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α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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Metformin and Systemic Metabolism.

Ling He1

  • 1Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA; Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

Trends in Pharmacological Sciences
|September 30, 2020
PubMed
Summary
This summary is machine-generated.

Metformin improves hyperglycemia by reducing liver glucose production and enhancing insulin sensitivity. It impacts gut metabolism and inflammation, creating a novel intestine-liver cycle for glucose regulation.

Keywords:
Metformininsulin resistancemitochondrianutrient metabolism

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Area of Science:

  • Endocrinology
  • Metabolic Medicine
  • Pharmacology

Background:

  • Metformin is a first-line treatment for type 2 diabetes, primarily known for reducing hepatic glucose production.
  • High intestinal concentrations of metformin suggest significant local effects on nutrient metabolism and the gut microbiome.
  • An intestine-liver metabolic cycle involving lactate has been proposed but requires further elucidation.

Purpose of the Study:

  • To review the systemic metabolic impact of metformin.
  • To elucidate the molecular mechanisms of metformin action in various tissues.
  • To discuss the role of metformin in modulating the gut-liver axis and inflammation.

Main Methods:

  • Literature review of preclinical and clinical studies on metformin's metabolic effects.
  • Analysis of metformin's impact on hepatic glucose production, intestinal metabolism, and gut microbiome.
  • Examination of metformin's effects on inflammation, oxidative phosphorylation, and insulin sensitivity.

Main Results:

  • Metformin suppresses hepatic glucose production and enhances insulin sensitivity in peripheral tissues.
  • Intestinal metformin accumulation alters epithelial cell metabolism and the microbiome, increasing lactate production.
  • A futile intestine-liver lactate cycle contributes to metformin's glucose-lowering effects.
  • Metformin reduces endotoxemia, low-grade inflammation, and modulates oxidative phosphorylation.

Conclusions:

  • Metformin exerts systemic metabolic benefits through multifaceted actions beyond hepatic glucose suppression.
  • The gut-liver axis and metformin-induced alterations in intestinal metabolism play a crucial role in its efficacy.
  • Understanding these complex mechanisms can inform future therapeutic strategies for metabolic diseases.