Time-response studies on development of cognitive deficits in an experimental model of insulin resistance

Sachdeva, Anand Kamal; Dharavath, Ravinder Naik; Chopra, Kanwaljit

doi:10.1016/j.clnu.2018.06.966

Cited by 17 publications

(9 citation statements)

References 49 publications

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“…The same metabolic pattern has been observed during fasting or glucoprivation [2,164]. There is evidence that, over time, insulin resistance may extend to the brain, leading to brain insulin resistance [210,145,190]. We suggest that migraine chronification could originate, at least partly, from a chronic mismatch between the brain's energy reserve and expenditure caused, at least in part, by a dysfunction of insulinoid signalling in neurons and astrocytes, due to insulin resistance, in particular in the nervous tissue, i.e., brain insulin resistance.…”

Section: The "Neuroenergetic" Hypothesismentioning

confidence: 56%

“…Current literature reports that the human brain is an insulin sensitive organ and, as such, may become insulin resistant [89,210]. Indeed, some researchers suggests that peripheral insulin resistance can extend to the brain, triggering brain insulin resistance [210,145,190].…”

Section: Glucose-insulin Metabolism and The Brainmentioning

confidence: 99%

“…A time response study on the development of cognitive deficits in an experimental model on peripheral insulin resistance, induced by a high fructose diet for 7 weeks, led to lasting symptoms of cognitive dysfunction, as from week 20 [190].…”

Section: The "Neuroenergetic" Hypothesismentioning

confidence: 99%

See 2 more Smart Citations

Migraine, Brain Glucose Metabolism and the “Neuroenergetic” Hypothesis: A Scoping Review

Moro¹,

Rota

Pirovano³

et al. 2022

The Journal of Pain

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Section: The "Neuroenergetic" Hypothesismentioning

confidence: 56%

Section: Glucose-insulin Metabolism and The Brainmentioning

confidence: 99%

See 1 more Smart Citation

Migraine, Brain Glucose Metabolism and the “Neuroenergetic” Hypothesis: A Scoping Review

Moro¹,

Rota

Pirovano³

et al. 2022

The Journal of Pain

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“…Insulin resistance is associated with depression and T2DM, possibly leading to DD [6,77]. The serum levels of IL-1β and homoeostatic model assessment-insulin resistance increase in patients with depression, and neuroinflammation and insulin resistance induced by metabolic imbalance can induce depressive disorder [78,79]. The activation of NLRP3 inflammasomes to produce IL-1β leads to the coexistence of depressive-like behavior and insulin resistance in CUMS mice [57].…”

Section: Role Of P2x7 Receptor and Nlrp3 Inflammasome In Ddmentioning

confidence: 99%

P2X7 receptor mediates NLRP3 inflammasome activation in depression and diabetes

Wang

Gao

et al. 2020

Cell Biosci

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The increasing prevalence of depression and diabetes mellitus has become a major public health problem worldwide. Studies have shown that people with diabetes are at a high risk of being diagnosed with depression, and diabetes complicates depression treatment by promoting the deterioration of glycemic control, reducing self-care ability and quality of life, and causing severe functional disability and early mortality. Moreover, health deterioration dramatically increases the financial cost of social and health care system. Thus, how to treat depression, diabetes, and diabetes complicated by depression has become one of the world's urgent concerns. The activation of nod-like receptor family pyrin domain containing 3 (NLRP3) is closely related to mental illness. This finding provides a new perspective for studying depression. NLRP3 plays an important role in the development of diabetes. In this review, we elaborate the definition and epidemiology of depression, diabetes, and diabetic depression and introduce the functional characteristics of an NLRP3 inflammasome and upstream P2X7 receptor. Moreover, related research on NLRP3 inflammasomes and P2X7 receptors is summarized and used as a reference for confirming that the excessive activation of P2X7-NLRP3 leads to the increased release of inflammatory cytokines, such as IL-1β, in depression and diabetes. We provide insights into the P2X7-NLRP3-IL-1β pathway as an important pathological mechanism and novel therapeutic target in diabetes and depression. Given that the P2X7-NLRP3-IL-1β pathway may play an important role in diabetes confounded by comorbid depression, the possibility of intervention with baicalin is proposed.

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“…Accruing evidence shows that insulin facilitates memory and cognition under normal conditions ( Watson et al, 2009 ; Tokarz et al, 2018 ) whereas chronic hyperinsulinemia impairs them ( Lee et al, 2016 ). For instance, fructose-induced insulin-resistant rat models show impaired spatial learning in the water-maze test ( Sachdeva et al, 2019 ). Moreover, intranasal insulin improves memory in humans ( Benedict et al, 2008 ; Krug et al, 2010 ).…”

Section: Insulin Resistance and Admentioning

confidence: 99%

Insulin Resistance Exacerbates Alzheimer Disease via Multiple Mechanisms

2021

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Alzheimer disease (AD) is a chronic neurodegenerative disease that accounts for 60–70% of dementia and is the sixth leading cause of death in the United States. The pathogenesis of this debilitating disorder is still not completely understood. New insights into the pathogenesis of AD are needed in order to develop novel pharmacologic approaches. In recent years, numerous studies have shown that insulin resistance plays a significant role in the development of AD. Over 80% of patients with AD have type II diabetes (T2DM) or abnormal serum glucose, suggesting that the pathogenic mechanisms of insulin resistance and AD likely overlap. Insulin resistance increases neuroinflammation, which promotes both amyloid β-protein deposition and aberrant tau phosphorylation. By increasing production of reactive oxygen species, insulin resistance triggers amyloid β-protein accumulation. Oxidative stress associated with insulin resistance also dysregulates glycogen synthase kinase 3-β (GSK-3β), which leads to increased tau phosphorylation. Both insulin and amyloid β-protein are metabolized by insulin degrading enzyme (IDE). Defects in this enzyme are the basis for a strong association between T2DM and AD. This review highlights multiple pathogenic mechanisms induced by insulin resistance that are implicated in AD. Several pharmacologic approaches to AD associated with insulin resistance are presented.

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Time-response studies on development of cognitive deficits in an experimental model of insulin resistance

Cited by 17 publications

References 49 publications

Migraine, Brain Glucose Metabolism and the “Neuroenergetic” Hypothesis: A Scoping Review

Migraine, Brain Glucose Metabolism and the “Neuroenergetic” Hypothesis: A Scoping Review

P2X7 receptor mediates NLRP3 inflammasome activation in depression and diabetes

Insulin Resistance Exacerbates Alzheimer Disease via Multiple Mechanisms

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