Circadian rhythms of insulin needs and action are a frequently discussed issue that is both of considerable physiological interest and of clinical importance in case of insulin substitution in type 1 diabetes. Basally, insulin is released in a pulsatile fashion which seemingly is erratic but at close analysis displays 'free-running' cyclical rhythmicity of 8-30 min duration that possibly guarantees optimal insulin action. This basal mode of insulin secretion is subject to a multitude of endogenous control systems that act on the B-cell both in a stimulatory (e.g., beta-agonists, glucagon as well as glucose and amino acids) and an inhibitory fashion (e.g., alpha-agonists, somatostatin). Since impairment of target cell sensitivity to insulin action and hyperglycemia may be caused by the stress hormones, cortisol, epinephrine and growth hormone included, with in part intrinsic rhythmicity, as well as by dehydration and by prolonged insulin withdrawal, a secondary feed-back signal on insulin release may easily be induced by rising blood glucose levels. In that modulators of insulin release and action are themselves secreted in a circadian fashion they tend to secondarily imprint the mode of insulin release. Therefore, any difference between a daily maximum and minimum in plasma insulin concentration besides its free-running short-term rhythmicity has to be regarded as a composite secondary circadian rhythm. It is in particular due to variable secondary early-morning and late-afternoon insulin resistance.