Blood Glucose Regulation

Blood Glucose · Glucose C6H12O6 o Glucose: 6C monosaccharide- type of carbohydrate o Destination: cell cytoplasm and mitochondria o Glucose converted (pyruvic acid which enter the mitochondria then) to ATP to release energy for movement, chemical synthesis, and nerve activity. o Particularly important to the brain – uses no other fuel (except in starvation mode) o Mid-range glucose levels 5mmolL-1, 0.09% by weight, or 90mg/100mL o Need for glucose is continuous by supply intermittent. Blood is glucose rich after meals but this must be stored to supply the body during night sleeping fast o Storage: liver and skeletal muscles · Glucose entering the blood stream o After consuming carbohydrates , bigger molecules are digested then smaller molecule breakdown products are stored . o Many processed foods contain sucrose which is far more easily digested than starch. It is digested and absorbed very quickly and over the years this may trigger diabetes. o Small amounts of glucose are derived from the breakdown of surplus amino acids which occurs in the liver. o Blood from the small intestines travels through the hepatic portal vein to the liver which means that surplus glucose can be taken · Glucose leaving the blood stream o The liver stores surplus glucose after a meal as glycogen (complex storage molecule). o After a meal the liver can store up to 10% of its mass as glycogen (sustain for 2 days) o Glycogen is also stored in muscles o Between meals glycogen is broken into glucose and released back into the bloodstream o Glucose should be needed to produced enough energy (ATP) but excess glucose is stored as fat which is stored in the liver, around the gut and under the skin. · Control of blood glucose o Rise in blood glucose (Insulin) – detected by IOL § Insulin output rises, glucagon output falls § Increase glycogen and fat synthesis and glycogen breakdown inhibited · = decrease in blood glucose o Drop in blood glucose (Glucagon) – detected by IOL § Glucagon output rises, insulin output falls § Decreased glycogen and fat synthesis and glycogen breakdown stimulated · = rise in blood glucose o Both are polypeptides o Both secreted by tiny patches of tissue in the pancreas (sensor) known as the Islets of Langerhans (part of endocrine system) § Alpha cells – secret glucagon in response to low blood glucose to increase blood glucose concentration § Beta cells- secret insulin in response to high blood glucose to decrease concentration · Insulin stimulates uptake of glucose by cells for cellular respiration, or liver cells to convert glucose to glycogen for storage. When glycogen store is full surplus is converted to fat. · The inability of beta cells to make insulin results in diabetes § Islets are independent of nerve control, they monitor and detect changes in blood glucose concentration and release appropriate hormone in correct amounts (both sensors and controllers) · Low glucose o Glycogen stores can maintain the body for about 24 hours, any longer then other resources are used § FAT is converted to fatty acids and glycerol (used respiration) § Glucose can be produced from PROTEIN once fat stores have been used. This is dangerous as this is the source of glucose the brain depends on for energy when starving § The hypothalamus controls appetite and can stimulate hunger when more glucose is required. · Main effector o Target of insulin: liver, skeletal muscles, fat cells § Liver cells convert glucose to glycogen and store in in insulin o Target of glucagon: liver only § Liver cells receive glucagon and convert glycogen into glucose then release it · Glucose into cells § Too big to pass through cell membrane via diffusion, depending on tissue entry is different. o Brain § Glucose constantly being used, must have constant supply – critical that levels maintained § Glucose transporters in cell membrane take glucose into brain by facilitated diffusion o Muscle and Fat § Regulated by insulin receptors that control whether glucose transporters are present or not in cell membrane · Specific glucose transporter needed to provide channel – GLUT4 (usually inside cell, only present on surface when insulin present – to inhibit transport) · Exocytosis / transduction: o Insulin binds to insulin receptor on plasma membrane. This changed intracellular part of molecule to change shape. o Enzyme activity is activated in insulin receptor. o Signal is then transmitted from extracellular environment to intracellular without the hormone entering the cell. o Insulin receptor then triggers chain reaction of enzymes which makes vesicles containing GLUT4 move to plasma membrane o Vesicles fuse with plasma membrane so GLUT4 is inside plasma membrane where it can transport glucose into muscle or fat cells. o To prevent excess glucose being released, the body breaks down insulin quickly – more will only be sent to cells if more glucose is needed · Glucose in emergencies o Glucagon and Insulin work under normal conditions (after meals) o Other hormones involved in emergencies o Adrenaline § Secreted by adrenal medulla in adrenal gland in times of fear and danger · Increases heart rate and blood pressure · Causes rapid breakdown of glycogen in the liver and release of glucose into the blood o Cortisol § Secreted by adrenal cortex in adrenal gland in times of stress and starvation · Simulates production of glucose from non-carbohydrate sources (amino acid / protein) · Diabetes o Type ONE: affects fewer than 1% § Caused: auto immune destruction of beta cells (no insulin produced). § Can appear at any age § Treatment: monitor food intake, inject insulin several times a day. Even then it is hard to control glucose levels. As injected it takes longer to act than naturally secreted insulin from pancreas. The body usually monitors how much to inject (beta cells) but a type 1 person has to guess. Too much causes hyperglycemia and too little causes hyperglycemia. o Type TWO: previously less than 3% now 10%-30% (some groups) § Caused: life style (obesity) and genetic influence (now an epidemic) § Insulin produced in pancreas but cells become resistant and insulin inhibits entry of glucose to cells § Develops gradually and is reversible pre-diabetic stages. When blood glucose falls below 3mmolL-1 (hypoglycemia) someone may become confused or unconscious (brain lack of supply) § When blood glucose rises above 11mmolL-1 (hyperglycemia) other problems develop § Diagnosis and Causes: Symptoms develop slowly (tiredness and weight loss). Insulin defense means higher glucose levels. Diagnosis based on blood test. § Prevention: Type 2 is mainly caused by lifestyle choices. · Active lifestyle with regular exercise · Eat less food (obesity is major factor) · Eat less high sugar food · Chose food with low glycemic index (GI) as they are digested and absorbed more slowly to reduce sugar rush effect. o Long term consequences § Kidneys: Above 11mmolL-1 glucose appears in urine. Osmotic imbalance develops, water moves out of the blood causing excessive volume of urine. This creates excessive thirst. High blood glucose levels also cause permanent damage to glomeruli – causes kidney damage and people need dialysis. § Ketosis: Diabetes results in by-product known as ketone bodies. These tend to reduce blood pH. Ketones can cause breath of badly controlled diabetics to smell like nail polish remover. § Eyes: can cause peripheral vascular disease (PVD) = damage to small blood vessels. This can result in retina damage and then blindness § Circulation: PVD can also cause problems to blood supply to feet and hands. Persistent infections and gangrene set in, and high proportion of advanced diabetics need amputations § Heart: Diabetes is linked to increased changes of coronary artery disease