Women have long bemoaned the fact that they tend to store more fat than men, particularly after menopause. Although it's well established that estrogen, the primary sex hormone present during women's childbearing years, is responsible for this effect, exactly how estrogen exerts this influence has been unknown. Previous research has shown that body fat both absorbs estrogen and other sex hormones circulating in the blood as well as produces its own sex hormones, though researchers have been unsure what role that plays in fat accumulation. Also not completely understood is why women tend to accumulate fat in the stereotypical "pear" shape, with more fat in the buttocks and thighs—a shape that's thought to be healthier than men's stereotypical "apple" shape, with more fat around the belly.
Gathering clues to answer these questions, Kathleen M. Gavin and her colleagues at East Carolina University examined how estrogen locally affects fat accumulation in these key areas by slowly infusing the hormone into the buttocks and belly in overweight women while also giving them drugs or having them exercise to speed up fat breakdown. They found that estrogen's effects on these fat deposits was highly dependent on the deposits' specific location and the fat-burning interventions themselves.
The article is entitled "Estradiol Effects on Subcutaneous Adipose Tissue Lipolysis in Premenopausal Women are Adipose Tissue Depot Specific and Treatment Dependent". It appears in the June edition of the American Journal of Physiology: Endocrinology and Metabolism, published by the American Physiological Society.
Gavin and her colleagues recruited 17 overweight-to-obese premenopausal women, all between the ages of 18 and 44 years old. After an initial visit to the lab to gather a variety of information on each study participant, including weight, height, percent fat and lean mass, and VO2 max (a measure of physical fitness), the researchers subjected each participant to a variety of interventions meant to speed up lipolysis, or fat breakdown/mobilization. Through probes inserted directly in the fat of the participants' buttocks and abdomen, the researchers slowly infused two drugs, either individually or together, that encourage lipolysis. They also had participants perform a bout of exercise at an intensity similar to a standard exercise session. Such "submaximal" exercise is known to optimally break down fat.
Participants performed this exercise both by itself and while the drugs were being infused. To test the effects of estrogen, the researchers also performed each of these conditions while estrogen was also being slowly infused into participants' fat deposits. To measure fat breakdown, the researchers used a technique called microdialysis to look for a marker (glycerol) left behind when stored fat is broken down for eventual production of energy.
The researchers found that estrogen's effects differed tremendously depending on the fat- mobilizing interventions themselves and where the fat deposit was located. For example, estrogen blunted fat breakdown in the abdomen if it was infused while a particular fat-mobilization drug called isoproterenol was also being infused, but it didn't have this effect in the buttocks. When a second fat mobilizing drug was given along with the first while participants were at rest, fat breakdown didn't change any further. However, when both drugs were injected together during exercise or when the volunteers exercised without the drugs, fat breakdown increased in the abdomen, but less so in the buttocks.
Importance of the Findings
These results suggest that estrogen has different effects within fat tissue depending on its location. Together, these effects could help maintain premenopausal women's "pear" shape even in the face of exercise or other signals the body receives to break down fat. They could also help generate some new ideas on how estrogen in fat may influence why postmenopausal women tend to accumulate more fat in the abdomen.
The authors suggest that more research is necessary to better understand the mechanisms behind how and why estrogen acts in these differential ways.
More information: ajpendo.physiology.org/content/304/11/E1167.full.pdf+html