HEALTH NEWS
Study Title:
Obesity: Pathophysiology, monosodium glutamate-induced model and anti-obesity medicinal plants.
Study Abstract
Obesity and overweight have increased at an alarming rate in the world during the last three decades. Obesity is a crucial factor in the development of metabolic abnormalities, including glucose intolerance, insulin resistance, metabolic syndrome, low-grade inflammation and oxidative stress. A similar scinario occurs during the aging process where alterations of the energetic metabolism homeostasis and a chronic systematic low-grade inflammation have been observed. Oxidative stress and poor physical performance can increase the risk of metabolic disease. Despite the diverse studies on the pathophysiological effects of obesity, its impact related to gender and through life, particularly during aging, hasn't received a reasonable attention. The purpose of this review is to outline the pathophysiological mechanisms and metabolic alterations associated with obesity, with an emphasis on the monosodium glutamate (MSG)-induced obese model. MSG-induced obesity associated inflammation and declined adiponectin were more obvious in male mice, while glucose tolerance, insulin sensitivity and the redox balance were altered with increased age of both male and female mice. These findings indicate that the metabolic alterations in MSG-induced obesity are associated with the gender as well as aging. Therefore, the MSG obesity model is of a resonable value to underlie the relationship between gender, aging and metabolic alterations in obesity. In addition, we reviewed the medicinal plants and their active constituents which have been used to treat MSG-induced obesity. Given the significat value of this model, studies are needed to scrutinize the benificial effects and underlying mechanisms of medicinal plants with proven anti-obesity activity.
Study Information
Biomed Pharmacother. 2019 Mar;111:503-516. doi: 10.1016/j.biopha.2018.12.108. Epub 2018 Dec 28. PMID: 30597304.Full Study
https://pubmed.ncbi.nlm.nih.gov/30597304/Recent News
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