Allulose mitigates chronic enteritis by reducing mitochondria dysfunction via regulating cathepsin B production.

Area of Science:

• Biochemistry
• Gastroenterology
• Immunology

Background:

• Metabolic alterations are implicated in inflammatory bowel disease (IBD) development, including colitis.
• Allulose, a bioactive monosaccharide, plays a role in metabolic processes, but its mechanism in colitis inhibition is unclear.
• Lower blood allulose levels correlate with IBD and colorectal cancer severity.

Purpose of the Study:

• To elucidate the biochemical mechanism by which allulose inhibits colitis.
• To investigate allulose's role in maintaining intestinal mucosal barrier integrity.
• To assess allulose's therapeutic potential for colitis.

Main Methods:

• Utilized dextran sodium sulphate (DSS)-induced and IL-10 knockout (IL-10-/-) mouse models of colitis.
• Administered allulose to mice with induced or naturally occurring colitis.
• Analyzed intestinal mucosal damage, tight junction integrity, and mitochondrial function.
• Investigated the molecular pathways involving cathepsin B, lysosomes, and myosin light chain kinase (MLCK).

Main Results:

• Allulose administration significantly reduced intestinal mucosal damage in colitis models.
• Allulose maintained tight junction integrity and prevented mitochondrial dysfunction.
• The mechanism involves inhibiting cathepsin B release and promoting lysosome cohesion, thereby blocking MLCK activity.

Conclusions:

• Allulose acts as an intrinsic protector of the intestinal mucosal barrier.
• By preserving barrier integrity, allulose effectively mitigates colitis progression.
• Allulose demonstrates significant potential as a therapeutic supplement for colitis treatment.