Background/objectives: Alzheimer's disease (AD), a leading cause of dementia, lacks effective long-term treatments. Current therapies offer temporary relief or fail to halt its progression and are often inaccessible due to cost. AD involves multiple pathological processes, including amyloid beta (Aβ) deposition, insulin resistance, tau protein hyperphosphorylation, and systemic inflammation accelerated by gut microbiota dysbiosis originating from a leaky gut.
View Article and Find Full Text PDFAlzheimer's disease is a neurodegenerative disorder characterized by the amyloid accumulation in the brains of patients with Alzheimer's disease. The pathogenesis of Alzheimer's disease is mainly mediated by the phosphorylation and aggregation of tau protein. Among the multiple causes of tau hyperphosphorylation, brain insulin resistance has generated much attention, and inositols as insulin sensitizers, are currently considered candidates for drug development.
View Article and Find Full Text PDFThe present study characterizes the oral pharmacokinetics of D-Pinitol, a natural insulin mimetic inositol, in human healthy volunteers (14 males and 11 females). D-Pinitol absorption was studied in (a) subjects receiving a single oral dose of 15 mg/kg ( = 10), or (b) 5 mg/kg pure D-Pinitol ( = 6), and (c) subjects receiving D-Pinitol as part of carbohydrate-containing carob pods-derived syrup with a 3.2% D-Pinitol (Dose of 1600 mg/subject, = 9).
View Article and Find Full Text PDFThe widespread use of added sugars or non-nutritive sweeteners in processed foods is a challenge for addressing the therapeutics of obesity and diabetes. Both types of sweeteners generate health problems, and both are being blamed for multiple complications associated with these prevalent diseases. As an example, fructose is proven to contribute to obesity and liver steatosis, while non-nutritive sweeteners generate gut dysbiosis that complicates the metabolic control exerted by the liver.
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