Intestinal glucose excretion: A potential mechanism for glycemic control

Ke, Zhigang; Lu, Zongshi; Li, Qing; Tong, Weidong

doi:10.1016/j.metabol.2023.155743

Cited by 2 publications

(1 citation statement)

References 94 publications

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“…Furthermore, the impact of metformin on glucose uptake in the digestive system is associated with the amount of GLUT2 expression, rather than relying on GLUT2 expression in the intestinal lining (Morrice et al, 2023). However, metformin has been shown to enhance the translocation of GLUT2 to the apical membrane of enterocytes (Ait-Omar et al, 2011), providing a potential mechanism for the release of glucose from enterocytes into the intestinal lumen in response to metformin treatment (Ke et al, 2023). Notably, mutations in the GLUT2 gene affect the glucose-lowering efficacy of metformin (Zhou et al, 2016), which may be one of the reasons for individual differences in metformin efficacy.…”

Section: Introductionmentioning

confidence: 99%

Understanding the action mechanisms of metformin in the gastrointestinal tract

Cheng,

Ren,

Jia

et al. 2024

Front. Pharmacol.

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Metformin is the initial medication recommended for the treatment of type 2 diabetes mellitus (T2DM). In addition to diabetes treatment, the function of metformin also can be anti-aging, antiviral, and anti-inflammatory. Nevertheless, further exploration is required to fully understand its mode of operation. Historically, the liver has been acknowledged as the main location where metformin reduces glucose levels, however, there is increasing evidence suggesting that the gastrointestinal tract also plays a significant role in its action. In the gastrointestinal tract, metformin effects glucose uptake and absorption, increases glucagon-like peptide-1 (GLP-1) secretion, alters the composition and structure of the gut microbiota, and modulates the immune response. However, the side effects of it cannot be ignored such as gastrointestinal distress in patients. This review outlines the impact of metformin on the digestive system and explores potential explanations for variations in metformin effectiveness and adverse effects like gastrointestinal discomfort.

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Section: Introductionmentioning

confidence: 99%

Understanding the action mechanisms of metformin in the gastrointestinal tract

Cheng,

Ren,

Jia

et al. 2024

Front. Pharmacol.

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Navigating contradictions: Salmonella Typhimurium chemotactic responses to conflicting effector stimuli

Franco,

Gentry-Lear,

Shavlik

et al. 2024

Preprint

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Many bacteria that colonize the guts of animals use chemotaxis to direct swimming motility and select sites for colonization based on sources of effectors derived from the host, diet, and microbial competitors of the local environ. The complex ecosystem of the gastrointestinal tract contains mixtures of chemoattractants and chemorepellents, but it remains poorly understood how swimming bacteria navigate conflicting signals. The enteric pathogen Salmonella Typhimurium possesses Tsr, a chemoreceptor protein that directs both chemoattraction and chemorepulsion responses, which we employed as a model to study chemotaxis in the presence of conflicting effector stimuli. We investigated how S. Typhimurium responds to human fecal matter, an effector source in the enteric lumen that contains high concentrations of indole, a bacteriostatic chemorepellent produced by the native commensals of the microbiota, and also nutrients such as L-serine, a chemoattractant. The indole concentration in human feces is more than 12-fold the concentration required for half-maximal chemorepulsion, however, we find S. Typhimurium, and various clinical isolates of non-typhoidal S. enterica serovars, are strongly attracted to liquid fecal matter. We further investigated the chemotactic responses of S. Typhimurium to titrations of indole and L-serine and revealed that chemorepulsion to indole is overridden in the presence of excess L-serine. We capture the inversion of these two opposing taxis behaviors in a phenomenon we define as "chemohalation" in which the bacteria organize into a halo around the treatment source with an interior zone of avoidance, which represents a compromise between chemoattraction and chemorepulsion. Growth analyses reveal that the chemotactic responses to these opposing effectors align chemoattraction and chemorepulsion with the relative growth of the bacteria in culture. Hence, our study supports the view that evolution has finely tuned chemotaxis to assess environmental habitability by evaluating the tradeoffs in bacterial growth based on the local combination of effectors.

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Intestinal glucose excretion: A potential mechanism for glycemic control

Cited by 2 publications

References 94 publications

Understanding the action mechanisms of metformin in the gastrointestinal tract

Understanding the action mechanisms of metformin in the gastrointestinal tract

Navigating contradictions: Salmonella Typhimurium chemotactic responses to conflicting effector stimuli

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