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This article originally posted 08 May, 2007 and appeared in  Issue 363
Diabetes Damaging Men's Sperm
Diabetes may be damaging to sperm, which could affect men's fertility
In one of the first studies to compare DNA in sperm from diabetic and non-diabetic men, the researchers found more DNA damage in sperm cells of men with diabetes -- a possible sign of reduced fertility.

Researchers at Queen's University in Belfast, Northern Ireland, studied sperm from 27 men with type 1 diabetes, with an average age of 34, and 29 non-diabetic men of similar age.

They found that while semen volume was lower in diabetic men, all other measures including sperm concentration, output, form, structure and ability to move appeared normal.

However, when they looked at the DNA, they found much more damage in the sperm of diabetic men.

Sperm damage can impair male fertility and has been associated in couples with a history of miscarriages, the team notes in the journal Human Reproduction.

They recruited their volunteers from a center for endocrinology in Belfast and among men who had sought to have their fertility tested. Because the volunteers who were not diabetic were men seeking fertility treatment, the researchers said they may also have more damaged sperm than the average man.

"Any significant differences demonstrated between diabetic men and this control group would be of even greater significance if compared with a fertile population," they write.

The study concluded that: "Diabetes is associated with increased sperm nuclear and mtDNA damage that may impair the reproductive capability of these men."  Deletions and fragmentation of DNA results in loss of genetic material which, in the case of nuclear DNA, causes infertility as the sperm is not able to deliver its full complement of genetic codes in fusion with the egg to create a viable embryo.

Mitochondrial DNA (MtDNA) is found in mitochondria -- tiny "power-stations" inside cells that make energy to fuel cell activity.  In humans and many other organisms, sperm cell mitochondria are destroyed when the sperm's nuclear DNA combines with the egg's nuclear DNA and only the egg's mitochondria go on to survive in the new individual.

A number of studies have suggested that high levels of mtDNA deletions in sperm cells is linked to lower fertility in men.

Dr Agbaje said: "As far as we know, this is the first report of the quality of DNA in the nucleus and mitochondria of sperm in diabetes. Our study identifies important evidence of increased DNA fragmentation of nuclear DNA and mitochondrial DNA deletions in sperm from diabetic men."  "These findings cause concern, as they may have implications for fertility," he added.

Dr Agbaje suggested that: "If the increasing trend in the incidence of type I diabetes continues, this will result in a 50% increase over the next ten years. As a consequence, diabetes will affect many more men prior to and during their reproductive years."

"Infertility is already a major health problem in both the developed and developing world, with up to one in six couples requiring specialist investigation or treatment in order to conceive," he added.

The researchers point out that semen quality has been declining over the last 50 years and poor sperm is thought to cause infertility in 40 to 50 per cent of infertile couples.

"The increasing incidence of systemic diseases such as diabetes may further exacerbate this decline in male fertility. However, it is not clear to what extent clinics consider information about the diabetic status of their patients when investigating fertility problems," said Dr Agbaje.

The researchers said the study was small and more research was needed to understand just how diabetes damages sperm and what it might mean. Given the rise in diabetes globally, the issue may be of increasing concern, they said.
journal Human Reproduction May 2007; "Insulin dependant diabetes mellitus: implications for male reproductive function." I.M. Agbaje, D.A. Rogers, C.M. McVicar, N. McClure, A.B. Atkinson, C. Mallidis, and S.E.M. Lewis.Hum. Reprod. Advance Access published on May 3, 2007.  Click here for Abstract.

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This article originally posted 08 May, 2007 and appeared in  Issue 363

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