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Martin M.A.,Institute Ciencia Y Tecnologia Of Alimentos Y Nutricion Ictan Csic | Martin M.A.,Research Center Biomedica En Red Of Diabetes | Ramos S.,Institute Ciencia Y Tecnologia Of Alimentos Y Nutricion Ictan Csic | Cordero-Herrero I.,Institute Ciencia Y Tecnologia Of Alimentos Y Nutricion Ictan Csic | And 2 more authors.
Nutrients | Year: 2013

Diabetes mellitus is associated with reductions in glutathione, supporting the critical role of oxidative stress in its pathogenesis. Antioxidant food components such as flavonoids have a protective role against oxidative stress-induced degenerative and age-related diseases. Flavonoids constitute an important part of the human diet; they can be found in most plant foods, including green tea, grapes or cocoa and possess multiple biological activities. This study investigates the chemo-protective effect of a cocoa phenolic extract (CPE) containing mainly flavonoids against oxidative stress induced by tert-butylhydroperoxide (t-BOOH) on Ins-1E pancreatic beta cells. Cell viability and oxidative status were evaluated. Ins-1E cells treatment with 5-20 μg/mL CPE for 20 h evoked no cell damage and did not alter ROS production. Addition of 50 μM t-BOOH for 2 h increased ROS and carbonyl groups content and decreased reduced glutathione level. Pre-treatment of cells with CPE significantly prevented the t-BOOH-induced ROS and carbonyl groups and returned antioxidant defences to adequate levels. Thus, Ins-1E cells treated with CPE showed a remarkable recovery of cell viability damaged by t-BOOH, indicating that integrity of surviving machineries in the CPE-treated cells was notably protected against the oxidative insult. © 2013 by the authors; licensee MDPI, Basel, Switzerland. Source


Cordero-Herrera I.,Institute of Food Science and Technology and Nutrition ICTAN | Martin M.A.,Institute of Food Science and Technology and Nutrition ICTAN | Martin M.A.,Research Center Biomedica En Red Of Diabetes | Goya L.,Institute of Food Science and Technology and Nutrition ICTAN | Ramos S.,Institute of Food Science and Technology and Nutrition ICTAN
Molecular Nutrition and Food Research | Year: 2015

Scope: Oxidative stress plays a main role in the pathogenesis of type 2 diabetes mellitus. Cocoa and (-)-epicatechin (EC), a main cocoa flavanol, have been suggested to exert beneficial effects in type 2 diabetes mellitus because of their protective effects against oxidative stress and insulin-like properties. In this study, the protective effect of EC and a cocoa phenolic extract (CPE) against oxidative stress induced by a high-glucose challenge, which causes insulin resistance, was investigated on hepatic HepG2 cells. Methods and results: Oxidative status, phosphorylated mitogen-activated protein kinases (MAPKs), nuclear factor E2 related factor 2 (Nrf2) and p-(Ser)-IRS-1 expression, and glucose uptake were evaluated. EC and CPE regulated antioxidant enzymes and activated extracellular-regulated kinase and Nrf2. EC and CPE pre-treatment prevented high-glucose-induced antioxidant defences and p-MAPKs, and maintained Nrf2 stimulation. The presence of selective MAPK inhibitors induced changes in redox status, glucose uptake, p-(Ser)- and total IRS-1 levels that were observed in CPE-mediated protection. Conclusion: EC and CPE recovered redox status of insulin-resistant HepG2 cells, suggesting that the functionality in EC- and CPE-treated cells was protected against high-glucose-induced oxidative insult. CPE beneficial effects on redox balance and insulin resistance were mediated by targeting MAPKs. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. Source


Testa R.,INRCA IRCCS National Institute | Genovese S.,IRCCS Gruppo Multimedica | Ceriello A.,Insititut dInvestigacions Biomediques August Pi i Sunyer IDIBAPS | Ceriello A.,Research Center Biomedica En Red Of Diabetes
Current Opinion in Clinical Nutrition and Metabolic Care | Year: 2014

