Examinando por Autor "Nava, Manuel"

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    Advanced glycation end products: New clinical and molecular perspectives
    (MDPI, 2021-07-02) Salazar, Juan; Navarro, Carla; Ortega, Ángel; Nava, Manuel; Morillo, Daniela; Torres, Wheeler; Hernández, Marlon; Cabrera, Mayela; Angarita, Lissé; Ortiz, Rina; Chacín, Maricarmen; D’marco, Luis; Bermúdez, Valmore
    Diabetes mellitus (DM) is considered one of the most massive epidemics of the twenty-first century due to its high mortality rates caused mainly due to its complications; therefore, the early identification of such complications becomes a race against time to establish a prompt diag-nosis. The research of complications of DM over the years has allowed the development of numer-ous alternatives for diagnosis. Among these emerge the quantification of advanced glycation end products (AGEs) given their increased levels due to chronic hyperglycemia, while also being related to the induction of different stress-associated cellular responses and proinflammatory mechanisms involved in the progression of chronic complications of DM. Additionally, the investigation for more valuable and safe techniques has led to developing a newer, noninvasive, and effective tool, termed skin fluorescence (SAF). Hence, this study aimed to establish an update about the molecular mechanisms induced by AGEs during the evolution of chronic complications of DM and describe the newer measurement techniques available, highlighting SAF as a possible tool to measure the risk of developing DM chronic complications. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
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    Ítem
    The Role of the α Cell in the Pathogenesis of Diabetes: A World beyond the Mirror
    (MDPI, 2021-09-01) Martínez, María Sofía; Manzano, Alexander; Olivar, Luis Carlos; Nava, Manuel; Salazar, Juan; D’marco, Luis; Ortiz, Rina; Chacín, Maricarmen; Guerrero-Wyss, Marion; Cabrera de Bravo, Mayela; Cano, Clímaco; Bermúdez, Valmore; Angarita, Lisse
    Type 2 Diabetes Mellitus (T2DM) is one of the most prevalent chronic metabolic disorders, and insulin has been placed at the epicentre of its pathophysiological basis. However, the involvement of impaired alpha (α) cell function has been recognized as playing an essential role in several diseases, since hyperglucagonemia has been evidenced in both Type 1 and T2DM. This phenomenon has been attributed to intra-islet defects, like modifications in pancreatic α cell mass or dysfunction in glucagon’s secretion. Emerging evidence has shown that chronic hyperglycaemia provokes changes in the Langerhans’ islets cytoarchitecture, including α cell hyperplasia, pancreatic beta (β) cell dedifferentiation into glucagon-positive producing cells, and loss of paracrine and endocrine regulation due to β cell mass loss. Other abnormalities like α cell insulin resistance, sensor machinery dysfunction, or paradoxical ATP-sensitive potassium channels (KATP) opening have also been linked to glucagon hypersecretion. Recent clinical trials in phases 1 or 2 have shown new molecules with glucagon-antagonist properties with considerable effectiveness and acceptable safety profiles. Glucagon-like peptide-1 (GLP-1) agonists and Dipeptidyl Peptidase-4 inhibitors (DPP-4 inhibitors) have been shown to decrease glucagon secretion in T2DM, and their possible therapeutic role in T1DM means they are attractive as an insulin-adjuvant therapy.