Table 2.

Summary of naringin action on clusters of Mets.

Naringin and Mets	Mechanism of Action	Outcome
Effect on visceral obesity	(i) Increases the intracellular calcium which increases the protein associated with cell death (calpain & caspase-12)	Leads to adipocyte apoptosis and reduce obesity
Effect on hypertension	(i) Suppresses the increased level of nitric oxide (NO) (ii) Radical scavenging ability of naringin increased SOD	Leads to failure in smooth muscle relaxation resulting in lower blood pressure
Effect on hyperglycemia	(i) Reduced the level of HbA1C and FBG (ii) Increased the level of insulin through proliferation of pancreatic β cells. (iii) Increased the hepatic and muscle glycogen content by lowering the activities of G6Pase and PEPCK.	Leads to reduction in circulating blood glucose
Effect on hyperlipidemia	(i) Reduced LDL levels by reducing VLDL and increasing the depuration of LDL receptors. (ii) Increased the levels of HDL due to inhibition of rho-signalling pathways with activation of PPAR-α and CETP. (iii) Inhibited the activity of HMG-CoA reductase that suppresses the cholesterol homeostasis. (iv) Reduced the ACAT activity by interacting with residues that play essential role in enzyme catalysis.	Leads to reduction in the lipid profiles and cholesterol biosynthesis
Effect on oxidative stress	(i) Naringin as a strong radical scavenger prevented the lipid peroxidation by trapping the free radicals through the donation of hydrogen atom and breaking the chain reaction.	Leads to prevention of the radicals attack on lipids, amino acid, fatty acids and DNA bases.
Effect on proinflammatory cytokines	(i) Reduced the levels of resistin and increased levels of adiponectin by suppressing the biological activity and production of the cytokines.	Leads to prevention of obesity, insulin resistance and lipid abnormalities