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Most prevalent diabetes complications includes the least clinically and mechanistically explored diabetic encephalopathy. Cognitive deficits could be exacerbated by metabolic syndrome, DM duration, and lack of glycemic control. Attention, memory and learning deficits are capital signs. KATP-channels have a neuroprotective role, and diabetes reduces its expression. CA3 hippocampus region is involved in diabetic cognitive imparement. Physical Exercise (PE) improves learning and memory, but its influence on protein expression hasn't been evaluated. PURPOSE: to evaluate aerobic PE effects on the expression of sulfonylurea receptors (SUR) subunits of the KATP-channels in CA3 hippocampal diabetic pyramidal cells. METHODS: 3 weeks male Wistar rats were randomly asigned to four groups, control with (EC) and without exercise (NEC), and diabetes with (ED) and without exercise (NED) groups (n=5, each). IP streptozotocin at 100 mg/Kg dosis was used to induce diabetes. DM was considered when glycaemia was ≥ 250 mg/dl in tail blood. EC and ED performed exercise in a treadmill 5 min at a 15 m/min pace, followed by 20 min at 20 m/min, along 13 consecutive days. NEC and NED were managed similarly, except not exercised. At the end of the program animals were eutanized and tissue samples were obtained from the hippocampus. Pyramidal cells were mechanically isolated from CA3, and Real Time Polymerase Chain Reaction (rtPCR) was used to SUR1, SUR2A, and SUR2B expression quantitation. RESULTS: Relative expression (mRNA SURx/β-actin genes) of SUR1, SUR2A, and SUR2B increased from 0.99±0.29 to 20.67±5.96 (p<0.001); 0.35±0.12 to 13.98±4.17 (p<0.001); 0.62±0.10 to 13.40±4.90 (p=0.003), respectively for ED compared to NED. CONCLUSIONS: It is the first demonstration that PE increases expression of KATP-channels SUR isoforms, from isolated CA3 pyramidal cells. It could correspond to molecular mechanisms for protection, maintenance, or improving cognitive functions in diabetes. [ABSTRACT FROM AUTHOR]

The pathological state of Diabetes Mellitus (DM) promotes the activation of proteolysis pathways that results in the overexpression of atrogin-1 and MurF-1, regulatory genes of the Ubiquitin-Proteasome pathway, linked to the degradation of cellular proteins in skeletal muscle. Exercise is a therapeutic tool to maintain muscle mass, however, the effects of Moderate-Intensity Training (MIT) on muscle atrophy in DM have not been fully described. PURPOSE: To assess the effect of MIT on the expression of atrogin-1 and MurF-1 in gastrocnemius muscle of diabetic male rats. METHODS: Male Wistar rats (25 days old) were randomly divided into four groups, among them: sedentary control (SC), sedentary diabetic (SD), trained diabetic (TD). Diabetes was induced by a single streptozotocin injection (100 mg/kg body weight), animals with fasting blood glucose levels ≥ 300 mg/dL were considered as diabetic. Groups with training program performed moderate-intensity training on a treadmill (30 minutes daily, 5 days/week) for 8 weeks. At the end of the intervention, atrogin-1 and MurF-1 were analyzed as proteolysis indicators and quantitative analysis of these genes was evaluated with real-time quantitative PCR. RESULTS: In the SD group, the expression of atrogin-1 was 13 times higher (8.947 ± 1.008 Arbitrary Units) than in SC (0.6885 ± 0.1209 AU). To TD, the effect of MIT decreased 0.5 times the atrogin-1 expression (0.335 ± 0.0347 AU) respect to SD. Similarly, the MurF-1 expression in SD was 4 times higher (3.922 ± 0.8161 AU) compared to SC group (1.019 ± 0.1162 AU), which was reduced with exercise 0.5 times versus SD. CONCLUSIONS: Our data demonstrate that in diabetes condition, the expression of atrogin-1 and MurF-1 increase, this determines the muscle atrophy. Interestingly, after 8 weeks of moderate-intensity training the expression of atrogin and murf-1 decreased, contributing to the maintenance of muscle mass of gastrocnemius muscle in diabetic male rats. [ABSTRACT FROM AUTHOR]

Diabetes mellitus (DM) is one of the most prevalent and rapidly increasing non-communicable chronic diseases around the world. It has been related to left ventricular disfunction, as well to its electric remodeling. Cellular and molecular underlying mechanisms remains unveiled, at least in part. Phenotypic consequences includes QT Interval prolongation, ventricular arrhytmia, and cardiac sudden death. KATP-channels are considered as couplers of metabolism to membrane electric behavior in ventricular cells. At early DM stages, reduction in KATP-channels expression has been claimed as one of the main cardiac dysfunction underlying mechanisms. Physical exercise (PE) is postulated as a preventive and therapeutic intervention for diabetic cardiomyopathy. PURPOSE: to explore aerobic PE effects on expression of KATP-channel sulphonylurea receptors (SURs) in diabetic cardiomyocites. METHODS: 3 weeks male Wistar rats were randomly asigned to four groups, control with (EC) and without exercise (NEC); diabetes with (ED) and without exercise (NED) groups (n=5, each). IP streptozotocin at 100 mg/Kg dosis was used to induce DM. DM was considered when glycaemia was ≥ 250 mg/dl in tail blood. EC and ED performed exercise in a treadmill 5 min at a 15 m/min pace, followed by 20 min at 20 m/min, along 13 consecutive days. NEC and NED spent similar periods of time in a nonfuctioning treadmill. At the end of the program animals were eutanized and tissue samples were obtained from the ventricular apex. Subsecuently, Real Time Polymerase Chain Reaction (rtPCR) was used to SURs expression quantitation. RESULTS: significant differences were found for weight and glycaemia between NEC and EC when compared to NED as well as to ED (p=0.05). Relative expression (mRNA SURx/β-actin genes) was higher in ED: for SUR1, ED vs. NED were 10.54±3.53 vs 1.32±0.38 (p=0.007), as well when compared to NEC (1.29±0.47, p=0.01). Similarly, SUR2A expression was higher in ED than in NED; 10.68±2.54/1.22±0.45 (p=0.002), and than in NEC (1.18±0.33, p=0.06). No differences were found in the expression of SUR2B. CONCLUSIONS: Aerobic PE increases SUR1 and SUR2A isoforms of the KATP-channels sulfonylurea receptors. This phenomenon could be related to cardioprotective effects of aerobic physical exercise in Diabetes Mellitus. [ABSTRACT FROM AUTHOR]