave-one-sample-out sensitivity analyses, treatment-adjusted covariance, and shrinkage regularization. Results: At week 16, HFD + quercetin reduced glucose AUC relative to HFD by 2415 mg·min/dL (q = 0.0029), visceral fat by 5.16 g (q = 0.004), and triglycerides by 47.03 mg/dL (q < 0.001), without a corresponding difference in final body weight. Diet × quercetin interactions were supported for week-16 AUC, visceral adiposity, triglycerides, and 15 of 21 hypothalamic transcripts. Sixteen of 21 transcripts met robustness criteria for the HFD + quercetin versus HFD contrast. PC1 and PC2 captured 73.5% of transcriptional variance, and all three predefined transcriptional modules showed robust diet-dependent responses. Regularized covariance sensitivity preserved the direction of all 210 treatment-adjusted transcript associations. Conclusions: The principal metabolic effects of quercetin were predominantly evident under HFD conditions and were accompanied by coordinated hypothalamic transcriptional remodeling across m6A-related, leptin–insulin-associated, and melanocortin-associated domains. These data define a transcriptional architecture for mechanistic follow-up without implying direct measurement of circulating leptin or insulin, m6A activity, protein abundance, or pathway activation.

Background/Objectives: High-fat diet (HFD) feeding disrupts systemic metabolism and hypothalamic mechanisms that coordinate energy balance. Whether quercetin modifies the coordinated transcriptional systems linking m6A-related regulation with leptin-insulin and melanocortin biology remains unclear. We examined the metabolic and hypothalamic transcriptional response to quercetin during chronic HFD exposure. Methods: Male Wistar rats were studied for 16 weeks in a 2 × 2 factorial design: Control (n = 8), Control + quercetin (n = 5), HFD (n = 5), and HFD + quercetin (n = 6). Quercetin was administered orally at 100 mg/kg/day. Body weight, fasting glucose, oral glucose tolerance, visceral adiposity, serum lipids, and terminal tissue measures were evaluated. Hypothalamic expression of 21 transcripts spanning m6A regulation, leptin-insulin signaling, melanocortin-associated genes, and oxidative response was quantified by RT-qPCR. Gene-level inference was complemented by principal component analysis, PERMANOVA, module-level analyses, bootstrap resampling, leave-one-sample-out sensitivity testing, and treatment-adjusted gene-gene covariance. Results: At week 16, HFD + quercetin reduced glucose AUC relative to HFD by 2415 mg·min/dL (q = 0.0029), visceral fat by 5.16 g (q = 0.004), and triglycerides by 47.03 mg/dL (q < 0.001), without a corresponding difference in final body weight. Sixteen of 21 transcripts met the predefined robustness criteria for the HFD + quercetin versus HFD contrast. PC1 and PC2 captured 73.5% of transcriptional variance, and the four groups differed in global molecular structure (PERMANOVA R² = 0.628, p = 0.0001). All three predefined transcriptional modules showed robust HFD + quercetin versus HFD differences. Conclusions: Quercetin attenuated major metabolic consequences of HFD feeding and was accompanied by coordinated hypothalamic transcriptional remodeling across m6A-regulatory, leptin-insulin, and melanocortin-associated domains. These data identify a transcriptional network for mechanistic follow-up without implying direct measurement of m6A activity or pathway activation.

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by endothelial dysfunction, vascular remodeling, and a sustained increase in pulmonary vascular resistance, causing cardiopulmonary damage. The apelin receptor (APJ), a member of the G protein-coupled receptor family, has emerged as an essential modulator of vascular homeostasis. Clinical and preclinical studies have demonstrated that its activation exerts beneficial effects on the progression of PAH. Its main actions include the restoration of endothelial function, reactivation of the BMPR2/SMAD axis, induction of nitric oxide-mediated vasodilation, inhibition of autophagy and the migration of the pulmonary artery smooth muscle cells (PASMCs). Furthermore, its expression and functionality are modulated by epitranscriptomic mechanisms, particularly by microRNAs involved in the post-transcriptional regulation of key genes for vascular homeostasis. These findings position the APJ as a relevant therapeutic target in PAH. However, the clinical application of its agonists still faces pharmacokinetic limitations that restrict their therapeutic use. Therefore, the aim of this review is to gather current information on APJ in the pathophysiology of PAH and focus attention on its potential as a therapeutic target.