Thyroid hormone improves insulin signaling and reduces the activation of neurodegenerative pathway in the hippocampus of diabetic adult male rats

Prieto-Almeida, Fernanda; Panveloski-Costa, Ana Carolina; Crunfli, Fernanda; Teixeira, Silvania da Silva; Nunes, Maria Tereza; Torrão, Andréa da Silva

doi:10.1016/j.lfs.2017.11.013

Cited by 16 publications

(8 citation statements)

References 43 publications

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Section: Insulinmentioning

confidence: 96%

“…There is literature which reports alteration in insulin level for reducing cognitive impairment. Triiodothyronine treatment reduced neurodegeneration by restoring insulin signaling in diabetic rats (Prieto‐Almeida et al, ). Intranasal insulin treatment in rats activated insulin signaling which reduced cognitive dysfunction induced by methamphetamine (Beirami, Oryan, Seyedhosseini Tamijani, Ahmadiani, & Dargahi, ).…”

Section: Factors Involved In Regulationmentioning

confidence: 99%

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Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Jash

Gondaliya

Kirave

et al. 2019

Drug Development Research

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Diabetes mellitus (DM) is a gradually rising metabolic disease which is currently affecting millions of people worldwide. Diabetes is associated with various complications like nephropathy, neuropathy, retinopathy, diabetic foot, cognitive impairment, and many more. Evidence suggests that cognitive dysfunction is a rising complication of diabetes which adversely affects the brain of patients suffering from diabetes. Age‐related memory impairment is a complication having its major effect on people suffering from diabetes and Alzheimer's. Patients suffering from diabetes are at two times higher risk of developing cognitive dysfunction as compared with normal individuals. Multiple factors which are involved in diabetes related complications are found to play a role in the development of neurodegeneration in Alzheimer's. The problem of insulin deficiency and insulin resistance is well reported in diabetes but there are many studies which suggest dysregulation of insulin levels as a reason behind the development of Alzheimer's. As the link between diabetes and Alzheimer disease (AD) is deepening, there is a need to understand the plausible tie‐ins between the two. Emerging role of major factors like insulin imbalance, advanced glycation end products and micro‐RNA's involved in diabetes and Alzheimer's have been discussed here. This review helps in understanding the plausible mechanism underlying the pathophysiology of amyloid beta (Aβ) plaque formation and tau hyperphosphorylation as well provides information about studies carried out in this area of research. The final thought is to enhance the scientific knowledge on this correlation and develop future therapeutics to treat the same.

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Section: Insulinmentioning

confidence: 96%

Section: Factors Involved In Regulationmentioning

confidence: 99%

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Jash

Gondaliya

Kirave

et al. 2019

Drug Development Research

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“…T 3 negatively regulates the amyloid-β precursor protein (APP) gene (Belandia et al, 1998;Belakavadi et al, 2011), and rendering rats hyperthyroid by giving oral T 3 for 5 days strongly suppressed overall brain APP expression (Belakavadi et al, 2011). However, the sole study that tested this trait in a rat model for AD by giving supraphysiological doses of T 3 for 4 weeks showed no significant changes in brain amyloid β content by western blotting (Prieto-Almeida et al, 2018) (Figure 2). T 3 did reduce Tau hyper-phosphorylation and glycogen synthase kinase 3 α/β (GSK-3β) expression (Prieto-Almeida et al, 2018).…”

Section: Thyroid Hormone As a Repair Cue In Alzheimer's Diseasementioning

confidence: 99%

“…However, the sole study that tested this trait in a rat model for AD by giving supraphysiological doses of T 3 for 4 weeks showed no significant changes in brain amyloid β content by western blotting (Prieto-Almeida et al, 2018) (Figure 2). T 3 did reduce Tau hyper-phosphorylation and glycogen synthase kinase 3 α/β (GSK-3β) expression (Prieto-Almeida et al, 2018). Hyperactivity of each of these factors underlies AD pathogenesis and associates with amyloid β deposition, plaque forming and memory impairment (Hooper et al, 2008).…”

Section: Thyroid Hormone As a Repair Cue In Alzheimer's Diseasementioning

confidence: 99%

Thyroid Hormone and Neural Stem Cells: Repair Potential Following Brain and Spinal Cord Injury

Vancamp¹,

Butruille²,

Demeneix³

et al. 2020

Front. Neurosci.

