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Published on: January 4, 2018
Insulin resistance and hippocampal dysfunction: Disentangling peripheral and brain causes from consequences
Claudia A Grillo1, Jennifer L Woodruff1, Victoria A Macht1
1University of South Carolina School of Medicine, Department of Pharmacology, Physiology, & Neuroscience, Columbia, SC, USA; WJB Dorn VA Medical Center, Columbia, SC 29209, USA.
Central nervous system (CNS) insulin resistance, common in type 2 diabetes and obesity, impairs neuroplasticity and cognitive function. Targeting brain insulin activity may reverse cognitive decline.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Endocrinology
Background:
- Insulin regulates metabolic homeostasis in the periphery and CNS neuroplasticity.
- Insulin resistance in both periphery and CNS is linked to type 2 diabetes (T2DM) and obesity.
- CNS insulin resistance causes neuroplasticity deficits, cognitive decline, and neuropsychiatric risks.
Purpose of the Study:
- Review neuroplasticity deficits in T2DM and obesity.
- Discuss causes and consequences of CNS insulin resistance.
- Focus on hippocampal neuroplasticity impacts.
Main Methods:
- Literature review of clinical and preclinical studies.
- Analysis of CNS insulin resistance mechanisms.
- Examination of hippocampal-specific insulin resistance effects.
Main Results:
- T2DM and obesity are associated with neuroplasticity deficits.
- CNS insulin resistance impacts cognitive function and increases neuropsychiatric disorder risk.
- Hippocampal insulin resistance can impair neuroplasticity independently of peripheral insulin resistance.
Conclusions:
- CNS insulin resistance contributes to cognitive decline in T2DM and obesity.
- Restoring brain insulin activity is a potential therapeutic strategy.
- Targeting brain insulin may ameliorate cognitive deficits in CNS insulin resistance conditions.
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