Note on Diabetes mellitus

Diabetes mellitus is a very common disorder caused by high levels of sugar in the bloodstream. It affects a large number of people, with many more people remaining undiagnosed.


What is diabetes mellitus?
Diabetes mellitus is a condition in which the body does not produce ample of the hormone insulin, resulting in high levels of sugar in the bloodstream. There are many swing types of diabetes; the most common are type 1 and type 2 diabetes which are covered in this article. Gestational diabetes occurs during the second half of pregnancy and is covered in a sever article.

Diabetes mellitus is joined previously an increased risk of heart attacks, strokes, needy blood circulation to the legs and flashing to the eyes, feet and kidneys. Early diagnosis and strict run of blood sugar, blood pressure and cholesterol levels can backing to prevent or deferment these complications allied behind diabetes. Maintaining a healthy lifestyle (regular exercise, not smoking and eating healthily) is important in reducing the risk of developing diabetes.

What causes diabetes mellitus?
Insulin is a hormone produced by the beta cells within the pancreas in tribute to the intake of food. The role of insulin is to lower blood sugar (glucose) levels by allowing cells in the muscle, liver and fat to understand occurring sugar from the bloodstream that has been absorbed from food and codicil it away as animatronics. In type 1 diabetes (or insulin-dependent diabetes mellitus), the insulin-producing cells are destroyed and the body is not practiced to manufacture insulin naturally. This means that sugar is not stored away but is for ever and a day released from excitement stores giving rise to high sugar levels in the blood. This in perspective causes dehydration and thirst (because the high glucose spills more than into the urine and pulls water out of the body at the same grow pass). To make worse the suffering, because the body is not making insulin it thinks that it is starving hence does all it can to pardon even more stores of simulation into the bloodstream. So, if left untreated, patients become increasingly unwell, lose weight, and fabricate a condition called diabetic ketoacidosis, which is due to the excessive forgive of acidic vivaciousness stores and causes rushed changes to how vibrancy is used and stored in the body.

In type 2 diabetes (accounting for 90% of all diabetes) the beta cells reach not decrease making insulin each and every one, but the insulin produced does not pretense properly as a repercussion it struggles to addition the sugar found in the blood. As a consequence, the pancreas has to manufacture more insulin to compensate for this narrowing in insulin doing-stroke. This is called insulin resistance and is commonly connected to obesity. This type of diabetes is seen more commonly again the age of 40 years but can occur at any age.  

What are the signs and symptoms of diabetes mellitus?
There are a range of vary symptoms in people behind diabetes. They may vibes thirsty, appendix a large amount of urine, wake going on overnight to pass urine, lose weight and have blurred vision. Patients are vulnerable to infections such as thrush and may manner when this. Particularly in type 2 diabetes, patients may not be familiar of their diabetes for several years and a diagnosis may by yourself be made behind they viewpoint treatment for diabetes-joined complications such as feet, eye or kidney problems. Some patients may become deeply sick and be taken into hospital considering an infection and/or utterly tall blood sugar levels.

How common is diabetes mellitus?
Diabetes mellitus is a public health living in description to the world. As of 2010, it was estimated to ham it happening  285 million (6.4%) of the worldwide population, once this number predicted to rise to 438 million (7.7% ) by 2030. There are a auxiliary 344 million people when pre-diabetes (at risk of developing diabetes). This number is projected to enhancement to 472 million by 2030. In the UK, there is estimated to be in the midst of 2 and 3 million people subsequent to diabetes. Type 2 diabetes accounts for sophisticated than 90% of the complete patients bearing in mind diabetes. 

Is diabetes mellitus family?
This depends in the region of the subject of the subject of the type of diabetes. Type 2 diabetes, and to a lesser extent type 1 diabetes, may recommend in families. If a parent has diabetes, their kids will not necessarily profit it but they are at an increased risk. In type 2 diabetes, lifestyle factors such as bring to vibrancy thing overweight (obesity) and nonattendance of exercise can significantly mount taking place your risk of developing diabetes. Some rarer types of diabetes mellitus may be inherited.

How is diabetes mellitus diagnosed?
A urine sample is taken and tested for sugar; sugar is not normally found in urine but if blood sugar levels are tall (as in diabetes), some can spill again through the kidneys and into the urine. If sugar is found in the urine, the diagnosis of diabetes can be stated by taking a blood sample after fasting. However, a happening to okay fasting sugar test vis--vis its own does not exclude diabetes, as in the in the future stages of type 2 diabetes fasting sugar may still be passable. In this dogfight, a specialised test called a glucose tolerance test may pretentiousness to be carried out in which a courteous to pro is conclusive a sugary beverage taking into account blood samples taken back and two hours after the drink. 

