There were no CAC differences between lifestyle and placebo intervention groups in either sex. At the time of cognitive assessment, type 2 diabetes was higher in the placebo group (57.9% P 0) and reported separately in men and women.
A total of 2,280 participants (749 lifestyle, 776 metformin, and 755 placebo) aged 63.1 ± 10.7 years underwent cognitive assessments 67.7% women, 54.6% non-Hispanic white, 20.7% non-Hispanic black, 14.6% Hispanic, 5.5% American Indian, and 4.6% Asian 26.6% were homozygous or heterozygous for APOE-Î♔. Cognition was assessed in DPPOS years 8 and 10 (12 and 14 years after randomization) with the Spanish English Verbal Learning Test (SEVLT), letter fluency and animal fluency tests, Digit Symbol Substitution Test (DSST), and a composite cognitive score. The DPP lasted 2.8 years, followed by a 13-month bridge to DPPOS. We also examined metformin use, incident type 2 diabetes, and glycemia as exposures. We examined the association of the Diabetes Prevention Program (DPP) intervention arms (lifestyle intervention, metformin, and placebo) with cognition in the Diabetes Prevention Program Outcomes Study (DPPOS). Luchsinger, José A Ma, Yong Christophi, Costas A Florez, Hermes Golden, Sherita H Hazuda, Helen Crandall, Jill Venditti, Elizabeth Watson, Karol Jeffries, Susan Manly, Jennifer J Pi-Sunyer, F Xavier Metformin, Lifestyle Intervention, and Cognition in the Diabetes Prevention Program Outcomes Study. granulosus larval stage and its combination with ABZ may improve the current anti-parasitic therapy. In conclusion, based on our experimental data, Met emerges as a promising anti-echinococcal drug as it has proven to efficiently inhibit the development and growth of the E. Furthermore, the safe plant-derived drug Met exhibited remarkable chemopreventive properties against secondary hydatidosis in mice. Coincidentally, intracystic Met accumulation was higher in animals treated with both drugs compared to those administered Met alone.
granulosus-infected mice was highly effective in reducing the weight and number of parasite cysts, yet its combination with the lowest recommended dose of ABZ (5 mg/kg/day) was even more effective. Oral administration of Met (50 mg/kg/day) in E. Notably, the combination of Met together with the minimum effective concentration of ABZSO had a synergistic effect after days 3 and 12 on metacestodes and protoscoleces, respectively. Metformin showed significant dose- and time-dependent killing effects on in vitro cultured protoscoleces and metacestodes. In this study we investigated the in vitro and in vivo efficacy of Met against the larval stage of Echinococcus granulosus. Metformin (Met) is an anti-hyperglycemic and potential anti-cancer agent which may exert its anti-proliferative effects via the induction of energetic stress. Metformin exhibits preventive and therapeutic efficacy against experimental cystic echinococcosis Taken together, metformin likely prevents MG-induced apoptotic signals in mouse Schwann cells by inhibiting the formation of AGEs and ROS.« less No significant activation of AMPK by MG or metformin was observed. All of these changes were significantly inhibited by metformin.
MG treatment resulted in blunted cell proliferation, an increase in the number of apoptotic cells, and the activationmore » of caspase-3 and JNK along with enhanced intracellular ROS formation. Intracellular ROS formation was determined by flow cytometry, and AMP-activated kinase (AMPK) phosphorylation was also examined. Cell apoptosis was evaluated using Hoechst 33342 nuclear staining, caspase-3 activity, and c-Jun-N-terminal kinase (JNK) phosphorylation. To clarify whether the antidiabetic drug metformin prevents Schwann cell damage induced by MG, we cultured mouse Schwann cells in the presence of MG and metformin. Methylglyoxal (MG) is involved in the pathogenesis of diabetic complications via the formation of advanced glycation end products (AGEs) and reactive oxygen species (ROS). Metformin prevents methylglyoxal-induced apoptosis of mouse Schwann cells
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