HE TERM ‘insulin hypersensitivity’is generally used to denote a greater than normal response to insulin. In the whole animal this is manifested by an exaggerated hypoglycemic response. Thus an injection of insulin results in a greater fall in the blood glucose level than in the normal animal, and is followed by a delayed return of the blood glucose concentration to the control level. It is apparent that the term is descriptive and not indicative of the underlying metabolic disturbances. It gives no indication whether the disturbances are in the processes responsible for the removal of glucose from the plasma and its subsequent utilization and transformation, or in the processes contributing to the replacement of the removed plasma glucose.

Numerous pathological conditions may be accompanied by an exaggerated response to insulin, but this review will be limited to the insulin hypersensitivity states which are attributable to endocrine deficiencies, and particularly those induced experimentally. Extirpation of various endocrine glands, especially the pituitary and adrenal glands, leads to development of insulin hypersensitivity. The first part of this review will deal with a) characterization of this disturbance, b) discussion of the factors contributing to it, and metabolic disturbances