[Show abstract][Hide abstract] ABSTRACT: Obesity is associated with a chronic and low-grade inflammation which may cause hypoferremia as seen in patients with chronic inflammatory diseases. The aim of the present study was to investigate the relationship between iron status and markers of inflammation in morbidly obese women and the effect of bariatric surgery.
Our cohort of patients consisted of 178 morbidly obese females selected for bariatric surgery. Clinical and biochemical data were recorded before surgery, and histopathological studies were carried out on preoperative liver biopsy samples. Fifty-five patients have been followed up after bariatric surgery.
A high prevalence of iron depletion was present in this cohort, with 53% having a transferrin saturation ratio below 0.20. Iron depletion was significantly correlated with raised levels of indices of inflammation, C-reactive protein (CRP), orosomucoid and haptoglobin), and with the white blood cell count. In multivariate analysis, orosomucoid and CRP were independently associated with iron depletion. Moreover, 6 months after bariatric surgery, inflammation level decreased, which was inversely correlated with the increase in transferrin saturation.
Iron depletion is common in morbidly obese women. Low-grade chronic inflammation associated with obesity could be a modulator of iron uptake and utilization. Bariatric surgery may reduce chronic inflammation and improve iron status.
Obesity Surgery 07/2008; 18(6):709-14. DOI:10.1007/s11695-007-9276-y · 3.75 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: C-Reactive Protein (CRP), a nonspecific marker of inflammation that is moderately elevated in obesity, metabolic syndrome (MS), and type 2 diabetes, has been proposed as a surrogate marker of nonalcoholic steatohepatitis (NASH). Its clinical usefulness in the diagnosis of NASH was evaluated in severely obese patients without or with MS, diabetes, and NASH and the potential roles of the liver and of the adipose tissue in CRP production were characterized.
Severely obese patients without NASH (without MS [N = 13], with MS [N = 11], or with MS and diabetes [N = 7]) and with NASH (without [N = 8] or with [N = 7] MS) were studied. For each patient, liver and adipose tissue biopsies were collected during a bariatric surgery and were used to determine the CRP gene expression by real-time PCR. The role of interleukin-6 (IL6) and lipopolysaccharide in CRP expression was also evaluated in subcutaneous adipose tissue obtained during cosmetic abdominoplasty.
Plasma CRP levels were elevated in severely obese patients independently from the presence or absence of MS, diabetes, or NASH. CRP gene expression was not only increased in livers but also in adipose tissues of obese patients compared with controls subjects. In human adipose tissue, CRP mRNA levels were positively correlated with those of IL-6 and the CRP expression was enhanced in vitro by IL-6 and lipopolysaccharide.
Plasma CRP levels are not predictive of the diagnosis of NASH in severely obese patients. The liver but also the adipose tissue can produce CRP, a process which could be dependent on IL6. Therefore, both tissues might contribute to the elevated plasma CRP levels found in obesity. In addition, the large amount of body fat may well produce an important part of the circulating CRP, further limiting its clinical usefulness in the evaluation of NASH in severely obese patients.
The American Journal of Gastroenterology 09/2006; 101(8):1824-33. DOI:10.1111/j.1572-0241.2006.00724.x · 10.76 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Hepcidin is an acute-phase response peptide. We have investigated the possible involvement of hepcidin in massive obesity, a state of chronic low-grade inflammation. Three groups of severely obese patients with or without diabetes or nonalcoholic steatohepatitis were investigated.
Hepcidin expression was studied in liver and adipose tissue of these patients. Hepcidin regulation was investigated in vitro by adipose tissue explant stimulation studies.
Hepcidin was expressed not only in the liver but also at the messenger RNA (mRNA) and the protein levels in adipose tissue. Moreover, mRNA expression was increased in adipose tissue of obese patients. The presence of diabetes or NASH did not modify the hepcidin expression levels in liver and adipose tissue. In adipose tissue, mRNA expression correlated with indexes of inflammation, interleukin-6, and C-reactive protein. Interleukin-6 also promoted in vitro hepcidin expression. A low transferrin saturation ratio was observed in 68% of the obese patients; moreover, 24% of these patients presented with anemia. The observed changes in iron status could be due to the role of hepcidin as a negative regulator of intestinal iron absorption and macrophage iron efflux. Interestingly, a feedback control mechanism on hepcidin expression related to low transferrin saturation occurred in the liver but not in the adipose tissue.
Hepcidin is a proinflammatory adipokine and may play an important role in hypoferremia of inflammation in obese condition.