<b>Aim:</b> The aim of this study was to investigate the effect and underlying signaling mechanisms of metformin on apoptosis and Cx43 expression in H9c2 cells presenting with hyperglycemia conditions.
<b>Background:</b> Increase in circulating dipeptidyl peptidase-4 (DPP4) activity and levels has been reported to associate both with hyperglycemia and obesity.
<b>Conclusion:</b> The results of our study show the hypoglycemic impact of black truffle on STZ-induced hyperglycemia in rats via Nrf2 and NF-κB pathways, and both pathways have significant improvement that may support the hypoglycemic impact of truffle.
<b>Conclusion:</b> The results of our study show the hypoglycemic impact of black truffle on STZ-induced hyperglycemia in rats via Nrf2 and NF-κB pathways, and both pathways have significant improvement that may support the hypoglycemic impact of truffle.
<b>Objective:</b> It was demonstrated that inflammation and oxidative stress induced by hyperglycemia were closely associated with alteration of miR-146a.
<b>Results:</b> Conditions of hyperglycaemia are characterized by a low affinity of hemoglobin to oxygen, which is manifested as a parallel decrease in the content of hemoglobin oxyform and the growth of deoxyform, methemoglobin and membrane-bound hemoglobin.
<b>Results:</b> MDA, IL-1β and TNF-α levels were significantly increased in blood samples of DC group rats with hyperglycemia induced by alloxan compared with NC group (<i>p</i> < 0.0001), and decreased in the TAX group compared with the DC group (<i>p</i> < 0.0001).
<i>In vitro</i> experiments in rat macrophages showed that hyperglycemia treatment suppresses Nrf2 activation, resulting in oxidative stress with decreased expression of antioxidant genes, including NAD(P)H:quinone oxidoreductase 1 and heme oxygenase 1, together with increased secretion of proinflammatory cytokines, including interleukin 1β (IL1β), IL6, and monocyte chemoattractant protein-1.
<i>In vitro</i> experiments in rat macrophages showed that hyperglycemia treatment suppresses Nrf2 activation, resulting in oxidative stress with decreased expression of antioxidant genes, including NAD(P)H:quinone oxidoreductase 1 and heme oxygenase 1, together with increased secretion of proinflammatory cytokines, including interleukin 1β (IL1β), IL6, and monocyte chemoattractant protein-1.
<i>In vitro</i> experiments in rat macrophages showed that hyperglycemia treatment suppresses Nrf2 activation, resulting in oxidative stress with decreased expression of antioxidant genes, including NAD(P)H:quinone oxidoreductase 1 and heme oxygenase 1, together with increased secretion of proinflammatory cytokines, including interleukin 1β (IL1β), IL6, and monocyte chemoattractant protein-1.
<i>In vitro</i> experiments in rat macrophages showed that hyperglycemia treatment suppresses Nrf2 activation, resulting in oxidative stress with decreased expression of antioxidant genes, including NAD(P)H:quinone oxidoreductase 1 and heme oxygenase 1, together with increased secretion of proinflammatory cytokines, including interleukin 1β (IL1β), IL6, and monocyte chemoattractant protein-1.
<i>In vitro</i> experiments in rat macrophages showed that hyperglycemia treatment suppresses Nrf2 activation, resulting in oxidative stress with decreased expression of antioxidant genes, including NAD(P)H:quinone oxidoreductase 1 and heme oxygenase 1, together with increased secretion of proinflammatory cytokines, including interleukin 1β (IL1β), IL6, and monocyte chemoattractant protein-1.
<i>In vitro</i> experiments in rat macrophages showed that hyperglycemia treatment suppresses Nrf2 activation, resulting in oxidative stress with decreased expression of antioxidant genes, including NAD(P)H:quinone oxidoreductase 1 and heme oxygenase 1, together with increased secretion of proinflammatory cytokines, including interleukin 1β (IL1β), IL6, and monocyte chemoattractant protein-1.
<i>Ishige okamurae</i> Extract Ameliorates the Hyperglycemia and Body Weight Gain of <i>db/db</i> Mice through Regulation of the PI3K/Akt Pathway and Thermogenic Factors by FGF21.
<i>Ishige okamurae</i> Extract Ameliorates the Hyperglycemia and Body Weight Gain of <i>db/db</i> Mice through Regulation of the PI3K/Akt Pathway and Thermogenic Factors by FGF21.
<i>Ishige okamurae</i> Extract Ameliorates the Hyperglycemia and Body Weight Gain of <i>db/db</i> Mice through Regulation of the PI3K/Akt Pathway and Thermogenic Factors by FGF21.
<i>Ishige okamurae</i> Extract Ameliorates the Hyperglycemia and Body Weight Gain of <i>db/db</i> Mice through Regulation of the PI3K/Akt Pathway and Thermogenic Factors by FGF21.
<i>S</i>-Equol Activates cAMP Signaling at the Plasma Membrane of INS-1 Pancreatic β-Cells and Protects against Streptozotocin-Induced Hyperglycemia by Increasing β-Cell Function in Male Mice.
(b) Differences in modulation of the insulin receptor signaling cascade are found with TNF-alpha and high glucose: Hyperglycemia-induced insulin receptor inhibition blocks both insulin receptor-dependent tyrosine phosphorylation and dephosphorylation of insulin receptor substrate proteins.
- In this post-hoc, exploratory analysis, serum copeptin, glomerular filtration rate (GFR<sub>Inulin</sub>), effective renal plasma flow (ERPF<sub>PAH</sub>), plasma renin angiotensin aldosterone system markers, HbA1c, 24-hour urine volume and sodium excretion were measured in 40 participants with T1D (24.3 ± 5.1 years) during eu- and hyperglycaemia before and after 8 weeks of 25 mg of daily empagliflozin.
138 preterm babies ≤30 weeks' gestation or ≤1500 g at birth who develop hyperglycaemia (two consecutive blood glucose concentrations ≥10 mmol/L, at least 4 hours apart) will be randomised to one of three groups: (1) CDD using the STAR-GRYPHON model-based decision support system: insulin dose and frequency of blood glucose testing advised by STAR-GRYPHON, with a maximum testing interval of 4 hours; (2) bedside titration: insulin dose determined by medical staff, maximum blood glucose testing interval of 4 hours; (3) standard care: insulin dose and frequency of blood glucose testing determined by medical staff.