“At the same time that hormones challenge the pubertal brain, they change the body. A girl’s high estrogen content helps in the deposition of body fat on the breasts, hips, thighs and buttocks, subcutaneously, everywhere. Because of estrogen and auxiliary hormones, women have more body fat than men…..We can look at the deposition of body fat that comes with womanhood and say it’s natural for girls to fatten up when they mature, but what ‘natural’ means is subject to cultural definition, and our culture still hasn’t figured out how to handle fat.” –Natalie Angier1
Sigmund Freud, the Austrian psychiatrist, may have been correct when he said that the “characteristics of what is male and female can be only be demonstrated in anatomy”. Although modern psychologists may no entirely agree because there may be inherent psychological differences as well. Apart from psychological issues, there are many evident physical gender differences. Depending on gender the typical shape of the adult human is often referred to as resembling an “apple or pear”. Adult men tend to accumulate bodyfat in the abdominal area and low back (called android deposition). Women’s bodyfat is generally deposited over the lower abdominals, buttocks and thighs (called gynoid deposition). These patterns of bodyfat deposition are similar to the shapes of apples (men) and pears (women). Deviations from these stereotypes do exist, such as in cases of insulin resistance and obesity in men and women. As well, a shift in bodyfat deposition occurs in post-menopausal women. Some physiology dysfunctions, such as Cushing’s disease, may cause bodyfat to be deposited in non-stereotypic patterns. Nevertheless, normal healthy adults tend to accumulate bodyfat following gender patterns.
One of the factors responsible for these differences in bodyfat deposition is our hormonal constitution. As we already know, the primary sex steroid in women is estrogen; in men, testosterone. How does this affect bodyfat deposition? After a brief description of the structure of fat, we will discuss the implications of estrogen and testosterone.
All fat is not created equal
Fat cells, or correctly called ‘adipose tissue’, are actually types of connective tissue, which provides structural and metabolic support for the body. Adipose tissue is responsible for storage and metabolism of fat for other tissues and organs in the body. It also supplies cushioning for some organs, such as the kidneys, and other areas of the body, such as the fat pads on our feet and hands.
Importantly, there are different kinds of bodyfat. Depots of adipose tissue are commonly referred to based on their location in the body. Visceral fat surrounds various internal organs in the body cavity, such as the kidneys and lymph glands. Accumulation of visceral adipose tissue in the innermost abdominal area is associated with increased risk factors for cardiovascular disease and Type 2 diabetes. Consequently, both men and women with large depots of abdominal visceral bodyfat are often counciled to partake in weight reduction programs.
Most of the total amount of bodyfat fat is deposited nearer to the outer surface of the body and called subcutaneous adipose tissue. This outer layer is actually composed of three layers of fat separated by sheets of connective tissue (septa) that carry blood vessels and nerves fibers. The predominant layer, often the middle layer, contains lobules that are oblong or rectangular shaped, standing somewhat upright. Thin layers of connective tissue separate these lobules and run perpendicular or diagonal and anchor the fat cells to the overlying dermal tissue. The connective tissue running between the fat lobules differs in men and women. In women, the lobules are larger and rectangular with the septa running perpendicular to the dermal layer. They look similar to tall boxes standing on end. Lobules in men are smaller and the septa run more diagonally, resembling small irregular-shaped lumps.
When fat lobules in the uppermost layer expand or when the tissue retains water (as in edema), the adipose tissue distorts the septa and projects into the dermis, extending the dermis and causing a quilting pattern in the skin. This is popularly referred to as ‘cellulite’, and is more commonly seen in women than men for several reasons. The upper layer of adipose tissue in men is thinner and the connective tissue separating the fat lobules has a different distribution. Also, the dermal layer in men is thicker and, therefore, is more resistant to protuberance.
German investigators showed that our fat structure is determined during fetal development and primarily associated with sex steroids. Toward the end of the third trimester and at birth, structure differences in adipose tissue and the dermis are apparent and conforming to those seen in females and males. The testis becomes hormonally active in the male fetus during the sixth to eighth month, whereas the ovaries are inactive in the female fetus. Authors hypothesize that androgenic hormones influence the fibroblasts from which adipose tissue and connective tissue are derived, and produce a denser connective tissue. Changes in adipose tissue structure are seen in adult women who receive long-term testosterone treatment, where the septa become thicker, confirming influences of sex hormones.
Historically, physiologists have been taught that patterns of adipose tissue accumulation are determined shortly after birth. Increase in fat cell number (hyperplasia) takes place in the womb and during our early childhood. The number of fat cells is hypothesized to be determined by genetic and environmental factors. Apparently, fat cells have a volume capacity for storing lipids (fatty substances) and new fat cells may proliferate after that capacity is reached. However, this concept is still challenged in the literature. Some in vitro studies show that adipocytes can increase in number, possibly from fat cell precursors, but this has not been confirmed in in vivo studies. Hyperplasia of fat cells in adults has been documented only in cases of extreme obesity.
During adulthood, our residing fat cells accumulate droplets of fat and grow in size (hypertrophy). Histological (the microscopic anatomy of tissues) studies have shown that as fat cells are depleted of lipids, as in dieting, they structurally collapse waiting to be refilled. Convention also teaches us that fat cells cannot be destroyed. It has yet to be confirmed if fat cells can actually be destroyed (i.e. ‘killed’) as some people have hypothesized. So, what determines the differences in number and volume of fat cells in different regions of the body?
