Obesity, insulin resistance, type 2 diabetes mellitus (T2DM) and metabolic syndrome have been largely correlated to a reduction in bacterial load and diversity, resulting in a condition known as intestinal dysbiosis. The recent emergence of novel antidiabetic medications has been demonstrated to exert a favourable influence on the composition of the intestinal microbiota. Incretin-based therapy exerts a multifaceted influence on the composition of the gut microbiota, leading to alterations in bacterial flora. Of particular significance is the capacity of numerous metabolites produced by the gut microbiota to modulate the activity and hormonal secretion of enteroendocrine cells. This review examines the effects of dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 (GLP-1) receptor agonists and GLP-1/gastric inhibitory polypeptide (GIP) receptor dual agonists on the composition of the gut microbiota in both mice and human subjects. The nature of this interaction is complex and bidirectional. The present study demonstrates the involvement of the incretinic axis in modulating the microbial composition, with the objective of providing novel preventative strategies and potential personalised therapeutic targets for obesity and T2DM.

The very low-calorie ketogenic diet (VLCKD), characterized by a marked energy restriction that induces rapid weight loss, has recently been proposed as a valid nutritional strategy for managing obesity. VLCKD is commonly considered dangerous for the kidneys due to the misconception that it is high in protein, beyond the risk of electrolyte imbalances and an increase in diuresis. We report a case of safe and effective weight loss induced by VLCKD in a 43-year-old Caucasian woman with a recent episode of acute kidney injury on advanced chronic kidney disease. Surprisingly, we observed that after the diet-induced weight loss, not only did renal function not worsen, but proteinuria also improved. The principal value of this case report is its singular demonstration of impressive weight loss induced by VLCKD in a complex obese patient that was apparently not accompanied by the development of serious adverse sequelae.