The role of melatonin in the onset and progression of type 3 diabetes.

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Term Occurence Count Dictionary
hyperglycemia 17 endocrinologydiseases
obesity 1 endocrinologydiseases
Insulin 6 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 4046 perspectives.The risk factors for diabetes contribute to the onset and progression of Alzheimer’s disease Insulin resistance leads to cognitive declineDiabetes is characterized by insulin resistance, diminished pancreatic
Insulin 5042 In the CNS, insulin signaling plays central roles in the cognitive dysfunction found in AD [[58]]. Insulin is known to be neuroprotective and has powerful effects on memory [[59]]. Previous studies have shown
Insulin 5996 hyperphosphorylation, and damage to neuronal cells contributes to impaired insulin signaling [[68], [69]]. Insulin receptors deficiency in the AD brain results in insulin resistance in AD neuropathology [[18], [70]].
Insulin 6354 mediated by impaired tau gene expression owing to the attenuation in insulin signaling [[72], [73]]. Insulin resistance in the AD brain reduces the phosphorylation of phosphoinositol-3-kinase (PI3K), and Akt [[72],
Insulin 8058 hyperphosphorylation and Aβ deposition in AD, and ultimately contribute to cognitive decline [[69]] (Fig. 1).Fig. 1 Insulin resistance triggers cognitive decline. Insulin resistance increases p-GSK3β phosphorylation, tau hyperphosphorylation,
Insulin 8105 contribute to cognitive decline [[69]] (Fig. 1).Fig. 1Insulin resistance triggers cognitive decline. Insulin resistance increases p-GSK3β phosphorylation, tau hyperphosphorylation, Aβ aggregation and reduces
Select Disease Character Offset Disease Term Instance
hyperglycemia 2396 dementia and results from common risk factors associated with dementia, including insulin resistance and hyperglycemia [[19]]. Many patients with metabolic diseases, such as cardiovascular disease, diabetes, and obesity,
hyperglycemia 4417 occurs more frequently in the global population than T1DM and is accompanied by insulin resistance, hyperglycemia , cognitive decline, and impaired circadian rhythms [[46], [47]]. T2DM is known to be associated with
hyperglycemia 8367 deficitsHyperglycemia triggers BBB disruption leading to cognitive dysfunctionAccording to previous studies, hyperglycemia in T2DM leads to cognitive dysfunction [[89]–[91]]. An abnormal glycemic condition is one of the main
hyperglycemia 8709 proteins which make up the BBB and the activation of matrix metalloproteinases (MMPs) was shown in hyperglycemia in vivo model [[94]] and in patients [[95], [96]]. The BBB is comprised of brain endothelial cells lining
hyperglycemia 9408 downregulation of BBB glucose transporters in hyperglycemic mice compared to wild-type mice [[100]]. In chronic hyperglycemia conditions, GLUT1 and GLUT3 expression was attenuated in diabetic animal brain and subsequently aberrant
hyperglycemia 10007 [[103], [104]] and downregulates glucose transporters in brain endothelial cells [[105]]. Moreover, hyperglycemia aggravates amyloid toxicity, independent of insulin resistance [[106]]. Numerous studies have demonstrated
hyperglycemia 10146 toxicity, independent of insulin resistance [[106]]. Numerous studies have demonstrated that diet-induced hyperglycemia triggers an increase in BBB permeability and BBB damage [[107]]. The expression of IgG as the marker
hyperglycemia 10344 IgG as the marker of BBB permeability was increased and tight junction proteins were attenuated in a hyperglycemia model [[107]]. In AD, BBB disruption promotes tau hyperphosphorylation [[108], [109]]. BBB disruption
hyperglycemia 10911 cells, and aggravates inflammation by recruiting leukocytes to the brain [[113]]. Given this evidence, hyperglycemia -induced BBB disruption might play an important role in the onset and progression of AD (Fig. 2).Fig.
hyperglycemia 14434 by Aβ toxicity and tau hyperphosphorylation.Melatonin protects cells against insulin resistance and hyperglycemia Diabetes is accompanied by dysregulation of the circadian system [[134]]. This is interesting given that
hyperglycemia 15599 [143]]. Type 3 diabetes is related to the prevalence of T2DM and results from insulin resistance and hyperglycemia [[144]–[146]]. Therefore, a method of reducing the cell damage induced by insulin resistance and hyperglycemia
hyperglycemia 15712 [[144]–[146]]. Therefore, a method of reducing the cell damage induced by insulin resistance and hyperglycemia is crucial in both diabetes and AD. Melatonin activates the expression of the MT2 receptor, which can
hyperglycemia 18669 and Aβ accumulationFig. 4Melatonin improve cognitive decline by regulating insulin resistance and hyperglycemia . Melatonin controls insulin resistance and glucose metabolism. Melatonin increases the expression of
hyperglycemia 19028 reactivity. Finally, melatonin improves cognitive decline in AD brainMelatonin protects the BBB against hyperglycemia Several studies have shown that disruption of the BBB is strongly associated with cognitive dysfunction
hyperglycemia 21754 called “type 3 diabetes” owing to the common risk factors, which include insulin resistance and hyperglycemia . Here, we reviewed the effect of melatonin in type 3 diabetes from various angles. Melatonin influences
hyperglycemia 21987 by 1) suppressing Aβ toxicity and tau hyperphosphorylation, 2) controlling insulin resistance and hyperglycemia , and 3) preventing hyperglycemia-induced BBB disruption. Hence, we suggest that melatonin would be a
hyperglycemia 22020 and tau hyperphosphorylation, 2) controlling insulin resistance and hyperglycemia, and 3) preventing hyperglycemia -induced BBB disruption. Hence, we suggest that melatonin would be a key in attenuating the pathogenesis
obesity 2503 hyperglycemia [[19]]. Many patients with metabolic diseases, such as cardiovascular disease, diabetes, and obesity , are reported to have a progressive decline in cognitive function, leading to the development of AD

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