Published October 6, 2011 This content is archived.
UB researchers have found that estrogen produced by body fat does not cause low testosterone levels in Type 2 diabetic men.
Instead, they believe that the mechanism for hypogonadism, or low testosterone, resides in the hypothalamus, the part of the brain that controls hormones influencing appetite, sleep, moods and sex drive.
Their findings unequivocally refute conventional wisdom that an enzyme expressed by body fat is increased in obese people.
“It was thought that this enzyme increased estradiol levels in the blood, which led to suppressed testosterone levels,” says Paresh Dandona, MD, UB Distinguished Professor of Medicine.
But the connection is not that simple, he adds, partly because not all type 2 diabetics are obese.
In their study, the UB researchers evaluated 240 obese and non-obese men with Type 2 diabetes and low testosterone.
They discovered that the men's estradiol levels were lower, not higher, than normal.
“We now need to look for other mechanisms for the rational understanding and treatment of hypogonadism syndrome,” Dandona says.
“If we can elucidate the specific underlying mechanism, we can develop a treatment for this condition.”
Low estradiol levels and low testosterone both probably contribute to the markedly increased risk of cardiovascular mortality in Type 2 diabetics, he adds.
The same team of UB researchers was the first to identify hypogonadism, a leading cause of male fertility, in a third of Type 2 diabetic men that they studied.
They are now extending their observations to non-diabetic obese adults and children, a quarter of whom have low testosterone.
Based on previous work with experimental animals, they are exploring the role of insulin resistance at the level of the brain to elucidate the mechanism underlying the defect in testosterone production.
The UB researchers published their paper, titled “Low Estradiol Concentrations in Men With Subnormal Testosterone Concentrations and Type 2 Diabetes,” in Diabetes Care.
Sandeep Dhindsa, MD, assistant professor of medicine, is lead author; Dandona is senior author.