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[Intestinal gluconeogenesis: an insulin-mimetic function].

Gilles Mithieux1

  • 1UMR-S Inserm 1213-UCB Lyon 1 « Nutrition, Diabète et Cerveau », Faculté Laennec-Lyon-Est, Rue Guillaume Paradin, 69372 Lyon cedex 8, France.

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Summary

Intestinal gluconeogenesis (IGN) regulates energy balance by producing glucose that influences appetite and glucose control. Activating IGN offers a potential strategy for treating metabolic diseases like obesity and diabetes.

Keywords:
Intestinal gluconeogenesisdiabetesdiabètegut-to-brain signalinginsulin sensitivitynéoglucogenèse intestinaleobesityobésitésensibilité à l’insulinesignalisation intestin-cerveau

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Area of Science:

  • Metabolic Physiology
  • Nutritional Science
  • Gastroenterology

Background:

  • Intestinal gluconeogenesis (IGN) is a key regulator of energy homeostasis.
  • IGN-derived glucose signals to the brain, influencing food intake and glucose metabolism.
  • IGN is activated by dietary factors (protein, fiber) and bariatric surgery.

Purpose of the Study:

  • To investigate the role of intestinal gluconeogenesis (IGN) in metabolic regulation.
  • To explore the therapeutic potential of activating IGN for metabolic diseases.

Main Methods:

  • The study discusses the substrates (glutamine, propionate, succinate) used in IGN.
  • It reviews evidence from dietary interventions and surgical procedures that activate IGN.
  • Genetic activation of IGN in a mouse model was examined.

Main Results:

  • IGN activation correlates with satiety effects of protein-rich diets.
  • IGN activation contributes to the anti-obesity and anti-diabetes effects of fiber and gastric bypass.
  • Genetic IGN activation in mice prevented hepatic steatosis during hypercaloric feeding.

Conclusions:

  • IGN activation plays a significant role in energy homeostasis and metabolic health.
  • Targeting IGN presents a promising avenue for novel therapeutic strategies against obesity and diabetes.
  • Harnessing IGN could offer a new approach to prevent and treat human metabolic disorders.