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. Yue Zeng from the Department of Gastroenterology at Shanghai Jiao Tong University School of Medicine in Shanghai (China), has found that colorectal pre-neoplasic lesions may be the most important factor leading to mucosal adherent bacterial dysbiosis in patients with colorectal adenomas.

A recent study, led by Prof. Maureen Hanson from the Department of Molecular Biology and Genetics at Cornell University in Ithaca, NY, USA, has found that ME/CFS patients have an altered composition of the gut microbiota that may play a role in increased microbial translocation and inflammatory symptoms in this condition.

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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