Examinando por Autor "Manzano, Alexander"
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Ítem Diagnostic criteria and management of metabolic syndrome: Evolution overtime(Saber UCV, Universidad Central de Venezuela, 2020) Rojas, Edward; Castro, Ana; Manzano, Alexander; Suarez, Maria Karina; Lameda, Victor; Carrasquero, Ruben; Nava, Manuel; Bermúdez, ValmoreThe beginnings of the Metabolic Syndrome (MetS) as a suspected, not yet recognized entity can be traced back to 1923 when a study concerning a particularly common clustering of metabolic entities observed in diabetic patients was first published. Years of research and endless debate yielded the currently accepted MetS definition and diagnostic criteria, even if some components and their cut-off points are still up for discussion. To date, MetS are defined as a clustering of metabolic risk factors that greatly increase the incidence of cardiovascular disease (CVD) and type 2 diabetes (T2D), while also being closely related to various potentially deadly comorbidities. Furthermore, since early detection and management of MetS have been shown to decrease the risk for CVD and T2D, current research has focused on unifying diagnostic criteria and proposing novel parameters to facilitate MetS identification, while also promoting a healthy lifestyle as a preventive measure. With a deeper understanding of MetS pathophysiology comes the broadening of therapeutic targets open for study, thus expanding and enhancing the treatment methods currently in use. This review aims to summarize the evolution of MetS as a concept, development of the diagnostic criteria, current management, and future directions.Ítem Probiotics and Gut Microbiota in Obesity: Myths and realities of a New Health Revolution(MDPI, 2022) León Aguilera, Xavier Eugenio; Manzano, Alexander; Pirela, Daniela; Bermúdez, ValmoreObesity and its comorbidities are humans’ most prevalent cardio-metabolic diseases worldwide. Recent evidence has shown that chronic low-grade inflammation is a common feature in all highly prevalent chronic degenerative diseases. In this sense, the gut microbiota is a complete ecosystem involved in different processes like vitamin synthesis, metabolism regulation, and both appetite and immune system control. Thus, dysbiosis has been recognised as one of the many factors associated with obesity due to a predominance of Firmicutes, a decrease in Bifidobacterium in the gut, and a consequent short-chain fatty acids (SCFA) synthesis reduction leading to a reduction in incretins action and intestinal permeability increase. In this context, bacteria, bacterial endotoxins, and toxic bacterial by-products are translocated to the bloodstream, leading to systemic inflammation. This review focuses on gut microbiota composition and its role in obesity, as well as probiotics and prebiotics benefits in obesity.Ítem Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review(MDPI, 2021) Cano, Raquel; Pérez, José L.; Angarita Dávila, Lissé; Ortega, Ángel; Gómez, Yosselin; Valero-Cedeño, Nereida Josefina; Parra, Heliana; Manzano, Alexander; Véliz Castro, Teresa Isabel; Díaz Albornoz, María P; Cano, Gabriel; Rojas-Quintero, Joselyn; Chacín, Maricarmen; Bermúdez, ValmoreNon-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.Ítem The Role of the α Cell in the Pathogenesis of Diabetes: A World beyond the Mirror(MDPI, 2021) 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, LisseType 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.Ítem Specialized Pro-Resolving Lipid Mediators: The Future of Chronic Pain Therapy?(MDPI, 2021) Chávez-Castillo, Mervin; Ortega, Ángel; Cudris-Torres, Lorena; Duran, Pablo; Rojas, Milagros; Manzano, Alexander; Garrido, Bermary; Salazar, Juan; Silva, Aljadis; Rojas-Gomez, Diana Marcela; De Sanctis, Juan B.; Bermúdez, ValmoreChronic pain (CP) is a severe clinical entity with devastating physical and emotional consequences for patients, which can occur in a myriad of diseases. Often, conventional treatment approaches appear to be insufficient for its management. Moreover, considering the adverse effects of traditional analgesic treatments, specialized pro-resolving lipid mediators (SPMs) have emerged as a promising alternative for CP. These include various bioactive molecules such as resolvins, maresins, and protectins, derived from ω-3 polyunsaturated fatty acids (PUFAs); and lipoxins, produced from ω-6 PUFAs. Indeed, SPMs have been demonstrated to play a central role in the regulation and resolution of the inflammation associated with CP. Furthermore, these molecules can modulate neuroinflammation and thus inhibit central and peripheral sensitizations, as well as long-term potentiation, via immunomodulation and regulation of nociceptor activity and neuronal pathways. In this context, preclinical and clinical studies have evidenced that the use of SPMs is beneficial in CP-related disorders, including rheumatic diseases, migraine, neuropathies, and others. This review integrates current preclinical and clinical knowledge on the role of SPMs as a potential therapeutic tool for the management of patients with CP.