Jefferson researchers have found that mice with low levels of the protein hormone adiponectin may also have high levels of a protein called albumin which, in humans, may be a sign of kidney disease. This study provides further support for the theory that kidney disease may be a more important risk factor for heart disease than is cholesterol.
Nephrologists at Thomas Jefferson University, Philadelphia, led by Kumar Sharma, M.D., director of Jefferson’s Center for Diabetic Kidney Disease, reported on the results during Renal Week in November 2005 at the American Society of Nephrology in Philadelphia.
The researchers worked with two sets of mice. They found a significant negative correlation between the urine albumin and levels of the hormone adiponectin in obese mice. To prove the relationship, they also studied mice without adiponectin (“adiponectin knockout”) compared to wild-type mice whose levels were normal. The team found that the knockout mice had three times the level of urine albumin than the wild-type mice.
In a separate study Jefferson researchers measured the adiponectin levels of a group of obese African American adolescents. They found similar results—subjects who had a low level of adiponectin also had the condition known as albuminuria—as indicated by high levels of the protein albumin in their urine. Albuminuria is an indicator for kidney disease.
“We found that people with obesity who have low adiponectin levels also have albuminuria,” explains lead author Kumar Sharma, M.D., who is also professor of Medicine at Jefferson Medical College of Thomas Jefferson University. “The data also suggest another piece of the puzzle that shows why obese people who have what is known as metabolic syndrome are at risk for, and are dying of, heart disease.” The metabolic risk syndrome is a combination of medical disorders that is a risk factor for cardiovascular disease.
“Cardiovascular risk factors that regulate albuminuria in association with the metabolic syndrome have not been established,” Dr. Sharma said. “As a next step, we would like to learn how levels of adiponectin become reduced in obese people. Then we can develop the treatments to offset this activity.”
Also contributing to the study are Bonita Falkner, M.D., professor of Medicine and Pediatrics at Jefferson; Barry Goldstein, M.D., Ph.D., professor of Medicine and director, Division of Endocrinology and Metabolic Diseases, Jefferson; Stephen Dunn, assistant professor of Medicine, Division of Nephrology, Jefferson; and Lawrence Chan, M.D., Ph.D., professor of Medicine at Baylor College of Medicine, Houston.
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