In 106 type II diabetics with persisting hyperlipidemia (i.e. persistently increased triglycerides greater than 200 mg/dl during intensive diabetes therapy) the Apo E polymorphism was examined in relation to IDDM (n = 68) and NIDDM (n = 38). It was shown that Apo E2 phenotypes are more (22.6% vs. 14.5%, p less than 0.05) and Apo E3 phenotypes less frequent in type II diabetics than in non-diabetic controls (86.8% vs. 94.7%, p less than 0.001). Looking at the increase in Apo E2 phenotypes it could be proved that the phenotype composition was distinctly different between diabetics with and in those without insulin therapy. While in NIDDM the increase was consequent to a higher concentration of Apo E2 homozygotes (p less than 0.005) it was caused by Apo E2 heterozygotes in IDDM (p less than 0.025) accompanied by a simultaneous decrease in Apo E3 homozygotes (p less than 0.025). Regarding blood lipids there was an increase in total cholesterol due only to VLDL cholesterol in IDDM as well as in NIDDM. It is concluded that in spite of similar hyperlipidemias in type II diabetics the increase in Apo E2 phenotypes is different; it is induced by heterozygotes in IDDM and by homozygotes in NIDDM.