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Aims: We aimed to determine if severe hypoglycemia (SH) independently increases the risk of hospitalization for heart failure (hHF) in type 2 diabetes, regardless of the prevalent or incident cardiovascular disease (CVD).Methods: This was a nationwide population-based propensity score-matched study using Korean National Health Insurance Service data (2002-2018). The hazards of hHF were compared in individuals who experienced SH (n = 8,965) and 1:3 matched controls, among adults with diabetes using oral anti-diabetes medications (OADs) with or without insulin and without previous hHF at baseline.Results: During 236,417 person-years, 1,189 cases of hHF occurred. The hazard of hHF was higher in individuals with SH compared to matched controls (adjusted hazard ratio [aHR] 1.503, 95 % confidence interval [CI] 1.324-1.707). The increase in aHR remained significant when excluding participants with prevalent or incident major adverse cardiovascular events (MACE; aHR 1.352, 95 % CI 1.228-1.622) and any CVD (aHR 1.342, 95 % CI 1.025-1.756). Two or more SH events were associated with further increase in hHF risk.Conclusion: SH was associated with increased risks of hHF among adults with diabetes using OAD with or without insulin. The increased risk was attenuated but remained significant in those without prevalent or incident MACE or CVDs. [ABSTRACT FROM AUTHOR]

Damage to pancreatic β-cells plays an important role in the development of type 2 diabetes, and oxidative stress is a likely contributor. In the present study, we investigated the effect of deuterohemin-AlaHisLys (DhHP-3), a microperoxidase-11 mimic, on rats with non-insulin dependent diabetes mellitus and examined the action mechanisms of DhHP-3. The induced hyperglycemia, glucose intolerance, and insulin resistance in diabetic rats were associated with increased oxidative stress and damage to pancreatic islets. DhHP-3 (3 mg/kg) ameliorated hyperglycemia and insulin resistance, protected pancreas islet, decreased the content of malondialdehyde, and increased the activity of superoxide dismutase in plasma and pancreatic tissue by reducing ROS levels. Furthermore, DhHP-3 stimulated the proliferation of INS-1 cells and inhibited apoptosis by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3-K/AKT) signaling pathway. Our results demonstrated for the first time that DhHP-3 decreased blood glucose level in rats with non-insulin dependent diabetes mellitus, scavenged reactive oxygen species, activated the PI3-K/AKT signaling pathway, and protected pancreatic β-cells against apoptosis. [ABSTRACT FROM AUTHOR]

Aim. – Analyze the effects of exercise training on cardiac sarco endoplasmic reticulum calcium ATPase (SERCA) 2 gene expression of genetically obese Zucker rats, an animal model of non-insulin dependent diabetes mellitus (NIDDM).Methods. – Twenty male and 20 female Zucker fatty rats ran 30–50 min/d at 35–40% VO2max, 6 d/week for 13 weeks. Semi-quantitative RT-PCR associated with specific restriction fragment analysis was used to detect and quantify the relative expression of SERCA mRNA isoforms.Results. – Fatty rats had an enhanced expression of SERCA2 and phospholamban (PLB) mRNA levels in ventricles. Moreover, fatty rats exposed to a moderate treadmill running exercise for 13 weeks exhibited a significant increase in ventricles SERCA2 mRNA levels, whereas, no change occurred in control lean rats. Exercise training produced a significant induction of α-myosin heavy chain mRNA levels only in fatty rats.Conclusion. – We hypothesize that exercise training may improve the cardiac function in diabetic rats by increasing the mRNA expression of SERCA2 since it is known that NIDDM rats have a reduced left ventricular diastolic compliance, and that exercise training improves the ventricular function in diabetic rats. [Copyright &y& Elsevier]