Ever wonder why there isn’t a birth control pill for men?

Part of the reason is that the physiological mechanisms governing sperm production in men are less well understood than those governing ovulation in women.

Androgens are known to play a key role in normal sperm production and male fertility generally, but the mechanism by which androgens exert these effects had been largely unknown.

Now, a recent paper published in the FASEB Journal may have shed some light on the matter.

In the paper, Michelle Welsh and colleagues at the Centre for Reproductive Biology in Edinburgh studied androgen levels and sperm production in 2 groups of mice. The first group was normal, but the second had been engineered such that the peritubular myeloid cells in their testes lacked a particular gene that codes for an androgen hormone receptor.

In latter group, testis weight did not increase normally at puberty, and by the time they matured to adulthood they could produce only about 14% as many sperm cells as their normal counterparts. The findings were not explained by differences in testosterone, luteinizing hormone, or follicle-stimulating hormone levels.

The authors concluded that androgen action on the peritubular myeloid cells was therefore essential for normal testis function, spermatogenesis, and fertility in male mice, and seemed quite confident in their write-up that the findings would be easily reproduced in other mammals including humans.

“This study…could provide new insight for the development of new treatments for male infertility and perhaps new male contraceptives,” Welch told BurrillReport.
 
“Not only does this research pinpoint androgenic hormones and their cellular receptors as prime targets for the development of new birth control drugs, but it promises to speed the development of new agents to boost sperm production,” added Gerald Weissmann, who edits the FASEB Journal.

Looking for another reason to avoid the Greasy Spoon on your lunch break?

Oxford University scientists have provided a doozy. In their study, rats receiving a fat-laden diet exhibited a 50% reduction in exercise capacity and diminished cognitive skills after just 9 days.

The findings could have implications for Average Joes who eat Sloppy Joes for lunch, athletes in search of an edge, and people at risk for metabolic syndrome and diabetes, say the authors who published their findings in the FASEB journal.
 
“We found that rats, when switched to a high-fat diet from their standard low-fat feed, showed a surprisingly quick reduction in their physical performance,” lead author Andrew Murray told BurrillReport.
 
The physiology behind the observations is fairly well understood. Exercise endurance is a function of the amount of oxygen that can be delivered to muscles and the efficiency with which muscles can extract the energy contained within the chemical bonds of the nutrients supplied to them (a process known as oxidation)

Fat oxidation is less efficient than the oxidation of simple carbohydrates like glucose.

For their study, Murray and Co. fed 42 rats a standard diet containing 7.5% fat, and measured exercise capacity as the maximal time they were able to run on a treadmill. They assessed short-term memory in the subjects using a maze task.

The scientists then switched half the rats to a diet in which 55% of the calories were derived from fat and reassessed the rats’ endurance and cognitive abilities.

Junk food diets can easily approach the 55% fat content used by the scientists.
 
By day 9, rats on the high fat diet managed to run only half as far as their counterparts. They were also making mistakes about 17% earlier in the maze task, suggesting diminished cognitive skills.