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Neurodegenerative diseases are characterized by chronic neuronal and/or glial cell loss, while traumatic injury is often accompanied by the acute loss of both. Multipotent neural stem cells (NSCs) in the adult mammalian brain spontaneously proliferate, forming neuronal and glial progenitors that migrate toward lesion sites upon injury. However, they fail to replace neurons and glial cells due to molecular inhibition and the lack of pro-regenerative cues. A major challenge in regenerative biology therefore is to unveil signaling pathways that could override molecular brakes and boost endogenous repair. In physiological conditions, thyroid hormone (TH) acts on NSC commitment in the subventricular zone, and the subgranular zone, the two largest NSC niches in mammals, including humans. Here, we discuss whether TH could have beneficial actions in various pathological contexts too, by evaluating recent data obtained in mammalian models of multiple sclerosis (MS; loss of oligodendroglial cells), Alzheimer's disease (loss of neuronal cells), stroke and spinal cord injury (neuroglial cell loss). So far, TH has shown promising effects as a stimulator of remyelination in MS models, while its role in NSC-mediated repair in other diseases remains elusive. Disentangling the spatiotemporal aspects of the injury-driven repair response as well as the molecular and cellular mechanisms by which TH acts, could unveil new ways to further exploit its proregenerative potential, while TH (ant)agonists with cell type-specific action could provide safer and more target-directed approaches that translate easier to clinical settings.

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“…Although both hyperthyroidism and hypothyroidism have been related to disturbances in insulin signaling and glucose metabolism (Teixeira et al 2012), exogenous thyroid hormone administration in IR and glucose intolerance conditions have recently attracted considerable attention with favorable outcomes. Accumulating recent reports have shown that exogenous triiodothyronine (T 3 ) administration can decrease glycemia and improve insulin signaling in diabetic (Prieto-Almeida et al 2018) and obese rats (Panveloski-Costa et al 2018). It has been also demonstrated that T 3 is able to enhance insulin-stimulated glucose transport and glycolysis in skeletal muscles (Moreno et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Triiodothyronine improves age-induced glucose intolerance and increases the expression of sirtuin-1 and glucose transporter-4 in skeletal muscle of aged rats

Agaty

2018

gpb

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To evaluate the potential beneficial impact and to clarify the underlying mechanisms of triiodothyronine (T 3) on glucose intolerance in aged rats. Rats were divided into adult group, aged group, and T 3-treated aged group (T 3-aged). T 3 was administered at a dose of 8 µg/kg body weight for 2 weeks. In comparison to adult group, aged rats presented significant higher levels of fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR). Glucose area under the curve (AUC), and peak glycemia, estimated from oral glucose tolerance curve, were significantly increased along with decreased mRNA expression of skeletal muscle sirtuin-1, glucose transporter-4 (GLUT-4) and uncoupling protein-3 (UCP-3) in aged versus adult group. T 3 administration significantly decreased the serum levels of fasting insulin, HOMA-IR, glucose AUC, and peak glycemia in T 3-aged versus aged rats. Skeletal muscle mRNA expression of sirtuin-1 and GLUT-4 were increased, whereas UCP-3 was not changed by T 3 administration. T 3 administration improved glucose intolerance, and decreased insulin resistance in aged rats. This was associated with upregulation of skeletal muscle sirtuin-1 and GLUT-4 which could mediate such beneficial effect.

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Thyroid hormone improves insulin signaling and reduces the activation of neurodegenerative pathway in the hippocampus of diabetic adult male rats

Cited by 16 publications

References 43 publications

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Thyroid Hormone and Neural Stem Cells: Repair Potential Following Brain and Spinal Cord Injury

Triiodothyronine improves age-induced glucose intolerance and increases the expression of sirtuin-1 and glucose transporter-4 in skeletal muscle of aged rats

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