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Diabetes Res Clin Pract. 2014 Sep;105(3):295-301. doi: 10.1016/j.diabres.2014.04.008. Epub 2014 Jun 11.

Intestinal glucose metabolism revisited.

Author information

1
Inserm U855, Faculté de Médecine Lyon-Est "Laennec", 69372 Lyon Cedex 08, France; Université Lyon 1, 69622 Villeurbanne, France; Université de Lyon, 69008 Lyon, France. Electronic address: gilles.mithieux@inserm.fr.
2
Inserm U855, Faculté de Médecine Lyon-Est "Laennec", 69372 Lyon Cedex 08, France; Université Lyon 1, 69622 Villeurbanne, France; Université de Lyon, 69008 Lyon, France.

Abstract

It is long known that the gut can contribute to the control of glucose homeostasis via its high glucose utilization capacity. Recently, a novel function in intestinal glucose metabolism (gluconeogenesis) was described. The intestine notably contributes to about 20-25% of total endogenous glucose production during fasting. More importantly, intestinal gluconeogenesis is capable of regulating energy homeostasis through a communication with the brain. The periportal neural system senses glucose (produced by intestinal gluconeogenesis) in the portal vein walls, which sends a signal to the brain to modulate hunger sensations and whole body glucose homeostasis. Relating to the mechanism of glucose sensing, the role of the glucose receptor SGLT3 has been strongly suggested. Moreover, dietary proteins mobilize intestinal gluconeogenesis as a mandatory link between their detection in the portal vein and their effect of satiety. In the same manner, dietary soluble fibers exert their anti-obesity and anti-diabetic effects via the induction of intestinal gluconeogenesis. FFAR3 is a key neural receptor involved in the specific sensing of propionate to activate a gut-brain reflex arc triggering the induction of the gut gluconeogenic function. Lastly, intestinal gluconeogenesis might also be involved in the rapid metabolic improvements induced by gastric bypass surgeries of obesity.

KEYWORDS:

Intestinal glucose metabolism

PMID:
24969963
DOI:
10.1016/j.diabres.2014.04.008
[Indexed for MEDLINE]

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