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    Excess Fructose Intake Activates Hyperinsulinemia and Mitogenic MAPK Pathways in Association With Cellular Stress, Inflammation, and Apoptosis in the Pancreas of Rats
    (Wiley, 2025) Guney, Ceren; Alcigir, Mehmet Eray; Akar, Fatma
    The increase in sugar consumption has been associated with current metabolic disease epidemics. This study aimed to investigate the pancreatic molecular mechanisms involved in cellular stress, inflammation, mitogenesis, and apoptosis in metabolic disease induced by high-fructose diet. Here, we used biochemical, histopathological, Western blot, and immunohistochemistry methods to determine the metabolic and pancreatic alterations in male Wistar rats fed 20% fructose in drinking water for 15 weeks. High-fructose consumption in rats increased the immunopositivity and protein expression of glucose transporter 2 (GLUT2) and insulin in the pancreatic tissue, in association with abdominal adiposity, hyperglycemia, and hypertriglyceridemia. The expressions of cellular stress markers, glucose-regulated protein-78 (GRP78) and PTEN-induced putative kinase 1 (PINK1), were increased in the pancreas. The levels of interleukin (IL)-6, nuclear factor kappa B (NF kappa B), tumor necrosis factor alpha (TNF alpha), and IL-1 beta and components of the Nod-like receptor protein 3 (NLRP3) inflammasome were elevated. Excess fructose intake stimulated the activation of mitogenic extracellular signal-regulated kinases 1/2 (ERK1/2), p38, and c-Jun N-terminal kinase (JNK)1 as well as the apoptotic p53 and Fas pathways in the pancreas of rats. There was also an increase in caspase-8 and caspase-3 cleavage. Our findings revealed that dietary high-fructose in the pancreas causes hyperinsulinemia due to the upregulation of GLUT2 together with cellular stress and inflammatory markers, thereby stimulates mitogenic mitogen-activated protein kinase (MAPK) and apoptosis pathways, resulting in a complex pathological situation.
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    Myricetin May Improve Cardiac Dysfunction Possibly Through Regulating Blood Pressure and Cellular Stress Molecules in High-Fructose-Fed Rats
    (Kare Publ, 2024) Bal, Nur Banu; Guney, Ceren; Yildirim, Onur Gokhan; Akar, Fatma; Demirel-Yilmaz, Emine
    Background: The aim of this study was to examine the effect of myricetin on cardiac dys- function caused by high fructose intake. Methods: Fructose was given to the rats as a 20% solution in drinking water for 15 weeks. Myricetin was administered by oral gavage for the last 6 weeks. Systolic blood pressure was measured by tail -cuff method. The effects of isoprenaline, phenylephrine, and ace- tylcholine on cardiac contractility and rhythmicity were recorded in the isolated right atrium and left ventricular papillary muscles. In addition to biochemical measurements, the cardiac expressions of cellular stress -related proteins were determined by western blotting. Results: Myricetin improved systolic blood pressure but did not affect body weight, plasma glucose, and triglyceride levels in fructose -fed rats. The impairment of isoprenaline- and phenylephrine-mediated increases in atrial contraction and sinus rate in fructose -fed rats was restored by myricetin treatment. Isoprenaline, phenylephrine, and acetylcho- line -mediated papillary muscle contractions were not changed by fructose or myricetin administration. The expression of the mitochondrial fission marker dynamin-related protein 1 and the mitophagic marker PTEN-induced kinase 1 (PINK1) was enhanced in the fructose -fed rat, and myricetin treatment markedly attenuated PINK1 expression. Highfructose intake augmented phosphorylation of the proinflammatory molecule Nuclear factor kappa B (NF-kappa B) and the stress -regulated kinase JNK1, but myricetin only reduced NF-kappa B expression. Moreover, myricetin diminished the elevation in the expression of the pro-apoptotic Bax. Conclusion: Our results imply that myricetin has a protective role in cardiac irregulari- ties induced by a high -fructose diet through reducing systolic blood pressure, improving cardiac adrenergic responses, suppressing PINK1, NF-kappa B, and Bax expression, and thus reflecting a potential therapeutic value.