The gut as a regulator of early inflammation in type 1 diabetes

Curr Opin Endocrinol Diabetes Obes. 2011 Aug;18(4):241-7. doi: 10.1097/MED.0b013e3283488218.

Abstract

Purpose of review: Several studies indicate that factors affecting the gut are capable of modulating the development of autoimmune diabetes. This review discusses the recent research on these mechanisms, which may reveal novel pathogenic pathways and new possibilities for prevention of type 1 diabetes (T1D).

Recent findings: The role of the gut as a regulator of T1D is mainly based on animal studies in which changes affecting the gut immune system have been shown to modulate the immune-mediated destruction of insulin-producing beta-cells. Dietary interventions, alterations in the intestinal microbiota and exposure to enteral pathogens regulate the development of autoimmune diabetes in animal models. In several studies, it has been demonstrated that these modulations affect the gut barrier mechanisms and intestinal immunity. Also, in humans, increased gut permeability and intestinal inflammation are associated with T1D. A recent report of dietary intervention study in infants at genetic risk of T1D showed that early diet could modulate the development of beta-cell autoimmunity in humans; weaning to hydrolyzed casein formula decreased the risk of beta-cell autoimmunity by age 10.

Summary: The gut modulation affecting permeability, inflammation and microbiota is evidently associated with the regulation of the inflammation leading to beta-cell destruction. Although the mechanisms of action are not fully understood, the recent research points out the lines of approach for the prevention of T1D.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoimmunity
  • Caseins / metabolism
  • Diabetes Mellitus, Type 1 / immunology*
  • Diabetes Mellitus, Type 1 / metabolism
  • Humans
  • Inflammation / immunology
  • Inflammation / metabolism
  • Insulin-Secreting Cells / metabolism
  • Intestinal Mucosa / metabolism*
  • Intestines / immunology

Substances

  • Caseins