Type 1 : Heredity is the cause. Several Genes are identified to predispose a person with type 1 DM. Some genes are genetically susceptible to infections by viruses (rubella, cytomegalovirus ), the antibodies built from our bodies attacks the beta pancreatic cells. Until a point where it cannot regulate sugar level in the body.
Type 2: It is not due to lack of insulin, but resistance to the insulin. Aka unresponsive. Certain ethnicity and environment plays a polygenic factor towards acquired Type 2 DM. Sedentary lifestyle shows that when muscle mass links with regulation of blood glucose, since muscle uses glucose, it is reasonably to say that it's important for regulating glycemia. It is known also that adipose tissue can secrete certain chemicals that prevent glucose transport to most kinds of cells- so more body fat means more glucose elevation.Therefore exercise can be a preventive measure.
Impact on Wound Healing
Chronic hyperglycemia can cause microvascular disease. In the skin, the vessels are poorly healed so it can easily ulcerate, becomes infected, and cause gangrene. The feet is the commonest example because blood supply to the distal part of body is poor, the feet also experience pressure making them susceptible to injury, and neuropathy cause a person to be unaware of the pain sensation to the lesion, so reluctantly the foot becomes amputated because of poor wound healing. ( they feel no pain when amputation ! No need pay for Anesthesia! )
Wound healing is slow
EPC endothelial progenitor cells are needed to regenerate wound healing at the lesion site. One study had found that when oxygen levels in diabetic mouse increase, hyperoxia increases the Bone marrow to mobilize the EPCs. High level oxygen activates enzyme Nitric Oxide (eNOs) that enhance production of EPCs. Increased presence of EPCs accelerates wound healing. SDF-1alpha factor helps guide EPCs to wound sites.
So the slow healing process is due to the SDF-1Alpha and eNOs impairment.
No comments:
Post a Comment