Diabetes is associated with changes in plasma
lipids and
lipoproteins into atherogenic direction. In
IDDM these changes are small or absent if good metabolic control can be maintained.
Diabetic nephropathy is, however, associated with the appearance of
dyslipoproteinemia. In
NIDDM plasma total and
VLDL triglyceride levels are elevated, and
HDL-cholesterol level is decreased, and this pattern of
dyslipoproteinemia does not always respond to improved control of
hyperglycemia. Abnormalities of
lipoprotein metabolism, not reflected in conventional plasma
lipid and
lipoprotein level measurements, and glucosylation of
lipoproteins and resulting alterations in
lipoprotein catabolism may be of importance in the enhanced
atherogenesis in diabetes. Both
IDDM and
NIDDM are associated with an increased frequency of
hypertension, but the underlying mechanisms appear to be different. In
IDDM hypertension is usually associated with the development of
diabetic nephropathy and thus with a long duration of the disease. In
NIDDM hypertension is often present already at the time of diagnosis, and also in IGT, the precursor stage of
NIDDM, the prevalence of
hypertension is already increased.
Obesity explains only in part the high prevalence of
hypertension in patients with
NIDDM. Diabetes is known to be associated with
multiple abnormalities in
hemostatic factors and, although these abnormalities may contribute importantly to the increased risk of ASVD in diabetic patients, information about their real role is scanty and conflicting. The impact of general major risk factors for ASVD, elevated plasma
cholesterol, elevated blood pressure, and smoking, on the risk of ASVD appears to be similar in diabetics and nondiabetics. Only a relatively small proportion of the excessive occurrence of ASVD in diabetics can, however, be explained by the effects of diabetes on the levels of general risk factors for ASVD. This proportion mediated through the effects of diabetes on risk factors is larger in female diabetics than in male diabetics. The major proportion of the excess of ASVD in diabetics remains, however, unexplained and must be due to effects of diabetes itself through mechanisms that are incompletely understood.