Insulin and Glucagon: Control of Blood Glucose

Although the pancreas is considered a major endocrine gland, hormone–secreting cells make up only 1–2% of its weight. The rest of the pancreas produces bicarbonate ions and digestive enzymes, which are released into small ducts and carried to the small intestine via the pancreatic duct. Tissues and glands that discharge secretions into ducts are described as exocrine. Thus, the pancreas is a dual endocrine and exocrine gland with important functions in both the endocrine and digestive systems.

Clusters of endocrine cells, the islets of Langerhans, are scattered throughout the exocrine tissue of the pancreas. Each islet has a population of alpha cells, which produce the hormone glucagon, and a population of beta cells, which produce the hormone insulin. Both of these protein hormones, like all endocrine signals, are secreted into the circulatory system.

 

 

This is a critical bioenergetic and homeostatic function, because glucose is a major fuel for cellular respiration and a key source of carbon skeletons for the synthesis of other organic compounds. Metabolic balance depends on maintaining blood glucose concentrations near a set point, which is about 90 mg/100 mL in humans. When blood glucose exceeds this level, insulin is released, and its effects lower blood glucose concentration. When blood glucose drops below the set point, glucagon is released, and its effects increase blood glucose concentration. Each hormone operates in a simple endocrine pathway that is regulated by negative feedback. The combination of the two pathways permits precise regulation of blood glucose.

Target Tissues for Insulin and Glucagon

Insulin lowers blood glucose levels by stimulating virtually all body cells except those of the brain to take up glucose from the blood. (Brain cells are unusual in being able to take up glucose without insulin; as a result, the brain has access to circulating fuel almost all the time.) Insulin also decreases blood glucose by slowing glycogen breakdown in the liver and inhibiting the conversion of amino acids and glycerol (from fats) to glucose.

The liver, skeletal muscles, and adipose tissues store large amounts of fuel and are especially important in bioenergetics. The liver and muscles store sugar as glycogen, whereas adipose tissue cells convert sugars to fats. The liver is a key fuel–processing center because only liver cells are sensitive to glucagon. Normally, glucagon starts having an effect before blood glucose levels even drop below the set point. In fact, as soon as excess glucose is cleared from the blood, glucagon signals the liver cells to increase glycogen hydrolysis, convert amino acids and glycerol to glucose, and start slowly releasing glucose back into the circulation.

The antagonistic effects of glucagon and insulin are vital to glucose homeostasis and thus to the precise management of both fuel storage and fuel consumption by body cells. The liver′s ability to perform its vital roles in glucose homeostasis results from the metabolic versatility of its cells and its access to absorbed nutrients via the hepatic portal vessel, which carries blood directly from the small intestine to the liver.

Diabetes Mellitus

When the mechanisms of glucose homeostasis go awry, there are serious consequences. Diabetes mellitus, perhaps the best–known endocrine disorder, is caused by a deficiency of insulin or a decreased response to insulin in target tissues. There are two major types of diabetes mellitus with very different causes, but each is marked by high blood glucose.

In people with diabetes, elevated blood glucose exceeds the reabsorption capacity of the kidneys, causing them to excrete glucose. This explains why the presence of sugar in urine is one test for diabetes. As glucose is concentrated in the urine, more water is excreted along with it, resulting in excessive volumes of urine and persistent thirst. (Diabetes, from the Greek diabainein, to pass through, refers to this copious urination; and mellitus, from the Greek meli, honey, refers to the presence of sugar in urine.) Without sufficient glucose available to meet the needs of most body cells, fat becomes the main substrate for cellular respiration. In severe cases, acidic metabolites formed during fat breakdown accumulate in the blood, threatening life by lowering blood pH.

Type I diabetes mellitus (insulin–dependent diabetes) is an autoimmune disorder in which the immune system destroys the beta cells of the pancreas. Type I diabetes, which usually appears during childhood, destroys the person′s ability to produce insulin. Treatment consists of insulin injections, usually several times daily. In the past, insulin for injections was extracted from animal pancreases, but now human insulin can be obtained from genetically engineered bacteria, a relatively inexpensive source.

Type II diabetes mellitus (non–insulin–dependent diabetes) is characterized either by a deficiency of insulin or, more commonly, by reduced responsiveness of target cells due to some change in insulin receptors. Although heredity can play a role in type II diabetes, research indicates that excess body weight and lack of exercise significantly increase the risk. This form of diabetes generally appears after age 40, but young people who are overweight and sedentary can also develop the disease. More than 90% of people with diabetes have type II. Many can manage their blood glucose level with regular exercise and a healthy diet; some require drug therapy.

Cardiovascular Disease

Most sudden deaths in Malaysia are caused by cardiovascular diseases, disorders of the heart and blood vessels. The tendency to develop cardiovascular disease is inherited to some extent, but lifestyle plays a large role, too. Nongenetic factors that increase the risk of cardiovascular problems include smoking, lack of exercise, a diet rich in animal fat, and high concentrations of cholesterol in the blood.

