Adiponectin level may underpin atherogenic haptoglobin phenotype

By Sally Robertson, B.Sc.Dec 4 2012

Researchers have suggested an active role for adiponectin in the pathophysiology of vascular disease in patients with diabetes, that depends on their haptoglobin phenotype.

Their study, published in Atherosclerosis, shows that diabetes patients who are homozygous for the 2 allele of the haptoglobin gene (Hp 2-2) are more atherogenic than other phenotypes, probably due to the lower levels of circulating adiponectin found in such individuals.

In the team's analysis of 47 patients, pulse wave velocity (PWV) was significantly higher in Hp 2-2 patients than in those heterozygous at the Hp locus (Hp 2-1) or homozygous for the 1 allele (Hp 1-1).

Also, circulating adiponectin levels were significantly lower in Hp 2-2 patients than in patients with the non-Hp 2-2 phenotpyes, at 9.52 ng/mL versus 16.13 ng/mL.

"Recently published data indicate that Hp gene expression occurs in major adipose tissue depots of mice as well as human adipose tissue, subcutaneous and omental," note Marina Shargorodsky (Wolfson Medical Center, Holon, Israel) and colleagues. "Moreover, the expression of the Hp gene is regulated by different adipokines, implicated in insulin sensitivity, inflammation, lipids metabolism and atherogenesis."

Further analysis showed that the cardiovascular disease risk associated with the Hp 2-2 phenotype was independent of differences in glycemic control, blood pressure level or presence of cardiovascular risk factors between the Hp 2-2 and non-Hp 2-2 patients.

Metabolic and inflammatory parameters including total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, 25-hydroxy vitamin D, and C-reactive protein did not differ significantly between the groups. Similarly no differences in fasting plasma glucose, glycated haemoglobin, or measures of insulin resistance, or β-cell function were detected.

The researchers say the findings support those of previous studies that have identified Hp phenotype and plasma adiponectin levels as significant independent predictors for early adverse changes and atherosclerosis progression.

However, they add: "A novel contribution of the present study is the identification of a relation between Hp phenotype and circulating adiponectin levels."

Future studies should be carried out into the treatment and prevention of microvascular and macrovascular complications by adiponectin increase in diabetic patients, in particular those with Hp 2-2 phenotype, concludes the team.

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