Abstract
Metformin is the first-line pharmacotherapy for treating type 2 diabetes mellitus (T2DM); however, its mechanism of modulating glucose metabolism is elusive. Recent advances have identified the gut as a potential target of metformin. As patients with metabolic disorders exhibit dysbiosis, the gut microbiome has garnered interest as a potential target for metabolic disease. Henceforth, studies have focused on unraveling the relationship of metabolic disorders with the human gut microbiome. According to various metagenome studies, gut dysbiosis is evident in T2DM patients. Besides this, alterations in the gut microbiome were also observed in the metformin-treated T2DM patients compared to the non-treated T2DM patients. Thus, several studies on rodents have suggested potential mechanisms interacting with the gut microbiome, including regulation of glucose metabolism, an increase in short-chain fatty acids, strengthening intestinal permeability against lipopolysaccharides, modulating the immune response, and interaction with bile acids. Furthermore, human studies have demonstrated evidence substantiating the hypotheses based on rodent studies. This review discusses the current knowledge of how metformin modulates T2DM with respect to the gut microbiome and discusses the prospect of harnessing this mechanism in treating T2DM.
Highlights
Type 2 diabetes mellitus (T2DM) is one of the most common chronic metabolic disorders and is characterized by hyperglycemia resulting from the combination of insulin resistance and inadequate insulin secretion [1,2,3,4]
Lee et al [88] suggested that gut microbiota could be affected by hormone levels, subsequently influencing glucose and lipid metabolism [102,103] and one of the studies demonstrated that progesterone promotes the growth of oral Bacteroides species [104]
Some scientists have investigated the relationship between metformin and the gut microbiome
Summary
Type 2 diabetes mellitus (T2DM) is one of the most common chronic metabolic disorders and is characterized by hyperglycemia resulting from the combination of insulin resistance and inadequate insulin secretion [1,2,3,4]. Several studies suggested that metforminaction suppresses hepatic gluconeogenesis resulting from glucose tolerance modulation mediated by the metformin when administered intravenously, instead of orally, demonstrated no adenosine monophosphate-activated protein kinase (AMPK). The jejunum tissue was found to exhibit a m evidence from three studies suggests that the gut is a major target of metformin action concentration of up to 2000 μmol/kg of tissue, which was 30–300 times higher and not the liver. Based on thegut mic hypothesis that metformin targets the human gastrointestinal tract, the gut microbiome abundance correlates with metabolic markers, such as adiposity, insulin resista has attracted attention as a key factor in the treatment of T2DM [36,37,38,39,40,41]. This review focused on the various studies related to the gut microbi its association with the anti-diabetic effects of metformin
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
