Obesity is a serious health issue impacting overall well-being, contributing to chronic conditions like heart disease, diabetes, and even affecting reproductive function. While it’s long been understood that obesity reduces fertility, the exact mechanism remained a mystery – until now.
A research team led by the University of California- Riverside discovered in a mice study that obesity causes chronic changes in the brain which affects sperm count.
The study published in the Journal of Neuroscience explains how obesity induces brain changes, leading to a significant reduction in neuronal connections. This, in turn, reduces the number of receptors that signal to the brain when enough energy is available, thereby regulating food intake.
“This may explain why we don’t stop excessive calorie intake,” Djurdjica Coss, who led the study, said in a news release.
The researchers also noted that overweight mice have lower testosterone in their blood and reduced sperm count. This is attributed to the dysregulation of the hypothalamus-pituitary-gonadal axis. The hypothalamus controls food intake, temperature, thirst, and reproduction. It manages hormone secretion from the pituitary gland, which regulates testosterone and sperm production in males and estrogen and ovulation in females, Coss explained.
“When these neurons in the hypothalamus are not functioning properly, as in obesity, it causes lower hormone levels from the pituitary gland and lower testosterone and sperm production. To our surprise, we found the primary site of obesity’s effects is the brain, rather than the testes or pituitary, in disrupting the normal functioning of the neurons that regulate reproduction,” Coss said, adding that the brain mechanism she observed in the lab mice exists in humans.
The researchers also noted that a high-fat diet reduces the brain synapses, the places where neurons connect and communicate with each other.
“We counted the numbers of synapses in the neurons that regulate reproduction in the brain and identified fewer synaptic connections in the mice that were fed high-fat diet. We still don’t know exactly how this happens, but now, after identifying specific neuronal populations and specific synaptic molecules that are affected by obesity, we can focus our future studies in trying to understand these observations,” Coss added.
The study has not explored if brain changes can be passed down through genes. The researchers plan to examine next if the brain changes induced by obesity can be reversed by switching the mice fed with a high-fat diet back to a normal diet.
“For many people, the fight against obesity is a losing battle. We hope to show that after a certain amount of time following weight loss, the brain is able to reset the body’s food intake, which would help people struggling to lose weight,” Coss said.
