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The development of formulations from plant or animal extracts and polymeric platforms has been well established toward emulsion-based delivery systems, avoiding the use of conventional surfactants. This approach involves the stabilization of poorly water-soluble extracts by polymers, improving their dispersion into food and pharmaceutical products, avoiding premature degradation, and resulting in better bioavailability. According to the literature, extracts are obtained via conventional and novel methods, which exhibit advantages and disadvantages related to using organic solvent, temperature, time, pressure, and equipment cost. Similarly, for polymer-based emulsifiers, there are different methods to obtain them. Also, their chemical composition and morphology (linear, branched, and crosslinked) play relevant roles in their performance as stabilizing agents. On the other hand, oil-in-water emulsions from plant-animal extracts and biocompatible polymers have been prepared using different strategies focused on achieving high stability of the colloidal system. Hence, this review provides current information regarding some protocols used for the extraction/synthesis of materials and the development of promising formulations.

Type 2 Diabetes Mellitus (T2DM) is a rapidly rising disease with cardiovascular complications constituting the most common cause of death among diabetic patients. Chronic hyperglycemia can induce vascular dysfunction through damage of the components of the vascular wall, such as vascular smooth muscle cells (VSMCs), which regulate vascular tone and contribute to vascular repair and remodeling. These functions are dependent on intracellular Ca2+ changes. The mechanisms by which T2DM affects Ca2+ handling in VSMCs still remain poorly understood. Therefore, the objective of this study was to determine whether and how T2DM affects Ca2+ homeostasis in VSMCs. We evaluated intracellular Ca2+ signaling in VSMCs from Zucker Diabetic Fatty rats using Ca2+ imaging with Fura-2/AM. Our results indicate that T2DM decreases Ca2+ release from the sarcoplasmic reticulum (SR) and increases the activity of store-operated channels (SOCs). Moreover, we were able to identify an enhancement of the activity of the main Ca2+ extrusion mechanisms (SERCA, PMCA and NCX) during the early stage of the decay of the ATP-induced Ca2+ transient. In addition, we found an increase in Ca2+ entry through the reverse mode of NCX and a decrease in SERCA and PMCA activity during the late stage of the signal decay. These effects were appreciated as a shortening of ATP-induced Ca2+ transient during the early stage of the decay, as well as an increase in the amplitude of the following plateau. Enhanced cytosolic Ca2+ activity in VSMCs could contribute to vascular dysfunction associated with T2DM.

Mexican oregano (Lippia graveolens) polyphenols have antioxidant and anti-inflammatory potential, but low bioaccessibility. Therefore, in the present work the micro/nano-encapsulation of these compounds in two different matrixes of chitosan (CS) and chitosan-b-poly(PEGMA2000) (CS-b-PPEGMA) is described and assessed. The particle sizes of matrixes of CS (~955 nm) and CS-b-PPEGMA (~190 nm) increased by 10% and 50%, respectively, when the phenolic compounds were encapsulated, yielding loading efficiencies (LE) between 90–99% and 50–60%, correspondingly. The release profiles in simulated fluids revealed a better control of host–guest interactions by using the CS-b-PPEGMA matrix, reaching phenolic compounds release of 80% after 24 h, while single CS retained the guest compounds. The total reducing capacity (TRC) and Trolox equivalent antioxidant capacity (TEAC) of the phenolic compounds (PPHs) are protected and increased (more than five times) when they are encapsulated. Thus, this investigation provides a standard encapsulation strategy and relevant results regarding nutraceuticals stabilization and their improved bioaccessibility.

Vitamin D (VD) deficiency has been associated with cancer and diabetes. Insulin signaling through the insulin receptor (IR) stimulates cellular responses by activating the PI3K/AKT pathway. PTEN is a tumor suppressor and a negative regulator of the pathway. Its absence enhances insulin signaling leading to hypoglycemia, a dangerous complication found after insulin overdose. We analyzed the effect of VD signaling in a model of overactivation of the IR. We generated inducible double KO (DKO) mice for the VD receptor (VDR) and PTEN. DKO mice showed severe hypoglycemia, lower total cholesterol and increased mortality. No macroscopic tumors were detected. Analysis of the glucose metabolism did not show clear differences that would explain the increased mortality. Glucose supplementation, either systemically or directly into the brain, did not enhance DKO survival. Lipidic liver metabolism was altered as there was a delay in the activation of genes related to β-oxidation and a decrease in lipogenesis in DKO mice. High-fat diet administration in DKO significantly improved its life span. Lack of vitamin D signaling increases mortality in a model of overactivation of the IR by impairing lipid metabolism. Clinically, these results reveal the importance of adequate Vitamin D levels in T1D patients.

Background Chronic kidney disease (CKD) is associated with increased atherosclerotic burden and higher risk for cardiovascular events (CVE). Atherosclerosis has a significant genetic component and, in CKD, it is influenced by mineral metabolism alterations. Therefore, genetic modifications of mineral metabolism–related proteins could affect atherosclerosis in CKD patients. In the present study we investigated the role of single nucleotide polymorphisms (SNPs) of the matrix gamma-carboxy glutamic acid protein (MGP) on atherosclerosis progression and CVE in a CKD cohort. Methods A total of 2187 CKD patients from the Observatorio Nacional de Aterosclerosis en Nefrologia (NEFRONA) study were genotyped for SNPs present in the matrix gamma-carboxy glutamic acid (Gla) protein (MGP) gene. Atheromatosis was detected by vascular ultrasound. Progression of atheromatosis, defined as an increase in territories with plaque, was assessed after 24 months. Patients were followed for 48 months for CVE. Association of SNPs with plaque progression was assessed by logistic regression and their capacity to predict CVE by Cox regression. Results Three SNPs of the MGP gene were analyzed. No association of the rs4236 or the rs1800801 SNPs was detected with any of the outcomes. However, patients homozygotes for the minor allele of the rs1800802 SNP showed higher adjusted risk for plaque progression [odds ratio 2.3 (95% confidence interval 1.06–4.9)] and higher risk of suffering a CVE [hazard ratio 2.16 (95% confidence interval 1.13–4.12)] compared with the rest of genotypes. No association of the SNP with total or dp-ucMGP levels was found in a subsample. Conclusions The rs1800802 polymorphism of MGP is associated with plaque progression and CVE in CKD patients. [ABSTRACT FROM AUTHOR]