The secretion of hypothalamic, pituitary, and target tissue hormones is under tight regulatory control by a series of feedback and feed- forward loops. This complexity can be demonstrated using the growth hormone (GH) regulatory system as an example. The stimulatory substance growth hormone releasing hormone (GHRH) and the inhibitory substance somatostatin (SS) both products of the hypothalamus, control pituitary GH secretion. Somatostatin is also called growth hormone-inhibiting hormone (GHIH). Under the influence of GHRH, growth hormone is released into the systemic circulation, causing the target tissue to secrete insulin-like growth factor-1, IGF-1. Growth hormone also has other more direct metabolic effects; it is both hyperglycemic and lipolytic. The principal source of systemic IGF-1 is the liver, although most other tissues secrete and contribute to systemic IGF-1. Liver IGF-1 is considered to be the principal regulator of tissue growth. In particular, the IGF-1 secreted by the liver is believed to synchronize growth throughout the body, resulting in a homeostatic balance of tissue size and mass. IGF-1 secreted by peripheral tissues is generally considered to be autocrine or paracrine in its biological action.
Several studies concluded that diets low in fat (under 15% of total calories) significantly decreased testosterone levels while diets higher in fat (above 30% of total calories) increased serum testosterone levels. Rather than continuing with this discussion I will provide a link to an article which covers the subject quite nicely. To simplify everything that I have said, it seems that one should not lower fat below 15% of daily calories unless they would like to face extreme testosterone deficiencies. Likewise, one should not increase fat to say 40% in order to increase testosterone. Although fat increases testosterone to a degree, it is important to remember that testosterone is only a small piece of the larger puzzle. There are many other hormones and factors involved in building muscle other than just testosterone. By increasing fat to extremely high levels, there will be less “space” for carbohydrates and protein, both of which are very important for aforementioned reasons.
In males with delayed puberty: Various dosage regimens have been used; some call for lower dosages initially with gradual increases as puberty progresses, with or without a decrease to maintenance levels. Other regimens call for higher dosage to induce pubertal changes and lower dosage for maintenance after puberty. The chronological and skeletal ages must be taken into consideration, both in determining the initial dose and in adjusting the dose. Dosage is within the range of 50 to 200 mg every 2 to 4 weeks for a limited duration, for example, 4 to 6 months. X-rays should be taken at appropriate intervals to determine the amount of bone maturation and skeletal development (see INDICATIONS AND USAGE and WARNINGS ).