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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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[Metabolic syndrome].

Miwa Ryo, Yoshiko Furiya, Satoshi Ueno

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    Reducing visceral fat may lower dementia risk. Targeting insulin resistance through hypertension treatments like renin-angiotensin system blockers may slow cognitive decline in Alzheimer

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    Area of Science:

    • Neuroscience
    • Metabolic Syndrome
    • Gerontology

    Background:

    • Non-genetic risk factors for dementia, including midlife obesity, are a significant public health concern.
    • Visceral obesity, linked to hyperglycemia, hypertension, and hypercholesterolemia, is increasingly recognized as a critical factor.
    • Insulin resistance, associated with visceral fat, is a potential risk for Alzheimer's disease (AD) and vascular dementia.

    Purpose of the Study:

    • To explore the link between visceral fat accumulation, insulin resistance, and the risk of dementia.
    • To investigate the potential of reducing visceral fat for dementia risk reduction.
    • To examine the role of hypertension treatments in modulating cognitive decline and insulin resistance in AD patients.

    Main Methods:

    • Review of existing literature on obesity, metabolic factors, and dementia.
    • Analysis of the relationship between visceral fat, insulin resistance, and neurodegenerative diseases.
    • Examination of pharmacological interventions for hypertension and their impact on cognitive function.

    Main Results:

    • Accumulating evidence suggests a strong association between insulin resistance, driven by visceral fat, and increased risk of AD and vascular dementia.
    • Reducing visceral fat may be a viable strategy to mitigate the onset and progression of dementia.
    • Renin-angiotensin system blockers used for hypertension may slow cognitive decline in AD patients by improving insulin resistance.

    Conclusions:

    • Visceral obesity and associated insulin resistance are key modifiable risk factors for dementia.
    • Interventions targeting visceral fat reduction and insulin sensitivity are crucial for dementia prevention.
    • Pharmacological management of hypertension, specifically with renin-angiotensin system blockers, shows promise in preserving cognitive function in AD.