Adipokines: Potential Therapeutic Targets for Vascular Dysfunction in Type II Diabetes Mellitus and Obesity

Table 1

The table shows the specific vascular functions of different adipokines and their roles as therapeutic targets for vascular dysfunction in type II DM and obesity.

Adipokine	Vascular effect	Diagnostic/therapeutic implications
Adiponectin	(i) Anti-inflammatory and endothelium-protective effects.; (ii) Promoting repair of endothelial damage and tissue ischemia.; (iii) Inhibition of smooth muscle cells’ proliferation and migration.; (iv) Reducing oxidative stress and associated cellular apoptosis.	(i) Increasing its plasma concentration by thiazolidinediones, RAS blockers, and cholesterol-lowering drugs.; (ii) Direct pharmacological administration of adiponectin.; (iii) Use of adiponectin agonists such as adipoRon or osmotin.; (iv) Enhancing adiponectin receptor expression by hypocaloric diet, exercise, or pharmaceutical agents.
A-FABP	(i) Accumulation of cholesterol-ester within macrophages and foam cell formation.; (ii) Positive feedback on C-Jun N-terminal kinase (JNK), a major mediator of insulin resistance and vascular dysfunction.	Using A-FABP pharmacological repressors such as arbazole-based repressors, benzylamino-6-(trifluoromethyl)pyrimidin-4(1H) repressors, and BMS309403.
Leptin	(i) At low levels, it induces hypotension and at high levels, it stimulates the sympathetic nervous system causing vasoconstriction and hypertension.; (ii) At high levels, it increases platelet aggregation, expression of vascular adhesion molecules, and prothrombotic tissue factor.	(i) Leptin/adiponectin ratio serves as an indicator of subclinical atherosclerosis.; (ii) Pharmacological administration of leptin can increase blood pressure in patients with human leptin deficiency syndrome.; (iii) Therapeutic investigations for hyperleptinemia are still under investigation.
Chemirin	Increasing the expression of endothelial adhesion molecules (ICAM-1 and E-selectin) that share in the early steps of forming an atherosclerotic plaque.	Pharmacological inhibition of omentin may slow the pathogenic process of atherosclerosis.
Omentin	(i) Omentin has a NO-mediated vasodilator effect that can antagonize TNF-α mediated vasoconstriction.; (ii) Inhibitory effect on smooth muscle migration and proliferation.	Potentiation of the molecular effects of omentin should be considered by pharmacological administration of its agonists or increasing the expression of its receptors.
Resistin	Promoting smooth muscle cells proliferation and migration and increasing the synthesis of prothrombotic tissue factor (TF) in human coronary cells.	It can serve as a prognostic factor for the severity of unstable angina and atherosclerosis.
Visfatin	Playing a significant role in plaque destabilization of unstable carotid and coronary atherosclerosis.	It can serve as a prognostic factor for cardiovascular mortality.
Apelin	Positive inotropic effect on the heart and exerting a relaxing effect on the aortic wall.	It may serve as an angiotensin II homologue, with a relaxing effect on the aortic wall.