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dc.contributorEspinoza Rojo, Monica
dc.contributor.advisorESPINOZA ROJO, MONICA; 30538
dc.contributor.authorBahena Cuevas, Oscar Ezequiel
dc.date.accessioned2023-10-26T01:54:53Z
dc.date.available2023-10-26T01:54:53Z
dc.date.issued2021-06
dc.identifier.urihttp://ri.uagro.mx/handle/uagro/4129
dc.description.abstractIntroduction: Insulin resistance (IR) is a condition that characterizes metabolic disorders, such as obesity and type 2 diabetes mellitus, which causes insulin-dependent tissues to alter their metabolism due to lack of response to the presence of the stimulus represented. by insulin. IR in the brain was recently related to the development of neurodegenerative diseases in obese people, however the mechanisms of damage that derive from the establishment of insulin resistance in the brain are not known, and whether it predisposes to the establishment of tissue alterations peripheral, in obesity, for this reason, the objective of our study is to determine if the establishment of peripheral insulin resistance (RIP) is related to the presence of cerebral insulin resistance (IQR) in an obesity model. Research design and methods: The effect of the administration of the high-fat diet (HFD) on the establishment of obesity was determined by the difference of 40% or more of the body weight of the mice on the standard low-fat diet (C and LFD). RIP in HFD mice was determined by measuring blood glucose levels, by incision in the tail of the mouse, every 30 minutes after administration of glucose and insulin. The effect of insulin administration in the preoptic area on core body temperature in mice was measured by radiotelemetry, to determine the establishment of IQR. Results: Mice developed obesity and weight gain 1, 2, and 3 months after consuming the high-fat diet (HFD). The glucose tolerance curves (CTG) and insulin (CTI) show that the group exposed to HFD had RIP at the third month of exposure, because the fasting glucose level during the CTG was above 150 mg / dl, in addition, the glucose level does not decrease when insulin is administered, compared to group C. On the other hand, the injection of insulin in the preoptic area does not induce an insulin response in the LFD groups (at the first and second month of diet) and HFD (at the third month), which shows the presence of IQR. Exposure to 10 ° C caused an increase in body temperature in the HFD group in the second month. Conclusions: Our results show that an HFD causes RIP and IQR, while LFD causes IQR in the first and second months.
dc.formatpdf
dc.language.isospa
dc.publisherUniversidad Autónoma de Guerrero (México)
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0
dc.subjectInsulin
dc.subjectinsulin resistance
dc.subjectobesity
dc.subjecthypothalamus
dc.subjectPOA
dc.subjecthyperthermia
dc.subject.classificationMEDICINA Y CIENCIAS DE LA SALUD::CIENCIAS MÉDICAS::BIOLOGÍA HUMANA::QUÍMICA CLÍNICA
dc.titleResistencia a la insulina cerebral y su relación con la resistencia a la insulina periférica en un modelo in vivo de obesidad.
dc.typeTesis de maestría
dc.contributor.committeeMemberBarragán Bonilla, Martha Isela
dc.contributor.committeeMemberMendoza Bello, Juan Miguel
dc.contributor.committeeMemberSalazar Hernández, Elena
dc.type.conacytmasterThesis
dc.rights.accesopenAccess
dc.audiencegeneralPublic
dc.identificator3||32||2410||230207
dc.format.digitalOriginBorn digital
dc.thesis.degreelevelMaestría
dc.thesis.degreenameMaestría en Ciencias Biomédicas
dc.thesis.degreegrantorUniversidad Autónoma de Guerrero
dc.thesis.degreedepartmentFacultad de Ciencias Químico Biológicas
dc.thesis.degreedisciplineMedicina y Ciencias de la Salud
dc.identifier.cvuagro13315132


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