Abstract
Recently, hesperidin, a flavonone mainly present in citrus fruits, has emerged as a new potential therapeutic agent able to modulate several cardiovascular diseases (CVDs) risk factors. Animal and in vitro studies demonstrate beneficial effects of hesperidin and its derived compounds on CVD risk factors. Thus, hesperidin has shown glucose-lowering and anti-inflammatory properties in diabetic models, dyslipidemia-, atherosclerosis-, and obesity-preventing effects in CVDs and obese models, and antihypertensive and antioxidant effects in hypertensive models. However, there is still controversy about whether hesperidin could contribute to ameliorate glucose homeostasis, lipid profile, adiposity, and blood pressure in humans, as evidenced by several clinical trials reporting no effects of treatments with this flavanone or with orange juice on these cardiovascular parameters. In this review, we focus on hesperidin’s beneficial effects on CVD risk factors, paying special attention to the high interindividual variability in response to hesperidin-based acute and chronic interventions, which can be partly attributed to differences in gut microbiota. Based on the current evidence, we suggest that some of hesperidin’s contradictory effects in human trials are partly due to the interindividual hesperidin variability in its bioavailability, which in turn is highly dependent on the α-rhamnosidase activity and gut microbiota composition.
Highlights
Cardiovascular diseases (CVDs) are the first cause of death in the world, causing about 31%of all deaths worldwide [1]
A reduction in inflammation and oxidative stress could be the underlying mechanisms involved in hesperidin effects on blood pressure in these animals [84]. These findings suggest that a potential mechanism whereby hesperidin and its derivatives, including G-hesperidin and hesperetin, exert their beneficial effects on hypertension through their demonstrated antioxidant effect [20,83,89], enhancing nitric oxide (NO) bioavailability and protecting endothelial function from reactive oxygen species
Hesperidin absorption is highly dependent on the conversion to its active form, hesperetin, by the microbiota, and this phenomenon occurs mainly in the large intestine, where gut microbiota releases the rutinose moiety for further absorption by the colonocytes [129] (Figure 3)
Summary
Cardiovascular diseases (CVDs) are the first cause of death in the world, causing about 31%. The number and specific position of hydroxyl groups in the flavanones aromatic rings, which produce important changes in their biochemical structure, are considered to be crucial for the reported beneficial effects of citrus polyphenols [18,19] Some of these effects include antitumor, antioxidant, anti-inflammatory, hypocholesterolemic, and hypoglycemic effects, related to an improvement in different pathologies, such as cancer, neurodegenerative diseases or CVDs [20,21]. Some of them are related with the food matrix and the physical form in which they are ingested (e.g., juice, soluble extract or capsules, among others), processing methods and storage techniques, as well as the structure of the compound and the host intrinsic characteristics, including intestinal microbiota composition [18] All these factors affect the solubility of flavanones and their uptake by the gastrointestinal tract [28,29]. This reported variability would explain the discrepancies observed between animal studies and human studies on beneficial effects of hesperidin over CVD risk factors
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