How to Improve the Fertility of Obese Boys in the Future?

Reproductive function in boys with obesity may be improved through weight loss, which could protect their fertility in adulthood, according to a study presented at the 59th Annual European Society for Paediatric Endocrinology Meeting.

The study suggests that even short-term weight loss can reverse the alterations in reproductive function in young boys with obesity. This study is published in the journal Hormone Research in Paediatrics.

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‘Early management of obesity in childhood can prevent future fertility problems.’

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Childhood obesity can have some profound effects on future health in adulthood, including a greater risk of cancer, heart disease, and type 2 diabetes.

Obesity is also been linked to fertility problems in both men and women. The commonest causes of fertility problems in men are usually sperm abnormalities or a low sperm count.

Leydig cells in the testes become active in puberty to produce the main male hormone, testosterone. Sertoli cells in the testes are critical for the production of healthy sperm and produce several reproductive hormones, essential for sperm maturation.

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Previous studies have shown that early alteration of Sertoli cell function from the age of 12, with later alteration in Leydig cell function from the age of 14 in obese boys. However, whether weight loss might reverse the altered function of these cells had not been investigated.

A new study investigated how a 12-week educational weight loss program in 34 boys, aged 10 – 18 years, affected Leydig and Sertoli cell function, as well as metabolism.

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The boys had a healthy, balanced diet, undertook physical activity for at least 1 hour per day, according to international recommendations, and had weekly individual sessions with a dietician.

Before and after the program, levels of reproductive hormones, body fat composition, and blood glucose were measured for comparison.

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After the 12 weeks, the boys significantly lost weight and had improved insulin levels, as well as increased testosterone levels. No significant changes were found in markers of Sertoli cell function.

Since fat cells produce an enzyme that converts testosterone to estrogen, the actual loss of fat mass may account for the increased testosterone levels, in addition to the reversal of Leydig cell altered function.

These findings underline the importance of childhood obesity as a factor in future fertility issues and recommend early weight loss is necessary to reverse these impairments.

This study only evaluated the effects in a small number of obese boys after a twelve-week therapeutic educational program. Further studies with longer follow-up are needed to help us fully study the effect of weight reduction on reproductive function.

Source-Medindia