In: Anatomy and Physiology
Blood glucose regulation involves maintaing blood glucose levels at constant levels in the face of dynamic glucose intake and energy use by the body. Glucose, is the key in the energy intake of humans. On average this target range is 60-100 mg/dl for an adult although people can be assymptomatic at much more varied levels. In order to maintain this range, there are two main hormones that control blood glucose levels: Insulin and glucagon. Insulin is released when there are high amounts of glucose in the bloodstream. Glucose is released when there are low levels of glucose in the bloodstream. There are other hormones that affect glucose regulation and are mainly controlled by the sympathetic nervous system. Blood glucose regulation is very important to the maintenance of the human body. The brain doesn't have any energy storage of its own and as a result needs a constant flow of glucose, using about 120 grams of glucose daily or about 60% of total glucose used by the body at resting state without proper blood glucose regulation the brain and other organs could starve leading to death.
role of Insulin
1) Enhances entry of glucose into cells; 2) Enhaces storage of glucose as glycogen or conversion to fatty acids.3) Enhances synthesis of fatty acids and proteins.4) Supresses breakdown of proteins into amino acids, or adipose tissue into free fatty acids.
Role of glucagon
1) Enhances the release of glucose from glycogen( glyconeolysis). 2) Enhances synthesis of glucose (gluconeogenesis) from amino acids or fats.
A variety of molecules are expressed on the endothelial cell surface that allow the neutrophil to be captured, then roll along the endothelium, then adhere. Following adherence, the neutrophil migrates into the subendothelial tissue to reach the site of infection.
The neutrophil engulfs the bacteria and eliminates them via breakdown within the phagosomes- a process known as phagocytosis.
In states of hyperglycemia, chemotaxis is reduced. Adherence is also adversely affected. Phagocytosis is also impaired by hyperglycemia. Hyperglycemia also adversely affects macrophage system. Under normal circumtances, circulating monocytes are attracted to sites of infection, roll, adhere and then migrate into the sunendothelial space. The monocyte then transforms into a macrophage which is the activated by cytokines released by the bacteria. The activated macrophages then engulfs the bacteria. However, hyperglycemia results in decreased activation of macrophages, thereby arresting the process of macrophage phagocytosis of bacteria. In addtion to affecting neutrophil and macrophage function, hyperglycemia also affects the complement cascade. Under situation of normal glycemia, bacteria can activate the complement cascade. Activation of the complement cascade results in the formation of transmembrane protein channels known as membrane attack complex in bacterial membrane. M embrane attack complexes make the bacterial membrane porous and the rapid influx of fluid results in the baterial cell death. Hyperglycemia inhibits the proper activation complement cascade, thereby reducing another pathway of the immune system.