Now a recent study, led by Dr. Nicola Santoro from the Department of Paediatrics at Yale University in New Haven, Connecticut (USA), has found that the gut microbiota of obese youth may drive a higher accumulation of energy than that of lean adolescents through an elevated production of short-chain fatty acids (SCFAs) and a higher capability to oxidize carbohydrates.

A recent randomized double-blind placebo-controlled trial, led by Dr. Ellen Blaak from the Department of Human Biology at Maastricht University Medical Centre in Maastricht (The Netherlands), has found that a 7-day antibiotic treatment does not affect host metabolism in obese humans in the short term, despite profound changes in gut microbial diversity and composition.

It is already known that a reduction in gut microbial richness is the hallmark change of human immunodeficiency virus (HIV) infection, but how this dysbiosis is established in the HIV-exposed uninfected infant is poorly understood. A recent cross-sectional study, led by Dr. Grace M. Aldrovandi from the Children’s Hospital Los Angeles in Los Angeles (USA), suggests that perturbations in the infant gut microbiome may explain the greater risk of morbidity and mortality in uninfected babies born to HIV-positive mothers.

A recent study, led by Dr. Wendy A. Henderson from the National Institute of Nursing Research at National Institutes of Health (NIH) in Bethesda (USA), and co-authored by Research Fellow Dr. Nicolaas Fourie, has found that the oral microbiota could be a useful source of information in patients with irritable bowel syndrome (IBS).

It has been previously reported that the gut microbiota could be involved in the pathogenesis of metabolic diseases such as diabetes. A recent study, led by Dr. Wolfgang zu Castell from the Scientific Computing Research Unit at Helmholtz Zentrum München in Munich (Germany) has found that butyrate may have a protective effect in the pathogenesis of type 1 diabetes.

In a recent paper by Perry et al., researchers describe an investigation into the putative mechanisms by which gut microbiota alterations may lead to obesity, insulin resistance, and metabolic syndrome. Authors describe increased production of acetate by altered gut microbiota in rats. They link this to activation of the parasympathetic nervous system, increased glucose-stimulated insulin secretion, higher ghrelin secretion, hyperphagia, and obesity. Thus, they point to increased acetate production as a driver of metabolic syndrome.

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