Î Visceral fat WHR
| Glucose tolerance | Insulin sensitivity J, Cholesterol
— glucose tolerance
J, Cholesterol J, Cholesterol
WHR, waist-to-hip ratio; tol, tolerance.
pose tissues (23). Lipid mobilization is stimulated in abdominal, but not in femoral, fat and evidence from rats (24) suggests that this might be more pronounced in visceral than in s.c. adipose tissue.
The total effects of testosterone on intra-abdominal tissue may, therefore, be to inhibit uptake and increase the mobilization of triglycerides in intraabdominal adipose tissue depots (Figure 32.2). Low testosterone values would then presumably result in lipid accumulation in the visceral fat region, a phenomenon frequently seen in men with abdominal distribution of adipose tissue.
The effects of testosterone on adipose tissue metabolism are probably mediated via a specific androgen receptor that in the rat shows marked regional differences in density, being higher in visceral than in s.c. adipose tissue (25). Therefore, it is suggested that the regional different effects of testosterone may be explained by differences in androgen receptor density.
Although the primary treatment of obesity is to induce a negative energy balance the prognosis of dietary treatment is poor with a high rate of relapse (26). Furthermore, there is currently no specific treatment of visceral obesity except surgery, which shows some promising results (27) but so far is only offered to the most obese subjects. Since aberrations in the sex steroid hormonres seem to be of major importance in the pathogenesis of visceral obesity several studies have recently been focused on the effect of hormone treatment.
Marin (28) treated abdominally obese men with low baseline testosterone values with two types of androgens, testosterone and dihydrotestosterone (DHT) for 8 months. Testosterone substitution was followed by a decrease in visceral fat mass, cholesterol, systolic and diastolic blood pressure, blood glucose and an increase in insulin sensitivity, whereas DHT treatment resulted in no such beneficial effects (Table 32.2). On the contrary, there was even an increase in visceral fat mass with DHT substitution. The rationale for testing DHT was that this androgen is generally considered to be the hormone acting on target tissues.
The explanation for these different results is presently unclear, but an obvious hypothesis is that testosterone has other important physiological functions in the body than to act only as a sex steroid on its target organs. It may be hypothesized that the specific regulatory effect of testosterone on the visceral adipose tissue is a more important background mechanism for the improvement in metabolic risk factors, than the sex steroid effect on different target tissues. This hypothesis is supported by recent identification of both testosterone and dihydrotestosterone receptors in intra-abdominal adipose tissue in man (29).
It is also possible that an increase of insulin sensitivity is the primary event followed by amelioration of metabolic risk variables and blood pressure, which are all closely dependent on insulin resistance. Supporting this hypothesis are the findings in male rats, where normalization of insulin sensitivity after castration was seen already after 48 hours of testosterone treatment (30).
Testosterone can be transformed to oestrogens by aromatization, particularly in the adipose tissue (31), but there was no evidence of increased oes-tradiol concentration in these studies, so obviously the observed effects of testosterone administration were those of testosterone alone.
However, there are also conflicting data on the beneficial effect of testosterone administration. Friedl et al. (32) observed no effect of short-term treatment with testosterone on glucose homeostasis in non-obese men (Table 32.2) and Lovejoy et al. (33) have recently reported that long-term treatment with testosterone in middle-aged obese males was followed by an increase in visceral fat, but a decrease in s.c. abdominal fat, whereas treatment with an anabolic steroid produced a decrease in visceral fat (table 32.2). The latter observation is inconsistent with previous findings of diminished glucose tolerance and insulin resistance in powerlif-ters ingesting anabolic steroids (13).
In the ageing male testosterone supplementation seems, though, to have positive effects on lipid profile but not on body fat (34) (Table 32.2).
There is no obvious explanation to the different outcome between these studies, but it may depend on difference in age, study population or the obese state per se. Because of this inconsistency further studies are warranted before testosterone treatment can be recommended to obese, hypogonadal men.
Previous studies have demonstrated that testosterone administration to women significantly increases the visceral fat depot and induces insulin resistance (15,35). However, in spite of these adverse effects there is currently considerable interest in the use of testosterone as a component of hormone replacement therapy for postmenopausal women (36).
Testosterone enhances sexuality and acts as an antiresorptive agent on bone, thus limiting bone loss (36), but testosterone should only be administered to women who are concurrently taking oestrogen replacement since otherwise the likelihood of adverse effects on lipids and insulin sensitivity is increased.
In men testosterone concentrations in the lower range are associated with accumulation of visceral fat and hyperinsulinaemia. Testosterone treatment may be followed by a decrease of insulin resistance and other metabolic risk factors, as well as, a specific decrease of the visceral adipose tissue mass, me diated by an inhibition of triglyceride assimilation and an enhanced turnover.
In women hyperandrogenicity is associated with enlarged visceral fat depots and insulin resistance leading to an increased risk of developing NIDDM and cardiovascular disease.
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