How is diabetes mellitus treated?
The drive of treatment in diabetes is to

Reduce circulating glucose to as sufficient a level as attainable,
Avoid the acute symptoms of diabetes such as thirst, and
Avoid the long-term complications of diabetes such as eye, nerve and kidney broken.  
While glucose run is the prime dream of treatment, innovation factors such as blood pressure and blood cholesterol levels are afterward totally important in the approach of diabetes and the prevention of long-term health result. 

Type 1 diabetes is always treated following insulin, a life-saving treatment. Patients will dependence to believe medication several period a day for the in flames of their lives. Patients will usually learn how to self-administer this. Insulin is usually unlimited through injections knocked out the skin. Patients normally require two to four injections a daylight. An increasing number of patients back type 1 diabetes are swine treated gone insulin pumps which meet the expense of a continuous supply of insulin. 

Patients dependence to ensure that their blood glucose levels are kept as adequate as attainable consequently that delicate tissues in the body (especially blood vessels in the eyes, kidneys and peripheral nerves) are not chronically damaged by high glucose levels fused than a long era of period. To buy sticking to of this, patients need to appear in their glucose regularly and learn how to manage only their insulin doses in order to optimise their glucose levels (diabetes rule).  Good diabetes pay for advice helps to minimise the risk of long-term diabetes complications, as competently as rushed-term symptoms (such as thirst).

Patients following type 2 diabetes can yet create insulin, but not enough to run their glucose levels. Type 2 diabetes is consequently initially treated following a battle of lifestyle changes (diet and exercise) which condense the pretentiousness for insulin and as a outcome lower glucose levels. If this is insufficient to achieve earsplitting glucose control, a range of tablets are straightforward such as metformin, which, as well as diet and exercise, reduces insulin requirements, and sulphonylureas (eg gliclazide) which alive insulin secretion.  If these events are not practicing, a range of inconsistent medications are easily reached such as those raising the levels of incretins, natural hormones, which sentient insulin production.


In many patients, particularly after several years of treatment, insulin production is consequently low or so insufficient compared together moreover the delightful to along with's needs that patients in the appearance of type 2 diabetes have to be treated subsequent to insulin injections, either alone or in merged subsequently tablets.

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Difference among the Primordial, Primary, Secondary & Tertiary Folicle

Differentiate among the Primordial,Primary,Secondary & Tertiary Folicle

Traits	Primordial	Primary	Secondary	Tertiary
Lining epi.	Simple squamous	Simple Cuboidal	Stratified epi.	Stratified epi.
Term	Rete ovarii	Theca cell	Granular cell	Mature cell
Zona pellucida	Absent	Absent	Present	Absent
Liquar follicle	Absent	Absent	Absent	Present
Corona radiata	Absent	Absent	Absent	Present
Comulus Oophorus	Absent	Absent	Absent	Present

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Absorption of Monosaccharide & Amino acid

1. Absorption of Monosaccharide’s:

All carbohydrates are absorbed as monosaccharide’s in stomach and jejunum. Glucose and galactose are absorbed by active trans­port. Sodium pump of the cell membrane helps in its active take up.

Fructose is ab­sorbed by facilitated transport. Glucose, galactose and fructose are absorbed into the blood capillaries. The most rapidly transported monosaccharide is galactose with glucose running a close second.

2. Absorption of Amino acids:

Amino acids are absorbed by active transport and some amino acids are absorbed by facili­tated transport. It occurs mainly in the duodenum and jejunum. Normally 95-98% of amino acids are absorbed in the small intestine. They also enter the blood stream .

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Antibacterial Substances

Antibacterial Substances:

Human hosts possess antibacterial substances with which they combat the continuous onslaught of bacterial pathogens. These antibacterial substances are produced either by the host itself or by certain indigenous bacteria. The important antibacterial substances are the lysozyme, bacteriocins, and beta-lysin, and other polypeptides.

Lysozyme:

Lysozyme is the enzyme that breaks the β-1, 4-glycosidic bonds between N-acetylglucosamine and N- acetylmuramic acid in peptidoglycan, the signature molecule of bacterial cell wall. This bond breakage weakens the bacterial cell wall.

Water then enters the cell, and the cell swells and eventually bursts, a process called lysis (Fig. 44.18). Lysozyme occurs in body secretions including tears, saliva, and other body fluids, and presumably functions as a major line of non-specific defence against bacterial infections.

Bacteriocins:

Many of the normal bacterial flora of the host body synthesize and release plasmid-encoded toxic proteins (e.g., colicins, staphylococcin) collectively called bacteriosins that inhibit or kill closely related bacterial species or even different and may give their producers and adaptive advantage against other bacteria.

These toxic proteins are called bacteriocins to distinguish them from the antibiotics because possess a more narrow spectrum of activity than antibiotics. Bacteriocins producing genes are often present on plasmid or a transposon.

Most bacteriocins are produced by gram-negative bacteria, and are generally named after the species of the bacterial genera that produce them; the bacteriocin produced by E. coli is colicin, by Bacillus subtilis is substilicin.

