Abstract
Haptoglobin is a putative adiposity marker because its concentration in blood is increased in obese humans. The present studies examined haptoglobin release by explants of adipose tissue in primary culture. Haptoglobin was released by explants of human visceral and subcutaneous adipose tissue at a nearly linear rate over 48 h. Explants of visceral adipose tissue released more haptoglobin than did explants of subcutaneous adipose tissue. The release of haptoglobin was quite variable, but there was a close correlation between haptoglobin release by visceral adipose tissue and that by explants of subcutaneous tissue from the same individual. Dexamethasone and niflumic acid, a cyclooxygenase-2 inhibitor, both inhibited haptoglobin release. There was release of haptoglobin by both isolated adipocytes and the adipose tissue matrix remaining after collagenase digestion of human adipose tissue. However, the amount of haptoglobin released by human adipose tissue explants in primary culture was quite low in relationship to the circulating level of haptoglobin.
Highlights
Haptoglobin is a putative adiposity marker because its concentration in blood is increased in obese humans
A genomic approach resulted in a similar finding, because haptoglobin mRNA was found to be significantly upregulated in the adipose tissue of obese rodents [2, 3]
The present studies were designed to determine if haptoglobin is released by human adipose tissue explants in primary culture, whether more haptoglobin is released by visceral than by subcutaneous adipose tissue, and what regulates haptoglobin release by adipose tissue
Summary
Haptoglobin is a putative adiposity marker because its concentration in blood is increased in obese humans. The present studies examined haptoglobin release by explants of adipose tissue in primary culture. Haptoglobin was released by explants of human visceral and subcutaneous adipose tissue at a nearly linear rate over 48 h. Haptoglobin release by human adipose tissue in primary culture. Haptoglobin is present at increased levels in the blood of obese humans [4, 5]. The circulating levels of haptoglobin in blood (ف2 mg/ml in obese humans) are manyfold greater than those of leptin or adiponectin, which are adipokines released by adipose tissue [6,7,8]. Treatment of mice with lipopolysaccharide (LPS) at 24 to 30 h before killing increased the haptoglobin mRNA content in adipose tissue to levels comparable to those in liver. The present studies were designed to determine if haptoglobin is released by human adipose tissue explants in primary culture, whether more haptoglobin is released by visceral than by subcutaneous adipose tissue, and what regulates haptoglobin release by adipose tissue
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