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GI inflammation Increases Sodium-Glucose Cotransporter Sglt1.

Jiyoung Park1,2, In-Seung Lee3,4, Kang-Hoon Kim5,6

  • 1College of Korean Medicine, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Korea. sdu1771@naver.com.

International Journal of Molecular Sciences
|May 26, 2019
PubMed
Summary

Gastrointestinal inflammation causes over-secretion of incretin hormones, impacting glucose regulation. This occurs due to increased glucose-sensing receptors, specifically sodium glucose cotransporter 1 (SGLT1), in inflamed conditions.

Keywords:
GI inflammationGIPGLP-1Sglt1glucose sensing receptorincretin secretion

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Area of Science:

  • Gastroenterology
  • Endocrinology
  • Immunology

Background:

  • Gastrointestinal (GI) inflammation is linked to gut hormone alterations.
  • Inflammatory stimuli can induce high incretin hormone levels, potentially causing glucose dysregulation.
  • Limited studies explore glucose-induced incretin secretion during inflammation.

Purpose of the Study:

  • To investigate if GI inflammatory conditions cause over-stimulated incretin secretion.
  • To determine if increased glucose-sensing receptors mediate this effect.
  • To examine the role of sodium glucose cotransporter 1 (SGLT1) in this process.

Main Methods:

  • Utilized a GI inflammatory mouse model to observe incretin secretion and glucose-sensing receptors.
  • Treated intestinal epithelial and enteroendocrine cells with conditioned media containing inflammatory cytokines.
  • Assessed the impact of SGLT1 inhibition on incretin secretion and cellular signaling.

Main Results:

  • GI-inflamed mice showed over-stimulated incretin secretion and insulin release in response to glucose.
  • Increased SGLT1 expression was observed in inflamed conditions, enhancing glucose-induced GLP-1 secretion.
  • SGLT1 inhibition reduced GLP-1 secretion, ERK activation, and calcium influx.

Conclusions:

  • GI inflammation leads to abnormal incretin secretion through increased SGLT1.
  • This mechanism contributes to metabolic disturbances observed in GI inflammatory diseases.
  • Targeting SGLT1 may offer therapeutic potential for managing metabolic issues in GI inflammation.