Two recent studies, led by Dr. Veena Taneja from the Department of Immunology and Division of Rheumatology at Mayo Clinic in Rochester (USA), allow a better understanding of the role of gut microbiota in people with rheumatoid arthritis and how manipulation of the gut microbiota may provide an additional approach to therapy.

The gut microbiome of individuals with human immunodeficiency virus (HIV) is a topic of growing scientific interest, as recent research has linked severe immunodeficiency in HIV infection with changes in both the bacterial and viral communities of the gut.

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.

It has been previously hypothesized that gut microbes could control a host’s eating behaviour through several potential mechanisms, including microbial manipulation of reward pathways, production of toxins that alter mood, changes to receptors (including taste receptors), and interference with neurotransmission via the vagus nerve—the main neural axis between the gut and the brain.

Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, affecting more than 10% of the population, with the highest impact in women. Although its origin is still unknown, reduced gut microbial diversity could be involved in its development.

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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