Quality of nutrition plays a central role in illnesses such as diabetes and its complications. Dietary and lifestyle habits may have a strong impact, either worsening or improving the evolution of diabetes mellitus. Some factors, such as obesity, worsen the illness, causing chronic inflammation, lipid metabolic disorder, accelerated atherosclerosis, increased risk for thrombosis, hypertension, hyperinsulinemia, insulin resistance, and cellular senescence. Some other nutritional components, however, have an opposite effect, probably increasing antioxidant defense. RECENT FINDINGS: The effects of nutritional factors on cellular senescence in diabetic patients are described in this review. In particular, we discuss some of the nutritional causes of cellular senescence in diabetes mellitus and focus on different nutraceutical compounds that can affect cellular senescence. Furthermore, relevant mechanisms of action are also described. SUMMARY: Diet and nutraceutical factors have important effects on diabetes mellitus. Some molecules, which improve antioxidant defense, may counteract cellular senescence. A good lifestyle with physical activity and good weight control can improve the quality of life in diabetic people; on the contrary, obesity and vitamin deficiencies may worsen the evolution of this illness, even inducing cellular senescence.Copyright © Lippincott Williams &Wilkins. Source


Duran J.,Barcelona Institute for Research in Biomedicine | Duran J.,Research Center Biomedica En Red Of Diabetes | Gruart A.,Pablo De Olavide University | Garcia-Rocha M.,Barcelona Institute for Research in Biomedicine | And 4 more authors.
Human Molecular Genetics | Year: 2014

Lafora disease is a fatal neurodegenerative condition characterized by the accumulation of abnormal glycogen inclusions known as Lafora bodies. It is an autosomal recessive disorder caused by mutations in either the laforin or malin gene. To study whether glycogen is primarily responsible for the neurodegeneration in Lafora disease, we generated malin knockout mice with impaired (totally or partially) glycogen synthesis. These animals did not show the increase in markers of neurodegeneration, the impairments in electrophysiological properties of hippocampal synapses, nor the susceptibility to kainate-induced epilepsy seen in the malin knockout model. Interestingly, the autophagy impairment that has beendescribedinmalin knockout animalswasalso rescued in this double knockout model. Conversely, two other mouse models in which glycogen is over-accumulated in the brain independently of the lack of malin showed impairment in autophagy. Our findings reveal that glycogen accumulation accounts for the neurodegeneration and functional consequences seen in the malin knockout model, as well as the impaired autophagy. These results identify the regulation of glycogen synthesis as a key target for the treatment of Lafora disease. © The Author 2014. Published by Oxford University Press. All rights reserved. Source


Bartolome A.,Complutense University of Madrid | Bartolome A.,Research Center Biomedica En Red Of Diabetes | Bartolome A.,Institute Investigacion Sanitaria Del Hospital Clinico San Carlos Of Madrid Idissc | Guillen C.,Complutense University of Madrid | And 2 more authors.
Vitamins and Hormones | Year: 2014

Exquisite regulation of insulin secretion by pancreatic β-cells is essential to maintain metabolic homeostasis. β-Cell mass must be accordingly adapted to metabolic needs and can be largely modified under different situations. The mammalian target of rapamycin (mTOR) complexes has been consistently identified as key modulators of β-cell mass. mTOR can be found into two different complexes, mTORC1 and mTORC2. Under systemic insulin resistance, mTORC1/mTORC2 signaling in β-cells is needed to increase β-cell mass and insulin secretion. However, type 2 diabetes arises when these compensatory mechanisms fail, being the role of mTOR complexes still obscure in β-cell failure. In this chapter, we introduce the protein composition and regulation of mTOR complexes and their role in pancreatic β-cells. Furthermore, we describe their main signaling effectors through the review of numerous animal models, which indicate the essential role of mTORC1/mTORC2 in pancreatic β-cell mass regulation. © 2014 Elsevier Inc. Source

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