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Diosmin can restore elevated blood sugar

Diosmin can restore elevated blood sugar
From Science Direct   2022.9.07

Diosmin is a flavone glycoside which is found in a natural structure in the pericarps of different citrus fruits and is called 3′,5,7-trihydroxy-40-methoxyflavone-7-rhamnoglucoside. In fact, this flavone glycoside is obtained by dehydrogenation of hesperidin. Diosmin was first isolated in 1925 from Scrophularia nodosa and first introduced as a therapeutic agent in 1969. Clinical evidence suggests that diosmin is a safe, nontoxic drug, and well-tolerated drug. This flavone glycoside has a sugar molecule attached to its three-ringed flavonoid structure and it contains imperative pharmacological applications (plasma half-life is 26–43 h), being the micronized nutraceutical formulation of diosmin, under the trade name Daflon, has been successfully used to treat chronic venous disease, hemorrhoids and diabetes for over a decade in Europe. Srinivasan and Pari46 divulged antihyperglycemic efficiency of diosmin by stimulating insulin production from the existing β-cells of the pancreas. Noteworthy, diosmin has also been demonstrated to activate the rate-limiting enzymes of carbohydrate metabolism and found to reverse the abnormalities in glycoprotein components in STZ-nicotinamide (NA)-induced diabetic rats. Studies from the same author claimed that diosmin alleviated the oxidative stress by enhanced the antioxidant status in the plasma, liver, and kidneys of STZ-NA-induced experimental rats. Moreover, administrations of diosmin to STZ-NA-induced type 2 diabetic rats alleviate dyslipidemia through enhanced the plasma and tissue levels of lipid profiles and lipid metabolizing enzymes. Recently, Hsu et al. suggest that intervention with diosmin at doses of 50 and 100 mg/kg significantly restored the elevated blood glucose and lipid profiles through enhance the secretion of endogenous β-endorphin from the adrenal glands, which can activate opioid receptors to increase glucose transporter 4 (GLUT4) expression in muscle and decrease hepatic gluconeogenesis, resulting in the reduction of hyperglycemia in STZ-diabetic rats. Hence, diosmin has been shown to improve factors associated with diabetic complications. Diosmin inhibits alloxan-induced diabetic neuropathy by modulating NF-kB-dependent signaling pathways resulting in reduced oxidative stress makers. Recently, Wojnar et al. authenticated the protective efficacy of diosmin on the oxidative stress markers in the lenses of STZ-induced type 1 diabetic rats (Fig. 2).

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