Energy metabolism and the intestinal barrier: implications for understanding and managing intestinal diseases

Abstract

The interplay between energy metabolism and the gut barrier is crucial for maintaining intestinal physiological homeostasis. Energy metabolism and the intestinal barrier perform distinct yet complementary roles that uphold intestinal ecological equilibrium. Disruptions in energy metabolism can compromise the integrity of the intestinal barrier; for example, inactivation of the AMPK pathway may lead to reduced expression of proteins associated with tight junctions. Conversely, impairment of the intestinal barrier can result in metabolic dysregulation, such as alterations in the gut microbiota that impede the production of short-chain fatty acids (SCFAs), which are essential substrates for energy metabolism. This disruption can affect energy production and modify the gut's hypoxic environment. Imbalances in these systems have been associated with the onset of various intestinal diseases. Research indicates that dietary interventions, such as a low FODMAP diet, can enhance the colonization of probiotics and improve the fermentation metabolism of SCFAs. Pharmacological strategies to elevate SCFA levels can activate the AMPK pathway and rectify abnormalities in energy metabolism. This review provides a comprehensive summary of recent advancements in elucidating the interactions between energy metabolism and the intestinal barrier.

Keywords: SCFAs; cross-talk; energy metabolism; intestinal barrier; intestinal diseases.

FIGURE 1

Biological barrier Tfh assist B cell proliferation and maturation, B cells produce IgA, which binds to pathogens and toxins, preventing their attachment to intestinal cells and neutralizing threats.

FIGURE 2

Anaerobic bacteria maintain an anaerobic environment in the intestine: anaerobic bacteria produce SCFAs via fermentation, which fuel oxidative phosphorylation in mitochondria, consuming oxygen to sustain intestinal hypoxia. These fatty acids also strengthen intestinal tight junctions through the AMPK pathway.