Insulin therapy may reduce cardiovascular disease in diabetics
Diabetics are more susceptible to the development of atherosclerosis than non-diabetics. According to a new study, published in the February issue of The American Journal of Pathology, insulin therapy might help repair atherosclerotic lesions in diabetic patients. Researchers at the Hospital for Sick Children and the Department of Laboratory Medicine and Pathobiology, University of Toronto reported that insulin applied in therapeutic doses selectively stimulates the formation of new elastic fibers in cultures of human aortic smooth muscle cells.
The researchers noted that their results advance the understanding of the molecular and cellular mechanisms of diabetic vascular disease.
“Our results particularly endorse the use of insulin therapy for the treatment of atherosclerotic lesions in patients with type 1 diabetes, in which the induction of new elastic fibers would mechanically stabilize the developing plaques and prevent arterial occlusions,” explained lead investigator Aleksander Hinek, MD, PhD, DSc, Professor, Division of Cardiovascular Research at the hospital. Type 1 diabetes is also known as juvenile, or early onset, diabetes because it appears at a young age, sometimes in infancy. Type 2 diabetes appears in adults; obesity is commonly linked to type 2 diabetes.
Primary insulin deficiency and decreased cellular sensitivity to insulin (insulin resistance) have been associated with the development of atherosclerosis, impaired healing, and hypertension. Arterial damage increases the risk of myocardial infarctions (heart attacks) and strokes. The investigators set out to determine whether determine whether low therapeutic concentrations of insulin would promote the production of elastic fibers in tissue cultures of human aortic smooth muscle cells.
The researchers found that insulin did indeed stimulate the deposition of elastic fibers in the tissue cultures. They noted that their results demonstrated, for the first time, that low doses of insulin induce the elastogenic effect solely through the activation of insulin receptor and trigger the downstream activation of the P13K signaling pathway. In addition, they explained, the ultimate up-regulation of elastic fiber deposition by insulin is executed through two parallel mechanisms: the initiation of elastin gene expression and the enhancement of tropoelastin secretion.