Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Nov;74(21):3941-3954.
doi: 10.1007/s00018-017-2611-0. Epub 2017 Aug 17.

Melatonin, mitochondria, and the metabolic syndrome

Daniel P Cardinali  1 , Daniel E Vigo  2
Affiliations
Review

Melatonin, mitochondria, and the metabolic syndrome

Daniel P Cardinali et al. Cell Mol Life Sci. 2017 Nov.

Abstract

A number of risk factors for cardiovascular disease including hyperinsulinemia, glucose intolerance, dyslipidemia, obesity, and elevated blood pressure are collectively known as metabolic syndrome (MS). Since mitochondrial activity is modulated by the availability of energy in cells, the disruption of key regulators of metabolism in MS not only affects the activity of mitochondria but also their dynamics and turnover. Therefore, a link of MS with mitochondrial dysfunction has been suspected since long. As a chronobiotic/cytoprotective agent, melatonin has a special place in prevention and treatment of MS. Melatonin levels are reduced in diseases associated with insulin resistance like MS. Melatonin improves sleep efficiency and has antioxidant and anti-inflammatory properties, partly for its role as a metabolic regulator and mitochondrial protector. We discuss in the present review the several cytoprotective melatonin actions that attenuate inflammatory responses in MS. The clinical data that support the potential therapeutical value of melatonin in human MS are reviewed.

Keywords: Aging; Diabetes; Inflammation; Insulin signaling; Melatonin; Metabolic syndrome; Mitochondria; Obesity.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
MS is the consequence of obesity-induced changes in adipocytokine secretion that lead to the development of systemic insulin resistance, type 2 and 3 diabetes mellitus, and cardiovascular disorders. Overnutrition that results from a combination of increased food intake and reduced energy expenditure leads to adipose tissue expansion, increased adipocyte size and number, and increased macrophage infiltration that, together, lead to increased free fatty acid release, dysregulated secretion from adipocytes of a variety of adipocytokines, including adiponectin, leptin, and resistin, and increased release from resident macrophages of the inflammatory cytokines (TNF-α, IL-6). Dysregulated secretion of these adipokines elicits a variety of adverse effects on numerous tissues
See this image and copyright information in PMC

References

    1. Smith CJ, Ryckman KK. Epigenetic and developmental influences on the risk of obesity, diabetes, and metabolic syndrome. Diabetes Metab Syndr Obes. 2015;8:295–302. - PMC - PubMed
    1. O’Neill S, O’Driscoll L. Metabolic syndrome: a closer look at the growing epidemic and its associated pathologies. Obes Rev. 2015;16:1–12. doi: 10.1111/obr.12229. - DOI - PubMed
    1. Bhatti JS, Kumar S, Vijayan M, Bhatti GK, Reddy PH. Therapeutic strategies for mitochondrial dysfunction and oxidative stress in age-related metabolic disorders. Prog Mol Biol Transl Sci. 2017;146:13–46. doi: 10.1016/bs.pmbts.2016.12.012. - DOI - PubMed
    1. Bhatti JS, Bhatti GK, Reddy PH. Mitochondrial dysfunction and oxidative stress in metabolic disorders—a step towards mitochondria based therapeutic strategies. Biochim Biophys Acta. 2016 - PMC - PubMed
    1. Fabbri E, Chia CW, Spencer RG, Fishbein KW, Reiter DA, Cameron D, Zane AC, Moore ZA, Gonzalez-Freire M, Zoli M, Studenski SA, Kalyani RR, Egan JM, Ferrucci L. Insulin resistance is associated with reduced mitochondrial oxidative capacity measured by 31P-magnetic resonance spectroscopy in participants without diabetes from the Baltimore Longitudinal Study of Aging. Diabetes. 2017;66:170–176. doi: 10.2337/db16-0754. - DOI - PMC - PubMed

Publication types