Endocrinology
AMAZING HORMONES
Counterbalance of Sugar and Fat Content between Insulin and Glucagon
Physical survival depends on the sustained availability and use of energy in the form of adenosine triphosphate or ATP from sufficient levels of a substance, called glucose (Bowen, 2001). The use of energy depends on the varying levels of activity. Hence, the amount of glucose needed for activity likewise varies each day. Too much or too little glucose is damaging to the body, hence the need for some system to regulate the availability of glucose. It must be present at the precise time and amount that it is needed in order to maintain what is called glucose homeostasis. Homeostasis is the tendency of the body to maintain internal stability and balance through the coordinated responses of body parts to stimuli or conditions (Bowen).
Insulin and Glucagon
The regulation of glucose availability begins with the pancreas, primarily by its production of the two antagonistic hormones, insulin and glucagon (Biomed, 2002; McGinnis, 2013). Insulin is the hormone produced and released by the pancreas when glucose levels get too high. Glucagon, in contrast, is that it produces and releases when glucose levels fall too low. Too much glucose in the blood is deadly to the cells, while too little can lead to starvation (Biomed, McGinnis).
Blood glucose levels are unstable as they change for different reasons (Biomed, 2002; Bowen, 2001; McGinis, 2013). These include digestion after eating and the release of insulin by the liver; the transport of glucose into the cells or its loss by urinating. The body first detects glucose in the bloodstream by receptors alpha cells and beta cells. Rising glucose levels prompt beta cells to produce insulin, which restores glucose levels to normal. At the same time, it signals body tissues to use glucose for energy. What is not used is converted to glycogen and lipids and stored in the liver as reserves. When glucose levels fall, on the other hand, alpha cells release the opposite or antagonistic hormone, glucagon to bring about the breakdown of glycogen into glucose and adipose tissue by skeletal muscle and liver. These organs digest lipids into fatty acids and glycerol. Glucagon furthermore causes the liver the synthesis of glucose from glycerol in the blood by the liver. These actions and reactions synergize and restore glucose levels to normal again. Thus do the insulin and glucagons counterbalance each other in maintaining glucose homeostasis (Biomed, Bowen, McGinnis).
Glycogenolysis
After the body uses needed glucose for functioning and brain power, un0used glycogen is stored in the liver and muscles through a process called glycogenesis (Bowen, 2001; Biomed, 2002; McGinnis, 2013). After activity or exercise, the body will automatically replace the stored glycogen used in the activity as soon as food is ingested. If the replacement does not occur or the reserve is depleted, the body turns to protein and breaks it down as source of energy (Bowen, Biomed, McGinnis).
Conclusion
The balance and control asserted by these hormones regulates tissue metabolism and blood levels of glucose, fatty acids, triglycerides and amino acids (Medbio, 2013). They are behind the maintenance of homeostasis on a minute-to-minute basis. Promoting it insures the body's integrated metabolism and stability of the body. Glucose is the key molecule in the process. Cells must receive a controlled amount for survival and health. Thus regulating glucose level in the blood is essential to maintain homeostasis (Medbio).
II. Effects of Epinephrine
Introduction
Epinephrine is a catecholamine hormone, secreted by the adrenal medulla in response to hypoglycemia, stress and other stimuli (The Free Medical Dictionary, 2013). It strongly stimulates the sympathetic nervous system and is also a powerful vasopressor. It raises blood pressure, stimulates the heart muscle, speeds up the heart rate and increases heart activity. It is also called adrenaline (The Free Medical Dictionary). It affects:
nutrient metabolism
Epinephrine increases the production of glucose by stimulating glycogenolysis and gluconeogenesis (Sherwin & Sacca, 1964). While its effect on glycogenolysis quickly dissipates, hyperglycemia persists because of its effect on gluconeogenesis and continued glucose disposal. Hyperglycemia is further enhanced by increased glucagons and cortisol or in diabetic persons. In either case, epinephrine's effect on the production of glucose by the liver changes from a temporary to a sustained response or an exaggerated hyperglycemia. Epinephrine thus exposes diabetics to the adverse metabolic effects of stress. During glucose feeding, a small increase in epinephrine with little effect on fasting glucose levels can develop marked glucose intolerance. Its sensitivity to the diabetogenic effects of epinephrine derives from its capacity to interfere with the components of the gluco-regulatory response. These include the stimulation of splanchnic and peripheral glucose uptake and the suppression of glucose production by the liver (Sherwin and Sacca).
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