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Browsing by Subject "Metabolic dysfunction"

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    Editorial: Nutrients, stress response, and human health
    (Frontiers Media, 2025-02-27) Misra, Jagannath; Liobikas, Julius; Biochemistry and Molecular Biology, School of Medicine
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    The Role of Beta Cell Dysfunction in Early Type 1 Diabetes
    (Wolters Kluwer, 2020-08) Sims, Emily K.; Mirmira, Raghavendra G.; Evans-Molina, Carmella; Pediatrics, School of Medicine
    Purpose of review: Emerging data have suggested that β-cell dysfunction may exacerbate the development and progression of type 1 diabetes (T1D). In this review, we highlight clinical and preclinical studies suggesting a role for β-cell dysfunction during the evolution of T1D and suggest agents that may promote β-cell health in T1D. Recent findings: Metabolic abnormalities exist years before development of hyperglycemia and exhibit a reproducible pattern reflecting progressive deterioration of β-cell function and increases in β-cell stress and death. Preclinical studies indicate that T1D may be prevented by modification of pathways impacting intrinsic β-cell stress and antigen presentation. Recent findings suggest that differences in metabolic phenotypes and β-cell stress may reflect differing endotypes of T1D. Multiple pathways representing potential drug targets have been identified, but most remain to be tested in human populations with preclinical disease. Summary: This cumulative body of work shows clear evidence that β-cell stress, dysfunction, and death are harbingers of impending T1D and likely contribute to progression of disease and insulin deficiency. Treatment with agents targeting β-cell health could augment interventions with immunomodulatory therapies but will need to be tested in intervention studies with endpoints carefully designed to capture changes in β-cell function and health.
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    Zinc sulphate attenuates metabolic dysfunctions induced by olanzapine via the reduction of insulin resistance, hepatic oxidative stress, and inflammation in albino rats
    (Springer Nature, 2025-04-14) Bashandy, Samir A. E.; Mostafa, Rasha E.; El-Baset, Marawan A.; Ibrahim, Fatma A. A.; Morsy, Fatma A.; Farid, Omar A.; Ibrahim, Halima M.; Mohamed, Bassim M. S. A.; Neurology, School of Medicine
    Olanzapine, an atypical antipsychotic drug, is used to treat psychological diseases. However, it's use carries common side effects. Those include weight gain, dyslipidemia, elevated glucose levels, and disrupted oxidative balance. We aimed to test the effect of zinc coadministration to lessen metabolic disturbances, inflammation and oxidative stress in a rat model. Four treatment groups (n = 6) were involved in this investigation. Group 1 was the control group (received no intervention). Group 2 received olanzapine (10 mg/kg, p.o.; daily) for six weeks, whereas Groups 3 and 4 received 50 mg/kg and 100 mg/kg of zinc sulphate (ZnSO4,p.o.; daily) respectively, in addition to olanzapine (10 mg/kg p.o.; daily). Following treatment completion, group 2 showed increased levels of stress markers (GSSG, MDA, and NO) and impaired levels of antioxidant markers (CAT, SOD, and GSH). Further, a strong positive correlation between insulin resistance index (HOMA-IR) and IL-6, TNF-α, and MDA of liver. Insulin resistance is a possible manifestation of the oxidative stress burden and the widespread inflammatory environment. In groups 3 and 4, however, ZnSO4 recovered each of these markers in a dose-dependent manner. Improvements were also noted in other homeostatic markers, such as taurine, coenzyme Q10, ascorbic acid, and vitamin E. Remarkably, in both combination groups, there was a significant improvement in all metabolic indicators of dyslipidemia (triglycerides, total cholesterol) and insulin resistance index. The biochemical study and the histological assessment of the liver slices agreed with the results. Thus, the results clearly suggest that Zinc supplementation can significantly improve oxidative stress, inflammation, metabolic perturbation (dyslipidemia and insulin resistance), and liver injury caused by olanzapine in Albino rats.
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