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New Insights into the Efficacy of Aspalathin and Other Related Phytochemicals in Type 2 Diabetes-A Review

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MDPI
DOI: 10.3390/ijms23010356

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aspalathin; bioavailability; diabetes; C-glucosyl flavones; gut microbiota; hyperuricemia; inflammation; insulin resistance; mitochondrial dysfunction; oxidative stress

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In the pursuit of bioactive phytochemicals for managing metabolic risk factors for type 2 diabetes (T2D), aspalathin, a C-glucosyl dihydrochalcone found in rooibos, has gained great attention. This review provides an overview of dietary sources, compound stability, bioavailability, and microbial biotransformation of aspalathin and its derivatives. It also discusses the role of these compounds in improving insulin resistance, gut dysbiosis, oxidative stress, inflammation, and hyperuricemia associated with T2D. Additionally, emerging targets for T2D management, such as enhancing insulin receptor signaling and reducing renal glucose reabsorption, are highlighted.
In the pursuit of bioactive phytochemicals as a therapeutic strategy to manage metabolic risk factors for type 2 diabetes (T2D), aspalathin, C-glucosyl dihydrochalcone from rooibos (Aspalathus linearis), has received much attention, along with its C-glucosyl flavone derivatives and phlorizin, the apple O-glucosyl dihydrochalcone well-known for its antidiabetic properties. We provided context for dietary exposure by highlighting dietary sources, compound stability during processing, bioavailability and microbial biotransformation. The review covered the role of these compounds in attenuating insulin resistance and enhancing glucose metabolism, alleviating gut dysbiosis and associated oxidative stress and inflammation, and hyperuricemia associated with T2D, focusing largely on the literature of the past 5 years. A key focus of this review was on emerging targets in the management of T2D, as highlighted in the recent literature, including enhancing of the insulin receptor and insulin receptor substrate 1 signaling via protein tyrosine phosphatase inhibition, increasing glycolysis with suppression of gluconeogenesis by sirtuin modulation, and reducing renal glucose reabsorption via sodium-glucose co-transporter 2. We conclude that biotransformation in the gut is most likely responsible for enhancing therapeutic effects observed for the C-glycosyl parent compounds, including aspalathin, and that these compounds and their derivatives have the potential to regulate multiple factors associated with the development and progression of T2D.

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