Cholesterol travels in the blood plasma mainly in the form of particles consisting of thousands of cholesterol molecules and other lipids bound to a protein. One type of particle—low–density lipoproteins (LDLs), often called the “bad cholesterol”—is associated with the deposition of cholesterol in arterial plaques, growths that develop on the inner walls of arteries. Another type—high–density lipoproteins (HDLs), or “good cholesterol”—appears to reduce the deposition of cholesterol. Exercise increases HDL concentration, whereas smoking has the opposite effect on the LDL/HDL ratio.

Healthy arteries have smooth inner linings that promote unimpeded blood flow. The deposition of cholesterol thickens and roughens this smooth lining. A plaque forms at the site and becomes infiltrated with fibrous connective tissue and still more cholesterol. Such plaques narrow the bore of the artery, leading to a chronic cardiovascular disease known as atherosclerosis.

 

The rough lining of an atherosclerotic artery seems to encourage the adhesion of platelets, triggering the clotting process and interfering with circulation.

Hypertension (high blood pressure) promotes atherosclerosis and increases the risk of heart attack and stroke. Atherosclerosis tends to raise blood pressure by narrowing the vessels and reducing their elasticity. According to one hypothesis, chronic high blood pressure damages the endothelium that lines arteries, promoting plaque formation. Fortunately, hypertension is simple to diagnose and can usually be controlled by diet, exercise, medication, or a combination of these. A diastolic pressure above 90 may be cause for concern, and living with extreme hypertension—say, 200/120—is courting disaster.

As atherosclerosis progresses, arteries become narrower, and the threat of heart attack or stroke increases. There may be warning signs. For example, if a coronary artery is only partially blocked, the person may feel occasional chest pain, a condition known as angina pectoris. The pain is most likely to appear when the heart is laboring hard as a result of physical or emotional stress, and it signals that part of the heart is not receiving enough O₂. However, many people with atherosclerosis are completely unaware of their condition until catastrophe strikes.

The final blow is usually a heart attack or a stroke. A heart attack is the death of cardiac muscle tissue resulting from prolonged blockage of one or more coronary arteries, the vessels that supply oxygen–rich blood to the heart. Because they are small in diameter to begin with, the coronary arteries are particularly vulnerable. Such blockage can destroy cardiac muscle quickly, since the constantly beating heart muscle cannot survive long without oxygen. A stroke is the death of nervous tissue in the brain, usually resulting from rupture or blockage of arteries in the head.

Heart attacks and strokes frequently result from a thrombus, or blood clot, that clogs an artery. A key process leading to the clogging of an artery by a thrombus is an inflammatory response triggered by the accumulation of LDLs in the artery′s inner lining. Such an inflammation, which is analogous to the body′s response to a cut infected by bacteria, can cause plaques to rupture, releasing fragments that form a thrombus. The thrombus may originate in a coronary artery or an artery in the brain, or it may develop elsewhere in the circulatory system and reach the heart or brain via the bloodstream. The transported clot, called an embolus, is swept along until it lodges in an artery too small for the clot to pass. An embolus is more likely to become trapped in a vessel that has been narrowed by plaques. The embolus blocks blood flow, and cardiac or brain tissue downstream from the obstruction may die from O₂ deprivation. If damage in the heart interrupts the conduction of electrical impulses through cardiac muscle, heart rate may change drastically or the heart may stop beating altogether. Still, the victim may survive if a heartbeat is restored by cardiopulmonary resuscitation (CPR) or some other emergency procedure within a few minutes of the attack. The effects of a stroke and the individual′s chance of survival depend on the extent and location of the damaged brain tissue.

 

Happy New Year

Keep the smile,
leave the tear,
Think of joy,
forget the fear,
Hold the laugh,
leave the pain,
Be joyous,
Coz its new year!
HAPPY NEW YEAR

Factors affecting the rate of photosynthesis

Affected by : 
Light intensity
Concentration of carbon dioxide
Temperature

Light intensity 

Light is essential during light reaction of photosynthesis.

When concentration of carbon dioxide & temperature are controlled at constant levels,

the rate of photosynthesis is directly proportional to light intensity up to a certain point.

As the light intensity increases, the rate of photosynthesis increases up to a saturated point

(point P).

Beyond the saturation point (point P), further increase in light intensity does not increase

the rate of photosynthesis because of concentration of carbon dioxide & temperature

become the limiting factors.
Both the concentration of carbon dioxide & temperature stop the rate of reaction from
increasing further along PQ.
The rate of photosynthesis will not increase although the light intensity is increases.        
When CO₂ concentration is raised to 0.13%, the rate of photosynthesis is higher. (graph II)
At very high light intensity, the rate of photosynthesis slows down because the chlorophyll
pigment is damaged by UV rays.

 

CO₂ is required in dark reaction as raw material used in the synthesis of glucose.
If there is no other limiting factors that limit the photosynthesis process, as the
concentration of carbon dioxide increases, the rate of photosynthesis increases.
Although the concentration of carbon dioxide keeps increasing, the rate of photosynthesis
will not increase further because light intensity acts as limiting factor.

 

Dark reaction is catalysed by enzymes; thus changes in temperature affects the rate of 
photosynthesis.
An increase in 10⁰C in the surrounding temperature will decrease the rate of photosynthesis
The optimum temperature of varies for each species.
But most plants : between 25⁰C to 30⁰. 
If temperature is too high, photosynthetic enzymes are destroyed by denaturation.
Photosynthesis stops.