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Difference between revisions of "Rodriguez de Yurre 2020 An Acad Bras Cienc"

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(Created page with "{{Publication |title=Yurre AR, Martins EGL, Lopez-Alarcon M, Cabral B, Vera N, Lopes JA, Galina A, Takiya CM, Lindoso RS, Vieyra A, SÁenz OC, Medei E (2020) Type 2 diabetes m...")
 
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|abstract=Type 2 diabetes mellitus (T2DM) is associated with an increase of premature appearance of several disorders such as cardiac complications. Thus, we test the hypothesis that a combination of a high fat diet (HFD) and low doses of streptozotocin (STZ) recapitulate a suitable mice model of T2DM to study the cardiac mitochondrial disturbances induced by this disease. Animals were divided in 2 groups: the T2DM group was given a HFD and injected with 2 low doses of STZ, while the CNTRL group was given a standard chow and a buffer solution. The combination of HFD and STZ recapitulate the T2DM metabolic profile showing higher blood glucose levels in T2DM mice when compared to CNTRL, and also, insulin resistance. The kidney structure/function was preserved. Regarding cardiac mitochondrial function, in all phosphorylative states, the cardiac mitochondria from T2DM mice presented reduced oxygen fluxes when compared to CNTRL mice. Also, mitochondria from T2DM mice showed decreased citrate synthase activity and lower protein content of mitochondrial complexes. Our results show that in this non-obese T2DM model, which recapitulates the classical metabolic alterations, mitochondrial function is impaired and provides a useful model to deepen study the mechanisms underlying these alterations.
|abstract=Type 2 diabetes mellitus (T2DM) is associated with an increase of premature appearance of several disorders such as cardiac complications. Thus, we test the hypothesis that a combination of a high fat diet (HFD) and low doses of streptozotocin (STZ) recapitulate a suitable mice model of T2DM to study the cardiac mitochondrial disturbances induced by this disease. Animals were divided in 2 groups: the T2DM group was given a HFD and injected with 2 low doses of STZ, while the CNTRL group was given a standard chow and a buffer solution. The combination of HFD and STZ recapitulate the T2DM metabolic profile showing higher blood glucose levels in T2DM mice when compared to CNTRL, and also, insulin resistance. The kidney structure/function was preserved. Regarding cardiac mitochondrial function, in all phosphorylative states, the cardiac mitochondria from T2DM mice presented reduced oxygen fluxes when compared to CNTRL mice. Also, mitochondria from T2DM mice showed decreased citrate synthase activity and lower protein content of mitochondrial complexes. Our results show that in this non-obese T2DM model, which recapitulates the classical metabolic alterations, mitochondrial function is impaired and provides a useful model to deepen study the mechanisms underlying these alterations.
|editor=[[Plangger M]]
|editor=[[Plangger M]]
|mipnetlab=BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry, BR Rio de Janeiro Vieyra A
}}
}}
{{Labeling
{{Labeling

Revision as of 20:28, 15 January 2021

Publications in the MiPMap
Yurre AR, Martins EGL, Lopez-Alarcon M, Cabral B, Vera N, Lopes JA, Galina A, Takiya CM, Lindoso RS, Vieyra A, SÁenz OC, Medei E (2020) Type 2 diabetes mellitus alters cardiac mitochondrial content and function in a non-obese mice model. An Acad Bras Cienc 92:e20191340.

» PMID: 32813865 Open Access

Yurre AR, Martins EGL, Lopez-Alarcon M, Cabral B, Vera N, Lopes JA, Galina A, Takiya CM, Lindoso RS, Vieyra A, SÁenz OC, Medei E (2020) An Acad Bras Cienc

Abstract: Type 2 diabetes mellitus (T2DM) is associated with an increase of premature appearance of several disorders such as cardiac complications. Thus, we test the hypothesis that a combination of a high fat diet (HFD) and low doses of streptozotocin (STZ) recapitulate a suitable mice model of T2DM to study the cardiac mitochondrial disturbances induced by this disease. Animals were divided in 2 groups: the T2DM group was given a HFD and injected with 2 low doses of STZ, while the CNTRL group was given a standard chow and a buffer solution. The combination of HFD and STZ recapitulate the T2DM metabolic profile showing higher blood glucose levels in T2DM mice when compared to CNTRL, and also, insulin resistance. The kidney structure/function was preserved. Regarding cardiac mitochondrial function, in all phosphorylative states, the cardiac mitochondria from T2DM mice presented reduced oxygen fluxes when compared to CNTRL mice. Also, mitochondria from T2DM mice showed decreased citrate synthase activity and lower protein content of mitochondrial complexes. Our results show that in this non-obese T2DM model, which recapitulates the classical metabolic alterations, mitochondrial function is impaired and provides a useful model to deepen study the mechanisms underlying these alterations.

Bioblast editor: Plangger M O2k-Network Lab: BR Rio de Janeiro Galina A, BR Rio de Janeiro Institute Biomedical Chemistry, BR Rio de Janeiro Vieyra A


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2021-01