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.

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BackgroundThis study investigated the effects of methylmercury intoxication on mice skeletal muscle subjected or not to progressive resistance training (RT).MethodsFour experimental groups were formed. Control and Con + RT received water and methylmercury (MeHg) and MeHg + RT groups received methylmercury (5 mg/kg/day), via gavage for 14 days. The Con + RT and MeHg + RT animals performed weighted ladder climbing RT, three times a week for 4 weeks. Animal muscle strength and gastrocnemius and soleus cross‐section area, fibrosis, myosin heavy chains (MyHCs), E3‐ligases MAFbx and MuRF1, 20S proteasome (P20S) and LC3‐II content were analysed. In addition, P20S chymotrypsin‐like activity was evaluated.ResultsResistance training protected MeHg + RT mice against strength loss but not against muscle atrophy. The latter appeared to be associated with MyHCs significant content reductions observed in the MeHg and MeHg + RT groups. In soleus muscle, there was an increase in E3‐ligases and P20S levels and P20S activity in both methylmercury groups compared with control ones. This pattern was also observed for gastrocnemius muscle, except for P20S content and activity that decreased. The P‐AKT content decreased in the soleus and gastrocnemius of the MeHg animals while significant elevation of LC3‐II content levels occurred.ConclusionsThe accumulation of methylmercury caused an increase in skeletal muscle MyHCs degradation, resulting in muscle atrophy that was reinforced by the elevated fibrosis area. Although RT did not reverse this condition, maintenance of muscle strength levels in animals submitted to MeHg + RT was detected. We believe that RT somewhat protected MeHg from damage to neural muscle structures, to be further investigated.