Metformin may help improve symptoms of Metabolic syndrome, finds study
The marked worldwide increased prevalence of type 2 diabetes (T2D) is thought to be driven, in large part, by increased prevalence of obesity. Obesity promotes an array of metabolic disorders collectively referred to as a metabolic syndrome, whose features include hypertension, hyperlipidemia, and, most importantly, insulin resistance, which is the central and defining cause of Type 2 Diabetes.
Metformin is among the world’s most widely prescribed drugs, largely because of its ability to effectively treat early-stage type 2 diabetes and, moreover, ameliorate many of the metabolic abnormalities including insulin resistance, obesity, and liver dysfunction, collectively referred to as metabolic syndrome, that is associated with dysglycemia Several mechanisms of action for metformin have been proposed, including that it acts as an anti-inflammatory agent, possibly as a result of its impact on intestinal microbiota.
The researchers at the institute of biomedical sciences, Georgia State University, Atlanta have found that Metformin Improves Diet-induced Symptoms of Metabolic Syndrome Independently of the gut microbiota. The study has been published in the American Journal of Physiology.
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Several mechanisms of action for metformin have been proposed, including that it acts as an anti-inflammatory agent, possibly as a result of its impact on intestinal microbiota. In accord with this possibility, we observed herein that, in mice with diet-induced metabolic syndrome, metformin impacts the gut microbiota by preventing its encroachment upon the host, a feature of metabolic syndrome in mice and humans.
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However, the ability of metformin to beneficially impact metabolic syndrome in mice was not markedly altered by reduction or elimination of gut microbiota, achieved by the use of antibiotics or germ-free mice. Although reducing or eliminating microbiota by itself suppressed diet-induced dysglycemia, other features of metabolic syndrome including obesity, hepatic steatosis, and low-grade inflammation remained suppressed by metformin in the presence or absence of gut microbiota.
These results support a role for metformin’s anti-inflammatory activity, irrespective of gut microbiota, in driving some of this drug’s beneficial impacts on metabolic syndrome.”
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