Pin1 Modulation in Physiological Status and Neurodegeneration. Any Contribution to the Pathogenesis of Type 3 Diabetes?

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Term Occurence Count Dictionary
glucose intolerance 3 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 3 endocrinologydiseases
Insulin 4 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 33082 resistance registered in the AD brain, thereby affecting negatively the insulin transduction pathway. Insulin /IGF-1 signaling upon binding to receptors activates the auto phosphorylation of receptors at Tyr residues
Insulin 34029 mitochondrial dysfunction, thereby increasing mitochondrial-mediated apoptosis and oxidative stress [[82]]. Insulin and IGFs levels were reduced in brain tissues of AD patients and this was associated with the reduced
Insulin 35558 cognitive performance in parallel with the improvement of the glucose metabolism [[17]]. 5.2. Pin1 and Insulin Pathways Pin1 modulated peripheral glucose metabolism influencing independently both insulin secretion
Insulin 46751 3Pin1 in the metabolic pathway acts as a negative regulator of AMPK and modulates the Akt active form. Insulin promotes neuronal cytoskeletal dynamics via Akt phosphorylation. Activation of insulin signaling leads
Select Disease Character Offset Disease Term Instance
glucose intolerance 1562 and peripherally, Pin1 KO mice are resistant to diet-induced obesity, insulin resistance, peripheral glucose intolerance and diabetic vascular dysfunction. In this review, we revise first critically the role of Pin1 in neuronal
glucose intolerance 30754 muscle) and brain impairment of glucose metabolism and altered insulin signaling that resulted in overt glucose intolerance [[3]]. Autopsy studies in AD brains and intracerebral injected mice with streptozocin (STZ) demonstrated
glucose intolerance 35745 both insulin secretion and sensitivity. β-cell-specific Pin1 KO (βPin1 KO) mice [[84]] developed glucose intolerance owing to reduced insulin secretion but preserved peripheral insulin sensitivity. βPin1 KO mice presented
hyperglycemia 36721 primary human endothelial cells and peripheral blood monocytes (PBMCs) of T2D patients demonstrated that hyperglycemia caused Pin1 upregulation and the latter, in turn, mediated vascular-damage occurring in diabetic patients
hyperinsulinemia 34778 AD phenotype [[17]].Therefore, insulin resistance that manifests in patients with T2D as peripheral hyperinsulinemia and increased release of IGF1, defective binding to receptors, impaired insulin signaling in muscle,
metabolic syndrome 3396 substrates has been implied in the onset of various diseases, i.e., cancer, neurodegenerative disorders and metabolic syndrome s including type 2 diabetes (T2D) [[2],[3],[4],[10],[11],[12]].Expression of Pin1 increases significantly
obesity 1522 modulates glucose homeostasis in the brain and peripherally, Pin1 KO mice are resistant to diet-induced obesity , insulin resistance, peripheral glucose intolerance and diabetic vascular dysfunction. In this review,
obesity 38138 AMP/ADP to the γ subunit of AMPK. Therefore, Pin1 KO mice were resistant to high-fat-diet (HFD) induced obesity [[88],[89]], with the activity level of AMPK in muscle significantly higher than in WT mice [[88]].
obesity 38331 WT mice [[88]]. In that interaction with AMPK, Pin1 may represent a therapeutic target also to treat obesity and diabetes. Indirect evidence in diabetic db/db treated by GLP1-analog demonstrated that PIN1 modulates

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