Causes and Correlations of Metabolic Syndrome

The mechanisms of the complex pathways of metabolic syndrome are under investigation. The pathophysiology is very complex and has been only partially elucidated. Most people affected by the condition are older, obese, sedentary, and have a degree of insulin resistance. Stress can also be a contributing factor. The most important risk factors are diet (particularly sugar-sweetened beverage consumption), genetics, aging, sedentary behavior or low physical activity, disrupted chronobiology/sleep, mood disorders/psychotropic medication use, and excessive alcohol use.

In a cohort study with 89,860 individuals, there was a strong and positive association between resting heart rate and metabolic syndrome in cross-sectional analysis; more importantly and interestingly, those subjects without metabolic syndrome at baseline but with higher resting heart rate had a greater risk in developing metabolic syndrome than those with lower resting heart rate in the near future in longitudinal analysis.

There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. Markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.

Research shows that Western diet habits are a factor in development of metabolic syndrome, with high consumption of food that is not biochemically suited to humans. Weight gain is associated with metabolic syndrome. Rather than total adiposity, the core clinical component of the syndrome is visceral and/or ectopic fat (i.e., fat in organs not designed for fat storage) whereas the principal metabolic abnormality is insulin resistance. The continuous provision of energy via dietary carbohydrate, lipid, and protein fuels, unmatched by physical activity/energy demand, creates a backlog of the products of mitochondrial oxidation, a process associated with progressive mitochondrial dysfunction and insulin resistance.

Endocrinology and Metabolism: Open Access is a peer reviewed journal which focuses on the publication of current research and developments on the endocrine glands and its secretions with their coordination with metabolism and reproduction.

Endocrinology and Metabolism: Open Access Journal is using Editorial Tracking System to maintain quality and transparency to the author in the peer-review process. Review processing will be performed by the editorial board members of the Journal Endocrinology and Metabolism: Open Access or by Reviewers (outside experts in the field). Two independent reviewer’s approval (Minimum reviewer’s approval) followed by editor approval is obligatory for acceptance of any manuscript excluding an editorial.

Journal is now accepting manuscripts for volume 5 for year 2021. We publish minimum of 5 and maximum of 20 articles per issue every month. Submissions to our journal are given high priority during the process.

Submit your manuscript at:

https://www.imedpub.com/submissions/endocrinology-metabolism-open-access.html 

You may also send the manuscript as an attachment to mail endometabol@emedscholar.com

Media Contact
Eliza Grace
Associate Managing Editor
Endocrinology and Metabolism: Open Access
E-Mail: endometabol@emedscholar.com