Catechins and Proanthocyanidins Involvement in Metabolic Syndrome

Abstract

Recent studies on natural antioxidant compounds have highlighted their potentiality against various pathological conditions. The present review aims to selectively evaluate the benefits of catechins and their polymeric structure on metabolic syndrome, a common disorder characterized by a cluster of three main risk factors: obesity, hypertension, and hyperglycemia. Patients with metabolic syndrome suffer chronic low inflammation state and oxidative stress both conditions effectively countered by flavanols and their polymers. The mechanism behind the activity of these molecules has been highlighted and correlated with the characteristic features present on their basic flavonoidic skelethon, as well as the efficient doses needed to perform their activity in both in vitro and in vivo studies. The amount of evidence provided in this review offers a starting point for flavanol dietary supplementation as a potential strategy to counteract several metabolic targets associated with metabolic syndrome and suggests a key role of albumin as flavanol-delivery system to the different target of action inside the organism.

Keywords: cardiovascular diseases; catechins; flavan-3-ols; inflammatory state; natural antioxidants; proanthocyanidins.

Figure 1

Schematic representation of the chemical structure of the treated compounds. (A) Basic skeleton of flavonoids and their main subclasses; (B) chemical structures of principal flavan-3-ols; (C) basic chemical structure of prohantocyanidin.

Figure 2

Beneficial effect of catechins in counteracting dysmetabolism by MetS. Catechins ameliorate cardiovascular flux: by modulation on eNOS that leads to increase NO production, which in turns improves vascular relaxation; by decreasing LDL, cholesterol, and triglycerides values that contribute to plaque buildup in arteries; by increasing HDL values. Catechins reduce inflammation process through reduction of ROS and NFkB, both triggering proinflammatory mediators including TNFa, IL-6, and IL-8. Catechins positively affect glucose homeostasis improving the glucose transport in cells via 4 and suppressing hepatic gluconeogenesis through G6Pase and PEPCK inhibition. Furthermore, catechins attenuate postprandial glycemia reducing GLUT 1 and 2 genes. Abbreviations: Nitric oxide endothelial synthase (eNOS); Nitric oxide (NO); Low-density lipoprotein (LDL); High-density lipoprotein (HDL); Reactive oxygen species (ROS); Tumor necrosis factor a (TNFα); Interleukin-6 (IL-6); Interleukin-8 (IL-8); Nuclear Factor kappa B (NK-kB); Glucose transporter (GLUT); Glucose 6-phosphatase (G6Pase); Phosphoenolpyruvate carboxykinase (PEPCK).

Figure 3

Schematic representation of the main molecular targets of catechins and PCAs. In general, they ameliorated MetS and related diseases improving cell antioxidant defenses while metal ions and ROS levels are reduced. MAPK, IRS-1/PI3K/Akt and Ca²⁺/CaMI/CaMKII pathways are improved while PTP1B, IKK/NFkB and ROS-ERK/KNK-p53 pathways are down-regulated.