Revista de síndrome metabólico

I am pleased to mention that during the year 2019, all issues of volume 8 were published online well within the time and the print issues were also brought out and dispatched within 30 days of publishing the issue online. JMS also brought out an online special issue in 2019. JMS Published 7 research Article 5 editorial and 2 short communication 2019. In 2018 JMS Published 4 Research Article, 5 Review Article and 1 short communication. The H-index of the journal, however, increased to 10. During the calendar year 2019, Jms received a total of 28 papers, out of which 14 articles (50%) were rejected in the preliminary screening due to plagiarism or being out of the format. During 2019 around 20 articles were subjected to the peer-review process and 14 of those were accepted. In the 8 Volume 14 published during the year 2019, a total of 14 articles were published (at an average of 5 articles per issue) of which, 50 % articles were by foreign authors. A total of 5 research scientists from India and abroad reviewed the 10 articles published in volume 7. Average publication lag time of an article was further reduced to 6-8 weeks. I take this opportunity to acknowledge the contribution of Liang-Kung Chen,during the final editing of articles published and the support rendered by the editorial assistant, Olivia Bratt bringing out issues of JMS in time. I would also like to express my gratitude to all the authors, reviewers, the publisher, the advisory and the editorial board of JMS, the office bearers and staff of IPA secretariat for their support in bringing out yet another volume of JMS and look forward to their unrelenting support to bring out the Volume 8 of JMS in scheduled time.

Background: The prevalence of metabolic syndrome is on the rise in developing countries like Bangladesh along with decreasing Vitamin D levels. As women are more vulnerable to metabolic syndrome and vitamin D deficiency, and connection among these were reported in various population, this research aims to quantify the association between vitamin D and metabolic syndrome and its components among Bangladeshi women from urban area.

Methods: Necessary data were collected from 233 participants over five months from 2015 to 2016 in Dhaka, Bangladesh. The concentration of Triglyceride, High- Density Lipoprotein (HDL) levels, fasting plasma glucose was measured with kits and vitamin D analysis was performed using High-Performance Liquid Chromatography.

Results: In this study, the prevalence of metabolic syndrome among the population was found to be 59.66%. When the subjects were divided into different quarters according to vitamin D sufficiency levels, subjects in all the quarters had significantly lower odds ratios of having metabolic syndrome compared to the lowest quarter.

Conclusion: The number of metabolic syndrome components were found to be inversely correlated with Vitamin D level and individual components were found to be correlated with Vitamin D, indicating the inverse association between vitamin D and prevalence of risk of metabolic syndrome.

Alzheimer's Disease (AD) is a global epidemic; every 3 seconds someone in the world develops dementia. An estimated 50 million people are living with a disease that cannot be prevented, treated or cured. Without novel breakthroughs, AD is predicted to exceed 130 million by 2050. Pharmaceuticals offer minimal relief with dismal evidence of reversing neurodegeneration. Research focuses on β-amyloid plaques and tau tangles; but, in a clinical trial, medications designed to sop-up toxic proteins in the brain fail to impede neural decline. Instead, plaques and tangles appear to be late-arrivers in the insidious progression of dementia. The recent explosion of comorbid metabolic pathologies (global prevalence of T2DM estimated @ 463 million) invites researchers into a deeper discussion of bioenergetics regulating cognitive impairment and metabolic dysregulation. Age-related energy deficits, driven by peripheral insulin resistance, exacerbate Aβ/tau accumulation, increase oxidative stress and impede mitochondrial function; work by Sergi et al. and Mastroeni et al. suggest that mitochondrial dysfunction with epigenetic impairment in oxidative respiration appear to be the earliest offenders in the progression of T2DM and AD . This case report highlights a novel, integrated intervention with a 69-year-old male dually diagnosed with T2DM and Mild Cognitive Impairment (MCI). Physiological biomarkers were measured pre/mid/post-intervention; the MoCA (Montreal Cognitive Assessment) measured cognitive function, pre/post. Statistically significant results were observed in the metabolic risk biomarkers, memory was restored to normal ranges, and the HbA1c normalized out of the diabetic range @ <5.6%. Furthermore, the metabolic and cognitive improvements were sustained @ 3 months postintervention. These promising results suggest that dietary ketogenesis restores peripheral insulin sensitivity, mitigates T2DM and improves cognition by circumventing neural starvation via the restoration of metabolic flexibility.

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