Insulin resistance in type 2 diabetes is a long-established fact and a target for therapeutic intervention. We present the case for there being similar resistance to testosterone causing a relative deficiency in the majority of cases of clinical onset of symptoms of deficiency of this hormone in the adult or comorbid conditions, especially metabolic syndrome. There are many parallels between resistances to the two hormones. This is seen in aetiology, age of onset, genetics, ethnicity, heredity, familial influences, association with obesity, links with viral diseases, and autoimmune conditions. Like diabetes, androgen deficiency can arise before birth, in early life, resulting in early onset, or later on leading to adult onset, with resistance playing a greater role. Similarly treatments such as weight loss and exercise have the effect of reducing resistance to both hormones. Clinical observations suggest that the duration of action of a standard dose of either pellet implants of testosterone, or an injection of testosterone undecanoate, might be a suitable measure of resistance to this hormone. Because of similar causation and co-existence of resistance to these two hormones in metabolic syndrome it is suggested that this may be new facet of the condition which because of its association with the male chromosome could be re-named as Syndrome-Y.