Regional and gender differences in adipose tissue
“But although a bearer of a rather prominent belly, I still have the bottom of my leg lean and the nerve salient as an Arab horse’s.” –Brillat-Savarin2
Rudolph Leibel (Rockefeller University, New York, NY), who has researched the differences in bodyfat distribution, aptly states “The amount of adipose tissue in any anatomical region of the body reflects both adipocyte size and number in that region.” As we know anecdotally and by research, women have larger deposits of fat mass on the lower body than men do. Conversely, men have greater fat mass in the abdominal region than premenopausal women. Histological studies show that adipocytes taken from the buttocks and thighs of premenopausal women are larger in size compared to those of men taken from the same area. However, fat cells taken from the abdominal subcutaneous area in both men and women are of similar size. Additionally, men have more visceral fat than women do. However, differences in the number of fat cells in specific areas may be responsible for the overall size of subcutaneous fat depots.
Regional differences exist within a sex as well. Fat cells from women’s buttocks and thighs are larger than the fat cells in their abdominal area. However, studies show that fat cells from visceral fat in men are equal in size or larger than depots of subcutaneous fat. Conversely, visceral fat cells in females are generally smaller than subcutaneous fat cells. Ultimately, abdominal subcutaneous fat mass in men is largely due to increased fat cell number. The factors directly responsible for regional fat cell number are not clearly understood. Scientists continue to study bodyfat deposition that occurs with specific endocrine dysfunctions, such as Cushing’s disease and androgen excess, to possibly explain the mechanisms responsible for regulating fat cell number. Unfortunately research lacks reliable methods to accurately determine whether increases in fat cell number occur with weight gain or hormone-related fat cell redistribution.
Metabolic control of fat cells
Metabolic activity of the fat cell is controlled mostly by two classes of hormones: insulin and the catecholamines (epinephrine and norepinephrine). These hormones influence the volume of fat cells by regulating the lipids stored inside and released from the cells. Insulin is the main regulator of fat synthesis within fat cells, although the role of insulin in determining bodyfat deposition has not been adequately studied. Some studies have determined that, after eating a meal, fat cells from the abdominal subcutaneous region in both men and women are more sensitive to the effects of insulin than those fat cells in the thigh and visceral areas. Other site- or gender-specific effects of insulin are not well demonstrated.
The catecholamines are the primary regulators of fat metabolism (lipolysis) in fat cells. The adrenergic receptors on the fat cells are mediators of these hormones’ effects. Stimulation of the beta-adrenoceptors (b-AR) prompt the breakdown of stored fat into products that are usually released from the fat cells and circulated to tissues and organs for fuel. Stimulation of the alpha2-adrenoceptors (a2-AR) puts the brake on b-ARs; that is, the a2-ARs prevent fat breakdown. Consequently, several authors have hypothesized that the relative numbers of b-ARs and a2-ARs largely controls the rate of fat breakdown in a fat cell.
Researchers confirmed that fat depots in the buttocks in both men and women have high levels of a2-AR activity that inhibit fat burning in those areas. Considering that women have more and larger fat cells in the buttock and thigh area than men, there is an overall tendency to store fat rather than breakdown fat in that region. Conversely, fat depots in the abdominal sites have higher b-AR activity. Although some studies indicate that women may have lower levels of b-AR activity in the buttock area, men and women have approximately equal a2-AR receptor activity. Women, however, have less a2-AR activity in the abdominal area. This may explain why men tend to accumulate more fat in this region.
Agreeing with what we see anecdotally, estrogens and progesterone may be associated with differences in site-specific fat accumulation in women. Sex hormones may influence the activity (most likely, the number) of the adrenergic receptors on fat cells, but this has not yet been confirmed in humans. Sex hormones also influence fat and carbohydrate metabolism throughout the body, which can have indirect influences on fat accumulation and breakdown. Also, sex steroids may not be the only hormones that explain site- and gender-related differences in fat accumulation. There is some evidence that catecholamine levels differ at rest and during stress in women and men. Bearing in mind that catecholamines regulate the rate of fat breakdown in adipose tissue, such variations in catecholamine levels may contribute to other regulatory factors (such as blood circulation). Can we use these known differences to predict fat loss when dieting or exercise?
Effects of diet and exercise
If status of adrenergic receptors play such an important role in fat accumulation and breakdown, one would suspect those fat depots with higher b-AR activity (e.g. women’s abdominal area) to lose fat faster than areas with higher a2-AR activity (e.g. women’s and men’s buttock area). Research has confirmed that compared to subcutaneous abdominal depots, visceral abdominal fat depots are preferentially reduced in response to dieting with and without exercise. Since the adipose tissue in women’s lower body is reportedly more resistant to catecholamine stimulation than men, we would expect men to lose more fat in their lower body than women during a diet or exercise. However, one study showed that this was not the case. There were no sex-related differences in fat loss during dieting and exercise. Nevertheless, results from this study must be used with caution because study subjects had a preponderance of upper-body obesity rather than typical gender-related patterns of obesity. Additionally, these patterns of fat loss may differ in non-obese men and women.
The same study showed in both genders that diet with exercise reduced abdominal fat more than lower-body fat, but not diet alone. This is consistent with other studies investigating bodyfat reduction regimes. The study also showed there were no sex-related differences in reduction of total bodyfat or in the lower body with diet or diet with exercise. A major finding was the preservation of skeletal muscle with exercise and diet versus diet alone. Another important implication of diet with exercise is that the increased reduction of visceral fat reduces metabolic risk factors, such as insulin resistance and cardiovascular disease.
While we are still unclear how female and male hormones influence bodyfat deposition, we know that a diet and exercise program will reduce overall fat deposition. We also know that both diet and exercise preferentially reduce visceral abdominal fat and increase health benefits. Including exercise in a weight reduction program also helps preserve skeletal muscle mass whereas dieting alone may not. In conclusion, I close this column with an appropriate quote:
“So we must exercise and control our bodies, because our natural lives won’t do it for us.”1