Do any of the agents used as ergogenic aids by athletes and bodybuilders cause insulin resistance? Over the years there have been a number of studies done on how androgens affect glucose sensitivity, some of them conflicting. Virtually all studies show that low testosterone causes insulin resistance. One of the most recent studies done in humans showed that supraphysiological testosterone had no effect on insulin sensitivity but nandrolone actually improved it (29). The doses were 300 mg/week.
In another recent study 600 mg of testosterone enanthate per week had no effect on glucose sensitivity in normal adult men (30). This is the highest dose that I've seen used in any studies. However, when 500 mg of testosterone was administered to obese men, glucose tolerance decreased, while 250 mg increased glucose tolerance (31). Obesity could be having an effect here, as the previously mentioned negative studies were done in non-obese individuals.
Hyperandrogenism is often associated with insulin resistance in women. Whether this is merely an association or an actual causal relationship is debated. In agreement with the latter hypothesis, when normal women were administered methyltestosterone, insulin sensitivity deteriorated (32). This could have widespread implications for women’s health as androgen administration becomes more common in the treatment of menopausal symptoms and sexual dysfunction
In other studies in animals, there appears to be a "window" of testosterone levels around the normal range that optimize insulin sensitivity (33).
So you can see why there is some confusion. We don't know what happens when androgen doses exceed 600 mg/week (It is hardly uncommon for bodybuilders to use doses of anabolic steroids far in excess of 600 mg/wk.), and studies in animals have given results in conflict with those done in men, but in agreement with studies performed in women. And the particular compound used seems to make a difference.
One anabolic agent that unquestionably is capable of causing (temporary) insulin resistance is recombinant human growth hormone, hGH. This side effect of hGH is discussed in detail in the M & M # 14 article on GH use to treat obesity, so I will refer interested readers to that piece for more information.
Hyperthyroidism is associated with elevated plasma glucose, and when rats are given high doses of thyroid hormone both fasting glucose and plasma glucose in response to a glucose load are elevated (34). This hyperglycemia does not appear to be the result of any thyroid hormone induced defect in insulin signaling, but rather decreased insulin secretion in response to glucose. The deceased insulin secretion is most likely a result of thyroid hormone induced apoptosis (programmed cell death) of pancreatic beta cells (35). A second factor contributing to the hyperglycemia seen in hyperthyroidism is increased gluconeogenesis (36). So technically, the elevated plasma glucose seen when supraphysiological doses of T3 or T4 are administered is not due to insulin resistance, but rather to lowered insulin production and increased glucose production from glucogenic substrates.