Insulin sensitivity of insulin dependent tissues (muscle, adipose tissue, liver) is subject to a variety of influences. Any change in insulin sensitivity is compensated in healthy subjects by a dynamic change in insulin secretion, which will decrease following a rise in insulin sensitivity and increase if insulin sensitivity is impaired (i.e. during insulin resistance induced by obesity, pregnancy, oral contraceptives, dehydration, saturated fatty acids, fever, drugs, etc.). In contrast to secondary insulin resistance idiopathic insulin resistance in type 2 diabetic individuals is associated with impaired insulin secretion, which thus is unable to overcome impaired insulin sensitivity. Idiopathic insulin resistance in type 2 diabetes is additionally characterized by reduced glucose storage, the basis of which may reside in an insulin receptor defect, in the presence of insulin receptor antibodies, in a postreceptor defect or in the synthesis of abnormal insulin molecules.