Novel investigation implies that intestinal bacteria could be vital to how the diabetes medication metformin acts.(Image credit: THOM LEACH / SCIENCE PHOTO LIBRARY via Getty Images)ShareShare by:
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From the decade of the 1990s onward, physicians have been prescribing metformin for treating type 2 diabetes, but the complete mechanism of action was not clear to experts.
Presently, fresh findings shed light on a component of the mystery: Metformin prompts the body to eliminate glucose from the bloodstream, dispatching it toward the intestines, where bacteria ingest the carbohydrate to produce substances that might aid in regulating sugar levels in the blood.
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Various Avenues
Most studies have been directed at metformin’s impact on the liver, enhancing cellular reaction to insulin and hindering the creation of glucose. However, some studies have hinted that the drug influences the gut as well, possibly through impeding glucose absorption into the circulation.
“Numerous researchers are examining metformin’s effect on the gut, given that when metformin is ingested, the intestines encounter significantly high concentrations,” stated Dr. Wataru Ogawa, primary author of the investigation and medical scientist at Kobe University in Japan. (Ogawa has benefited from research funding and honorariums for speaking from Sumitomo Pharma, the manufacturer of metformin.)
Previously, Ogawa’s group demonstrated that the organism discharges glucose into the central channel of the human digestive system, the pathway for food and waste. This is observed across individuals with and without diabetes. “This indicates this represents a normal biological process present in humans,” Ogawa communicated with Live Science.
Nourishing Intestinal Bacteria
In the recent study, the researchers discovered that metformin nearly quadrupled the rate by which glucose was excreted into the gut among five individuals dealing with type 2 diabetes, which was confirmed in murine models.
Preventing glucose from circulating through the system by directing it towards the gut might diminish blood sugar levels immediately; however, specialists informed Live Science that they believe this clarifies merely a section of metformin’s helpful impacts.
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Nicola Morrice, a researcher of metformin at the University of Dundee in Scotland who had no role in the research, shared via email with Live Science, “I am of the opinion that this is not the principal process by which the drug operates.”
Moreover, beyond eradicating glucose from the bloodstream, discharged glucose may exert an indirect impact upon blood sugar through nourishing intestinal bacteria, as relayed to Live Science by additional specialists.
Dr. José-Manuel Fernández-Real, a medical researcher at the University of Girona in Spain with no link to the research, communicated in an email to Live Science, “Certain bacteria, notably those flourishing upon simple sugars, might exhibit accelerated development, whereas others relying upon complex carbs or the process of fiber fermentation might be influenced less.”
Given that a glucose molecule possesses a foundation composed of six carbon atoms, Ogawa sought a method to track these carbons for quantifying the pace at which gut bacteria dismantle glucose into divergent compounds. His team infused murine models with glucose incorporating a “heavy” isotope—a form of carbon bearing an additional neutron. This strategy facilitated tracking of heavy carbons as bacteria morphed glucose into new substances.
Examination of stool samples indicated that bacteria inside the metformin-treated mice had transformed the labeled glucose into short-chain fatty acids (SCFAs). “Bacterial strains responsible for the development of short-chain fatty acids typically represent ‘beneficial’ bacteria,” indicating that metformin’s impacts could promote the formation of a favorable microbiome, Ogawa specified.
Metformin administration led to an increase of labeled SCFAs by merely 1% within stool specimens. Regardless, Manuel Vázquez-Carrera, a pharmacological investigator at the University of Barcelona lacking involvement in the research, communicated via email with Live Science that “the preponderance of SCFAs undergo rapid absorption and consumption rather than excretion.” This proposes that the assessment potentially constitutes an underestimation.
Furthermore, “even a marginal increase in SCFA genesis can amplify the functionality of the intestinal barrier, alleviate inflammation, and bolster insulin responsiveness, each offering advantages in addressing diabetes,” Fernández-Real hypothesized.
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The investigation encountered constraints. At first, the investigators neglected to evaluate the effects of heightened intestinal SCFA concentrations upon the health of the murine subjects. In addition, it encompassed “a reduced quantity of participants who were obtaining fluctuating amounts of metformin as a feature of their treatment plans,” Morrice pointed out.
The murine component similarly involved solely male rodents, implying a lack of exploration into potential sex-based variations of the drug’s influence. Beyond analyzing metformin’s impacts upon five diabetes participants, Ogawa disclosed he has concluded a more expansive, gold-standard assessment in humans to probe further into the medication’s impacts upon the gut. Although the analysts haven’t finalized the analysis, they have yet to observe sex-related dissimilarities.
Morrice suggested that future research might dissect the influence of metformin upon glucose secretion within murine subjects ingesting varying diets, such as diets abundant in fats and sugars, recognized to correlate with obesity.
Disclaimer
The purpose of this article is solely informational and not to provide medical consultation.
Kamal NahasSocial Links NavigationLive Science Contributor
Kamal Nahas holds the position of a freelance contributor and is situated in Oxford, U.K. His contributions have been showcased in New Scientist, Science, and The Scientist, among other publications, primarily focusing on exploration of research pertaining to evolution, wellness, and technology. He has secured a PhD in pathology sourced from the University of Cambridge alongside a master’s degree in immunology from the University of Oxford. Presently, he fulfills the duties of a microscopist at the Diamond Light Source, the U.K.’s synchrotron installation. Outside of writing engagements, he can be found on the Jurassic Coast, engaged in fossil pursuits.
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Eliminating ‘senescent cells’ within blood vessels might be essential for addressing diabetes, an initial investigation reveals