Metabolic syndrome is a multifaceted condition associated with a greater risk of various disorders (e.g., diabetes and heart disease). In a rat model of metabolic syndrome, an acute in vitro application of rosuvastatin causes relaxation of aortic rings. Since the outcome of a subchronic rosuvastatin treatment is unknown, the present study explored its effect on acetylcholine-induced vasorelaxation of aortic rings from rats with metabolic syndrome. Animals were submitted to a 16-week treatment, including a standard diet, a cafeteria-style diet (CAF-diet), or a CAF-diet with daily rosuvastatin treatment (10 mg/kg). After confirming the development of metabolic syndrome in rats, aortic segments were extracted from these animals (those treated with rosuvastatin and untreated) and the acetylcholine-induced relaxant effect on the corresponding rings was evaluated. Concentration-response curves were constructed for this effect in the presence/absence of L-NAME, ODQ, KT 5823, 4-aminopyridine (4-AP), tetraethylammonium (TEA), apamin plus charybdotoxin, glibenclamide, indomethacin, clotrimazole, and cycloheximide pretreatment. Compared to rings from control rats, acetylcholine-induced vasorelaxation decreased in rings from animals with metabolic syndrome, and was maintained at a normal level in animals with metabolic syndrome plus rosuvastatin treatment. The effect of rosuvastatin was inhibited by L-NAME, ODQ, KT 5823, TEA, apamin plus charybdotoxin, but unaffected by 4-AP, glibenclamide, indomethacin, clotrimazole, or cycloheximide. In conclusion, the subchronic administration of rosuvastatin to rats with metabolic syndrome improved the acetylcholine-induced relaxant response, involving stimulation of the NO/cGMP/PKG/Ca2+-activated K+ channel pathway.

Boron-containing compounds (BCCs) have emerged as potential drugs. Their drug-like effects are mainly explained by their mechanisms of action in enzymes. Nowadays, some experimental data support the effects of specific BCCs on GPCRs, provided there are crystal structures that show them bound to G protein-coupled receptors (GPCRs). Some BCCs are recognized as potential ligands of GPCRs—the drug targets of many diseases. Objective: The aim of this study was to collecte up-to-date data on the interactions of BCCs with GPCRs. Methods: Data were collected from the National Center of Biotechnology Information, PubMed, Global Health, Embase, the Web of Science, and Google Scholar databases and reviewed. Results: Some experimental reports support the interactions of BCCs with several GPCRs, acting as their labels, agonists, or antagonists. These interactions can be inferred based on in silico and in vitro results if there are no available crystal structures for validating them. Conclusions: The actions of BCCs on GPCRs are no longer hypothetical, as the existing evidence supports BCCs’ interactions with and actions on GPCRs.

Ruth Mery L?pez, Jorge Skiold L?pez, Jair Lozano, H?ctor Flores, Rosa Angelica Carranza, Antonio Franco, and Enrique Fernando Castillo. Korean J Physiol Pharmacol 2020;24:339-48. https://doi.org/10.4196/kjpp.2020.24.4.339

El sobrepeso afecta a millones de lactantes y preescolares en el mundo afectando su calidad y esperanza de vida. La exposición a guarderías puede jugar un papel importante para prevenir un peso no saludable (PNS). indicar la prevalencia y la asociación de la exposición a guarderías y otros factores asociados con el PNS en lactantes y preescolares. se realizó un estudio transversal analítico. Se incluyó población infantil de 6-47 meses sin comorbilidades que comprometieran su estado nutricional y se excluyeron a aquellos con un cuidado infantil formal diferente al de las guarderías seleccionadas. Se evaluó la exposición a guardería, y otros factores (perinatales, actividad física, nutricionales, y familiares). Se consideró PNS una puntuación z > 1 DE. Se obtuvieron prevalencias, razones de momios (RM), intervalos de confianza del 95% (IC95%) y RM ajustadas por edad, bajo peso al nacer, inicio de la alimentación complementaria, consumo de bebidas azucaradas, siestas diurnas, estado nutricional materno y quintil de ingreso familiar a través de regresión logística. la prevalencia general de PNS fue de 17.84% (IC95%:14.93-21.16), 11.84 (IC95%: 8.54-16.14) para la población infantil expuesta a guarderías, y 23.78% (IC95%: 19.21-29.02) en no expuestos, mostrando diferencias significativas entre ambas prevalencias (p < 0.001). La RM ajustada para la presentación de PNS fue de 0.39 (IC95%: 0.23-0.66) para exposición a guardería. la exposición a guarderías IMSS mostró ser un posible ambiente protector contra el desarrollo de un PNS.

Insulin resistance is a feature of pregnancy and is associated with increased levels of angiotensin II (Ang II) and insulin. Therefore, pregnancy may change insulin-induced vasodilation through changes in Ang II receptors. Insulin-induced vasorelaxation was evaluated in phenylephrine-precontracted aortic rings of pregnant and non-pregnant rats, using a conventional isolated organ preparation. Experiments were performed in thoracic or abdominal aorta rings with or without endothelium in the presence and absence of N^G-nitro-L-arginine methyl ester (L-NAME) (10⁻⁵ M), losartan (10⁻⁷ M), or PD123319 (10⁻⁷ M). AT1 and AT2 receptor expressions were detected by immunohistochemistry. Insulin-induced vasodilation was endothelium- and nitric oxide–dependent and decreased in the thoracic aorta but increased in the abdominal segment of pregnant rats. The insulin’s vasorelaxant effect was increased by losartan mainly on the thoracic aorta. PD123319 decreased insulin-induced vasorelaxation mainly in the pregnant rat abdominal aorta. AT1 receptor expression was decreased while AT2 receptor expression was increased by pregnancy. In conclusion, pregnancy changes insulin-induced vasorelaxation. Moreover, insulin vasodilation is tonically inhibited by AT1 receptors, while AT2 receptors appear to have an insulin-sensitizing effect. The role of pregnancy and Ang II receptors differ depending on the aorta segment. These results shed light on the role of pregnancy and Ang II receptors on the regulation of insulin-mediated vasodilation.

Boron-containing compounds (BCC) have emerged as potential drugs. The effects of letting act as drugs are mainly by means of action on enzymes. Moreover, no crystal structure shows binding to G-Protein coupled receptors (GPCRs), albeit if those are recognized as targets in many diseases. However, some experimental data support the effects of specific BCC on GPCRs. Objective: Updating data about the reported effects that suggest or support interactions of BCC on GPCR. Methods: Data were collected and reviewed from the National Center of Biotechnology Information, PubMed, Global Health, Embase, the Web of Science, and Google Scholar databases. Results: Some experimental reports support the interactions of BCC in several GPCRs, acting as labels, agonists, or antagonists on them. Details of interaction can be inferred by in silico and in vitro results. Albeit if not a crystal structure showing such a complex. Conclusions: The action of BCCs on GPCR is beyond a presumptive proposal. Evidence supports the interaction and actions of BCCs on GPCRs.