Coenzyme Q10, Glucose Homeostasis and the Probable Mediating Role of Adipokines.
Obesity, the major growing health problem worldwide, is one the most important contributors of initiation and progression of insulin resistance.16 The potential mechanisms include higher production of fatty acids, activation of Toll-like receptor 4 and the innate immune system, alterations in endocrine and inflammatory mediators and activation of nuclear factor-κB
(NF-κB).
Recently the metabolic functions of adipose derived peptides, adipokines, have been investigated progressively in different disorders. The changes in the secretion of adipokines in obesity could inhibit insulin signalling through increasing inflammatory adipocytokines and other mediators interfering the IRS phosphorylation and integrity. Direct leptin actions might inhibit insulin and glucagon secretion from pancreatic cells. Moreover, leptin could potentially affect insulin signaling in adipocytes, liver and skeletal muscles.
There are obvious commonalities between the mechanisms of modulating glucose metabolism by adipokines and Q10. Nevertheless, despite the available data on the functions of adipokines on insulin signalling, there are few studies investigated the probable role of these peptides in mediating the beneficial effects of dietary supplements such as coenzyme Q10 on glucose homeostasis and insulin resistance. There are also recently recognized adipokines with insulin sensitizing features like adipolin (CTRP12). Adipolin improves insulin actions by suppressing the gluconeogenesis via PI3K-Akt pathway and improving glucose uptake of adipocytes and hepatocytes. It increases phosphorylation of IRS-1 and Akt in adipose tissue and liver while this effect is not observed in muscle cells. Adipolin might also have anti-inflammatory effects. Adipolin administration have decreased macrophages accumulation and the gene expression of proinflammatory cytokines in experimental studies.
Obes Res Open J. 2016; 3(1): e3-e5. doi: 10.17140/OROJ-3-e008
