María del Rosario Ferreira

Objective: The aim of the present study was to analyze the effects of an Astaxanthin (ASTX)- rich extract—a powerful antioxidant—obtained from freshwater crustaceans ( Dilocarcinus pagei crabs) on liver disturbed lipid metabolism and oxidative stress in rats fed a high-sucrose diet (HSD). Methods: Male Wistar rats were fed for 13 weeks with either: 1—a standard commercial rodent diet (RD), 2—a HSD, 3—a RD plus ASTX, or 4—a HSD plus ASTX. The rats were given orally either ASTX (10 mg/kg body weight/day in sunflower oil) or only the vehicle. Results: ASTX supplementation attenuated liver injury, as reflected by a reduction in steatosis severity and hepatic triglyceride accumulation. This effect appears to be primarily achieved by promoting mitochondrial fatty acid β-oxidation, as suggested by increased hepatic carnitine palmitoyltransferase-1 (CPT-1) activity, without significantly affecting lipogenesis. In addition, ASTX improved intracellular redox status by preventing the increase in hepatic reactive oxygen species (ROS) levels and by promoting a significant increase in the activity of the antioxidant enzymes catalase (CAT) and glutathione S-transferase (GST). ASTX was also able to restore altered GSH levels. Furthermore, ASTX induced an up-regulation of Nrf2 and a down-regulation of p-NFκB p65 protein expression, key transcription factors that govern cellular responses under pro-oxidant and pro-inflammatory conditions. Conclusion: This study suggests that ASTX obtained from the freshwater crustacean D. pagei exerts beneficial effects against altered hepatic lipid metabolism and oxidative stress in HSD-fed rats, positioning this species as a promising novel source of ASTX for functional nutrition strategies.

Skeletal muscle (SkM) is a plastic and dynamic tissue, essential in energy metabolism. Growing evidence suggests a close relationship between intramuscular fat accumulation, oxidative stress (OS), extracellular matrix (ECM) remodeling, and metabolic deregulation in SkM. Nowadays natural products emerge as promising alternatives for the treatment of metabolic disorders. We have previously shown that chia seed administration reverts SkM lipotoxicity and whole‐body insulin resistant (IR) in sucrose‐rich diet (SRD) fed rats. The purpose of the present study was to assess the involvement of OS and fibrosis in SkM metabolic impairment of insulin‐resistant rats fed a long‐term SRD and the effects of chia seed upon these mechanisms as therapeutic strategy. Results showed that insulin‐resistant SRD‐fed rats exhibited sarcopenia, increase in lipid peroxidation, altered redox state, and ECM remodeling‐increased collagen deposition and lower activity of the metalloproteinase 2 (MMP‐2) in SkM. Chia seed increased ferric ion reducing antioxidant power and glutathione reduced form levels, and the activities of glutathione peroxidase and glutathione reductase enzymes. Moreover, chia seed reversed fibrosis and restored the MMP‐2 activity. This work reveals a participation of the OS and ECM remodeling in the metabolic alterations of SkM in our experimental model. Moreover, current data show novel properties of chia seed with the potential to attenuate SkM OS and fibrosis, hallmark of insulin‐resistant muscle.

Metabolic syndrome (MS) is a cluster of risk factors for the development of cardiovascular disease and type 2 diabetes mellitus. Some dietary bioactive compounds such as peptides can exert dual antioxidant and anti-inflammatory effects. The aim of this study was to analyze the effects of microencapsulated brewers’ spent grain peptides (BSG-P-MC) on hepatic injury, lipid peroxidation, oxidative stress and inflammation in the liver-spleen axis in Wistar rats fed with a sucrose-rich diet (SRD). Male rats received for 100 days a reference diet (RD), SRD or RD and SRD containing 700 mg per kg body weight per day of BSG-P-MC. The results demonstrated that BSG-P-MC reversed injury, lipid peroxidation, and oxidative stress in the liver. For the spleen, BSG-P-MC decreased the levels of lipid peroxidation, CAT activity, NFκB, PAI-1 and F4/80 protein mass levels with respect to the SRD-fed rats. Three peptides identified by LC-MS/MS from BSG-P-MC after in vitro gastrointestinal digestion showed high in silico free radical scavenging activity (LPRDPYVDPMAPLPR, ANLPRDPYVDPMAPLPRSGPE and ANLPRDPYVDPMAPLPR). Moreover, two identified peptides presented high in silico anti-inflammatory properties (LTIGDTVPNLELDSTHGKIR and VDPDEKDAQGQLPSRT). This study is the first report of antioxidant and anti-inflammatory properties of microencapsulated BSG-peptides exerted in the liver-spleen axis in a MS rodent model.

The aim of this study was to analyze blood coagulation, endothelial dysfunction and liver fibrosis in an experimental model of Metabolic Syndrome and to evaluate the effects of chia seed as a therapeutic strategy.

Introducción: la disfunción del tejido adiposo constituye un punto central en el desarrollo de la resistencia insulínica y otras alteraciones asociadas al Síndrome Metabólico. La proteína quinasa activada por AMP (AMPK) es considerada un sensor metabólico celular, con un importante rol en la regulación de la actividad metabólica del tejido adiposo blanco. Objetivos: evaluar los efectos de la administración crónica de una dieta rica en sacarosa sobre algunos mecanismos involucrados en la disfunción del tejido adiposo y su relación con la resistencia insulínica. Materiales y métodos: ratas macho Wistar recibieron una dieta de referencia (DR) o una dieta rica en sacarosa (DRS) durante seis meses. Al final del período experimental se analizaron parámetros antropométricos e índice de adiposidad visceral. En tejido adiposo epididimal se midió: contenido de triglicéridos, actividad enzimática carnitina palmitoil transferasa (CPT1, CPT2 y CPTtotal), ácidos grasos no esterificados, glucosa, insulina y TNFα. La sensibilidad insulínica se midió por la técnica clamp euglucémica-hiperinsulinémica. Resultados: los animales dislipémicos insulinoresistentes alimentados con DRS presentaron un aumento significativo en los parámetros antropométricos peso corporal, circunferencias toráxica y abdominal e indíce de masa corporal y de adiposidad visceral. En el tejido adiposo epididimal, se observó un aumento en el contenido de triglicéridos, sin modificaciones en el transporte de ácidos grasos hacia la mitocondria (estimado por la medida de la actividad CPT). Además, se observó una disminución en la masa proteica de la AMPK fosforilada que se correlacionó con altos niveles séricos de TNFα. Conclusiones: los hallazgos aportan nuevos mecanismos que involucran a la AMPK en la disfunción del tejido adiposo visceral en ratas dislipémicas insulinorresistentes.