Obesity reduces testosterone and sperm count

Obesity reduces testosterone and sperm counts by disrupting brain circuits, according to a new study published in The Journal of Neuroscience.

Obesity: what are the objectives of the study?

“One of the long-term goals of my research is to identify the molecular and cellular mechanisms that regulate the reproductive function, which is necessary for the survival of the species,” says the author of the essay Djurdjica Coss, a professor at the University of California.

“My research is also important for people struggling with unexplained infertility. It is also essential for the survival of endangered species whose preservation depends on assisted reproduction,” he adds.

“The rise in infertility in the Western world has coincided with the increasing prevalence of obesity, which now affects 35% of individuals in the United States,” he continues. “Obese people have a higher incidence of various diseases, including reproductive disorders” he completes.

Obesity: tests carried out on male mice

To replicate the effects of obesity in men, Djurdjica Coss and her team used male mice fed a high-fat diet. These animals were compared to a control group fed a standard diet.

After 12 weeks of experimentation, the researchers measured levels of luteinizing hormone (LH), an essential component of testosterone production and sperm development, in all rodents.

The team also evaluated two groups of neurons in the hypothalamus:
– proopiomelanocortin (POMC) neurons, which play a role in regulating energy balance and food intake;
– kisspeptin neurons, which are essential for controlling the release of gonadotropin-releasing hormone (GnRH) and therefore luteinizing hormone.

Obesity: what are the results of the study?

The researchers then found that obesity led to significant changes in the brain’s reproductive circuits. In obese mice, the frequency of luteinizing hormone (LH) pulses was reduced, leading to lower testosterone levels and sperm counts.

The chronic effects of obesity also suppressed the activity of kisspeptin neurons, which are essential for triggering the release of GnRH and LH.

Another important finding was that glutamate signaling was reduced in obese mice.

“The magnitude of the changes has been surprising,” says Djurdjica Coss. “Our analyses demonstrated that the brain is the primary site of the impact of obesity on reproductive function, particularly at the level of neuronal populations that regulate the reproductive hormone axis and food intake,” he summarizes.

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