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.
Highlights
IntroductionType 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes and about 90% of diabetic patients develop this syndrome, which is characterized by sustained high blood glucose levels and insulin resistance (Kaiser et al 2018)
The prevalence and incidence of diabetes mellitus (DM) is increasing worldwide
The data obtained here allow us to propose a new Type 2 diabetes mellitus (T2DM) mice model that mimics the natural history of this syndrome in humans to deepen study the metabolic and cardiac characteristics
Summary
Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes and about 90% of diabetic patients develop this syndrome, which is characterized by sustained high blood glucose levels and insulin resistance (Kaiser et al 2018). This syndrome can lead to cardiovascular complications such as hypertension, coronary disease and stroke (Zimmet et al 2001). Development of better animal T2DM models, which accurately reflect the pathogenesis of the human syndrome, are needed
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