Clinical

Hepcidin contributes to hypoferremia of inflammation in obese patients

Last Updated: 2006-10-13 17:07:13 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Hepcidin expression by adipocytes may contribute to hypoferremia of inflammation in obese patients, according to a report in the September issue of Gastroenterology.

Hepcidin plays a key role in the anemia of inflammation, the authors explain, but it is not known whether obesity, a low-grade inflammatory state, affects hepcidin expression.

Dr. Soumeya Bekri from Faculte Medecine de Nice, France and colleagues studied hepcidin expression in liver and adipose tissue from severely obese patients with or without diabetes or nonalcoholic steatohepatitis.

Expression of hepcidin in subcutaneous adipose tissue was significantly enhanced in all obese conditions, the authors report, although expression in the liver was not influenced by diabetes or non-alcoholic steatohepatitis.

In adipose tissue, but not in liver, hepcidin expression was closely related to the expression of C-reactive protein and IL-6, the results indicate, and treatment of adipose tissue explants with lipopolysaccharide or IL-6 significantly increased hepcidin expression.

Hepcidin expression in liver correlated with serum transferrin saturation, the researchers note, whereas there was no such correlation with hepcidin expression in adipose tissue.

"We have demonstrated that hepcidin expression in adipose tissue was enhanced in severe obesity," the investigators conclude. "This increase is due to the chronic and constant inflammatory stimuli of obesity state."

"This high expression level is not modified upon iron depletion, which influences hepatic expression," the authors add. "These data suggest that obese patients should be investigated in terms of iron status."

Gastroenterology 2006;131:788-796.