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Barajas Vélez, Miguel Ángel

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https://academica-e.unavarra.es/handle/2454/48659

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Barajas Vélez

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Miguel Ángel

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Ciencias de la Salud

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IMAB. Research Institute for Multidisciplinary Applied Biology

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0000-0003-4004-1432

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810192

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2016 - 20193
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Now showing 1 - 3 of 3
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    PublicationOpen Access
    Generation and characterization of human iPSC line generated from mesenchymal stem cells derived from adipose tissue
    (Elsevier, 2016) Zapata Linares, Natalia; Rodríguez, Saray; Mazo, Manuel; Abizanda, Gloria; Barajas Vélez, Miguel Ángel; Ciencias de la Salud; Osasun Zientziak
    In this work, mesenchymal stem cells derived from adipose tissue (ADSCs) were used for the generation of the human-induced pluripotent stem cell line G15.AO. Cell reprogramming was performed using retroviral vectors containing the Yamanaka factors, and the generated G15.AO hiPSC line showed normal karyotype, silencing of the exogenous reprogramming factors, induction of the typical pluripotency-associated markers, alkaline phosphatase enzymatic activity, and in vivo and in vitro differentiation ability to the three germ layers.
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    PublicationOpen Access
    New insights into immunotherapy strategies for treating autoimmune diabetes
    (MDPI, 2019) Cabello Olmo, Miriam; Araña Ciordia, Miriam; Radichev, Ilian; Smith, Paul; Huarte, Eduardo; Barajas Vélez, Miguel Ángel; Ciencias de la Salud; Osasun Zientziak; Gobierno de Navarra / Nafarroako Gobernua
    Type 1 diabetes mellitus (T1D) is an autoimmune illness that affects millions of patients worldwide. The main characteristic of this disease is the destruction of pancreatic insulin-producing beta cells that occurs due to the aberrant activation of different immune effector cells. Currently, T1D is treated by lifelong administration of novel versions of insulin that have been developed recently; however, new approaches that could address the underlying mechanisms responsible for beta cell destruction have been extensively investigated. The strategies based on immunotherapies have recently been incorporated into a panel of existing treatments for T1D, in order to block T-cell responses against beta cell antigens that are very common during the onset and development of T1D. However, a complete preservation of beta cell mass as well as insulin independency is still elusive. As a result, there is no existing T1D targeted immunotherapy able to replace standard insulin administration. Presently, a number of novel therapy strategies are pursuing the goals of beta cell protection and normoglycemia. In the present review we explore the current state of immunotherapy in T1D by highlighting the most important studies in this field, and envision novel strategies that could be used to treat T1D in the future.
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    PublicationOpen Access
    A fermented food product containing lactic acid bacteria protects ZDF rats from the development of type 2 diabetes
    (MDPI, 2019) Cabello Olmo, Miriam; Oneca Agurruza, María; Torre Hernández, Paloma; Sainz, Neira; Moreno Aliaga, María J.; Guruceaga, Elizabeth; Díaz, Jesús Vicente; Encío Martínez, Ignacio; Barajas Vélez, Miguel Ángel; Araña Ciordia, Miriam; Ciencias de la Salud; Osasun Zientziak; Ciencias; Zientziak; Gobierno de Navarra / Nafarroako Gobernua
    Type 2 diabetes (T2D) is a complex metabolic disease, which involves a maintained hyperglycemia due to the development of an insulin resistance process. Among multiple risk factors, host intestinal microbiota has received increasing attention in T2D etiology and progression. In the present study, we have explored the effect of long-term supplementation with a non-dairy fermented food product (FFP) in Zucker Diabetic and Fatty (ZDF) rats T2D model. The supplementation with FFP induced an improvement in glucose homeostasis according to the results obtained from fasting blood glucose levels, glucose tolerance test, and pancreatic function. Importantly, a significantly reduced intestinal glucose absorption was found in the FFP-treated rats. Supplemented animals also showed a greater survival suggesting a better health status as a result of the FFP intake. Some dissimilarities have been observed in the gut microbiota population between control and FFP-treated rats, and interestingly a tendency for better cardiometabolic markers values was appreciated in this group. However, no significant differences were observed in body weight, body composition, or food intake between groups. These findings suggest that FFP induced gut microbiota modifications in ZDF rats that improved glucose metabolism and protected from T2D development.