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http://repositorio.ugto.mx/handle/20.500.12059/1079
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DC Field | Value | Language |
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dc.rights.license | http://creativecommons.org/licenses/by-nc-nd/4.0 | es_MX |
dc.creator | JUAN MANUEL MALACARA HERNANDEZ | es_MX |
dc.date | 2012-02-10 | - |
dc.date.accessioned | 2019-06-25T19:44:37Z | - |
dc.date.available | 2019-06-25T19:44:37Z | - |
dc.date.issued | 2012-02-10 | - |
dc.identifier.uri | http://repositorio.ugto.mx/handle/20.500.12059/1079 | - |
dc.description.abstract | La causa de la diabetes mellitus tipo 2, la enfermedad metabólica más frecuente, no es bien conocida. Tiene un componente genético y otro ambiental, en éste destacan la obesidad y el sedentarismo. El conocimiento de las nuevas hormonas que controlan la alimentación: la leptina, la ghrelina y el péptido YY3-36, es una esperanza para el control de la obesidad. No se han identificado los genes asociados con la enfermedad, lo que hace sospechar que bien se trata de una herencia compleja, o intervienen otros mecanismos. La teoría del gen ahorrador busca explicar el aumento de la obesidad y la diabetes en los grupos humanos en transición a la industrialización. | es_MX |
dc.format | application/pdf | - |
dc.language.iso | spa | es_MX |
dc.publisher | Universidad de Guanajuato | es_MX |
dc.relation | http://www.actauniversitaria.ugto.mx/index.php/acta/article/view/264 | - |
dc.rights | info:eu-repo/semantics/openAccess | es_MX |
dc.source | Acta Universitaria. Multidisciplinary Scientific Journal. Vol 13 No 2 (2003) | - |
dc.source | ISSN: 2007-9621 | - |
dc.title | El Enigma de las Causas de la Diabetes Mellitus Tipo 2 | es_MX |
dc.type | info:eu-repo/semantics/article | es_MX |
dc.creator.id | info:eu-repo/dai/mx/cvu/320 | es_MX |
dc.subject.cti | info:eu-repo/classification/cti/3 | es_MX |
dc.subject.keywords | Diabetes Mellitus Tipo 2 (DMT2) | es_MX |
dc.subject.keywords | Genética | es_MX |
dc.subject.keywords | Inflamación | es_MX |
dc.subject.keywords | Metabolismo | es_MX |
dc.subject.keywords | Bajo peso al nacer | es_MX |
dc.subject.keywords | Type 2 Diabetes Mellitus (T2DM) | en |
dc.subject.keywords | Genetics | en |
dc.subject.keywords | Inflammation | en |
dc.subject.keywords | Metabolism | en |
dc.subject.keywords | Low birth weight | en |
dc.type.version | info:eu-repo/semantics/publishedVersion | es_MX |
dc.description.abstractEnglish | Type 2 diabetes mellitus the most frequent metabolic disease, is induced by factors so far largely unknown. Genetic and environmental causes are implicated, among the latter obesity and sedentary life are the most important.The discovery of new hormones controlling food intake such as leptin, ghrelin and the YY3-36 peptide, are expected to provide new tools to reduce overfeeding. The genes associated with type 2 diabetes are intensively sought without success.It is possible that the genetic transmission is more complex than suppossed. The theory of the thrifty gene proposes an explanation for the increased obesity and diabetes in ethnic groups in transition from pre-industrial to industrialized cultures.The theory of the fetal origins of adult disease, proposes that in the fetal life there is a window for metabolic programming under stress or caloric restriction. If the subject, however, at the adult life consumes excessive caloric intake, has a high risk for the metabolic syndrome. The mechanisms involved in insulin resistance are complex, and several molecules are under study as candidates to explain it. The diminution in insulin secretion is another important factor for the initiation of type 2 diabetes.Glucotoxicity and lipotoxicity are factors that further reduce insulin secretion. Recent evidence indicates that inflammation is implicated in the onset of both diabetes and atherosclerosis. The elucidation of the nature of this process, as well as the pathways involved will be another important tool for a better management of this disease. | en |
Appears in Collections: | Revista Acta Universitaria |
Files in This Item:
File | Description | Size | Format | |
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264-Article Text-1006-1-10-20120210.pdf | 419.42 kB | Adobe PDF | View/Open |
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