Статья

Impaired insulin signaling and Insulin resistance in neurodegeneration

Tаlаt SааtоvInstitute of Biophysics and Biochemistry at the National University of Uzbekistan named after M.Ulugbek, Tashkent, Toshkent, UzbekistanGulnora ArtikbaevaInstitute of Biophysics and Biochemistry at the National University of Uzbekistan named after M.Ulugbek, Tashkent, Toshkent, UzbekistanTokhir IshankhodjaevInstitute of Biophysics and Biochemistry at the National University of Uzbekistan named after M.Ulugbek, Tashkent, Toshkent, UzbekistanElvira IbragimovaInstitute of Biophysics and Biochemistry at the National University of Uzbekistan named after M.Ulugbek, Tashkent, Toshkent, UzbekistanZafar IbragimovInstitute of Biophysics and Biochemistry at the National University of Uzbekistan named after M.Ulugbek, Tashkent, Toshkent, UzbekistanMukhammadjon MustafakulovInstitute of Biophysics and Biochemistry at the National University of Uzbekistan named after M.Ulugbek, Tashkent, Toshkent, UzbekistanSunnatilla AbdurakhimovInstitute of Biophysics and Biochemistry at the National University of Uzbekistan named after M.Ulugbek, Tashkent, Toshkent, UzbekistanZulaykho ShamansurovaCentral Asian University School of Medicine, Tashkent, Toshkent, Uzbekistan

Physiologyjournal2026en

ABI

Аннотация

Introduction: Impaired secretion of insulin and its signaling are common mechanisms for Alzheimer’s disease (AD) and type 2 Diabetes Mellitus (DM2). The aim of this study were investigation of relationship between impaired insulin signaling and the level of markers of neurodegeneration in the blood and various brain areas in experimental animals with sporadic neurodegeneration model (SND). Material and methods: The experimental model of SND were created in 30 albino rats. Rats were treated by high-calorie atherogenic diet following by intranasal administration of neurotoxin streptozotocin (STZ) in dosage of 3 mg/kg body weight coated by liposome for better crossing blood-brain barrier. Feeding animals with high-calorie atherogenic diet leads to increasing of carbohydrate and lipid metabolism, insulin resistance index HOMA-IR and CARO and changes in behavioral activity of animals. Results: Determination in the blood parameters of neurodegeneration showed increasing content of S100B protein as a marker of brain tissue ischemic state before and after injection of STZ. When experimental model of SND reproducing significant changes in content of β amyloid protein and tau protein were shown, with the latter increasing in 3-fold after STZ administration. Despite the absence of significant changes in insulin receptor expression, glycogen synthase kinase-3β expression was increased in the hippocampus, striatum, and olfactory bulb. These changes have correlation with increased level of beta-amyloid protein Aβ in the brain areas after both high-calorie diet and STZ administration. Conclusion: Thus, impaired insulin signaling leads to increasing of neurodegeneration markers in various brain areas and content in the blood of animals with both metabolic syndrome and SND. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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Темы

Alzheimer's disease research and treatments Advanced Glycation End Products research Neurological Disorders and Treatments

Идентификаторы

DOI: 10.1152/physiol.2026.41.s1.2299972

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