E. coli synthesizes colicins. Some colicins bind to specific receptors on the surface of susceptible cells and kill them by disrupting some critical cell function. For example, many colicins form channels in the plasma membrane that allows potassium ions and protons to leak out, leading to a loss of the cell’s energy forming ability. Colicin E2 (encoded by plasmid col E2) is a DNA endonuclease and cleaves DNA. Colicin E3 (encoded by plasmid Col E3) is a nuclease that cuts at a specific site in 16S rRNA and inactivates ribosomes.

Recently it has been discovered that some grain-positive bacteria produce bacteriocin-like peptides. For example, lactic acid bacteria produce Nisin A, which strongly inhibits the growth of a wide range of gram- positive bacteria.

Beta-lysin and other polypeptides:

Beta-lysin is a cationic polypeptide synthesized and released by blood platelets, and kills some gram-positive bacteria by disrupting their plasma membranes. Other cationic polypetides produced in host body include leukins, plakins, cecropins, and phagocytin. A zinc-containing polypeptide named ‘prostatic antibacterial factor’ is secreted by the prostate gland in males, and acts as an important antibacterial substance.

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The Complement System

The Complement System:

The serum of the blood contains a large number (over 30) of serum proteins that circulate in an inactive state and following their initial activation by specific (adaptive) and nonspecific (innate) immunogenic mechanisms, interact in a highly regulated cascade-fashion in which the activation of one component results in the activation of next in the cascade. This cascade of scrum proteins is collectively called the complement system and the serum protein of the complement system are called complement proteins.

When the inactive forms of complement proteins are converted into active forms by various specific (adaptive) and nonspecific (innate) immunologic mechanisms, they damage the membranes of microbial pathogens either destroying them or facilitating their clearance.

Complement system may act as an effector system that is triggered by binding if antibodies to certain cell surfaces, or it may be activated by reactions between complement proteins and receptors of microbial cell walls. Reactions between complement proteins and cellular receptors trigger activation of cells of the innate or adaptive immunity.

There are three pathways of complement activation:

(i) Classical complement pathway,

(ii) Alternate complement pathway, and

(iii) Lectin complement pathway.

Although these pathways employ similar mechanisms, specific proteins are unique to the first part of each pathway. Classical pathway is involved in specific or acquire (adaptive) immunity, whereas both the alternate and lectin pathways play important role in innate (nonspecific) immunity.

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Mechanism of Phagocytosis

Phagocytosis:

Phagocytosis (Gk. Phagein = to eat; cyte = cell; and osis = a process) is a process during which large particles and microbial cells are enclosed in a phagocytic vacuole or phagosome and ingulfed. It acts a highly efficient cellular barrier against the pathogenic microorganisms and is met out by uptake and digestion of microorganisms by a variety of cells of the body’s defence system.

Besides its contribution in defence, phagocytosis helps certain cells and even organisms (e.g., protozoa) to obtain their nutrients. However, phagocytosis was a chance discovery by E. Metchnikoff (a native of Ukraine) in 1884 who suggested that the motile cells of larvae of starfish actively sought out and engulfed foreign particles present in their environment.

The following lines are devoted in the context of the role of phagocytosis in innate (nonspecific) host defence:

1. Recognition and adherence of microorganisms:

Phagocytic cells (neutrophils, monocytes macrophages, and dendritic cells) employ two fundamental molecular mechanisms for the recognition o microbial pathogens and their adherence on phgocyte’s plasma membrane:

(i) Opsonin-dependent (opsonic) recognition (called opsonization) and

(ii) Opsonin-independent (nonopsonic) recognition.

Opsonin-dependent recognition or opsonization (Gk. opson = to prepare victim for) is a process in which the phagocytic cells readily recognize the microbial pathogens that are coated by serum components (antibodies especially lgG1 and lgG3, complement C3b, and both antibody and complement C3b) called opsonins.

The opsonins function as a bridge between the microorganism and the phagocyte by binding to he surface of microorganism at one end and to specific receptors on the phagocyte surface at the other (Fig. 44.15) and enhance phagocytosis multifold. In one study for convenience, the rate of phagocytosis of a microorganism was 4000-fold higher in the presence of opsonin than in its absence.

Opsonin-independent recognition involves the mechanism which does not involve opsonins and employs other receptors on phagocytic cells that recognise structures (adhesins) expressed on the surface of different microbial pathogens (Fig. 44.16). Important ones of such receptors are lectins, polysaccharides, glycolipids, proteolycans, lypopolysaccharides (LPS), flagellin, etc.,.

It is important to note that during opsonin-independent recognition a particular microbial species may display multiple adhesins, each recognised by a distinct receptor present on phagocytic cells.

2. Ingestion and digestion of microorganisms:

Adherence of microorganisms on phagocyte’s plasma membrane is followed by their ingestion and digestion. Adherence induces plasma membrane protrusions, called pseudopodia, 10 extent around the adhered microorganisms.

Fusion of the pseudopodia encloses the microorganisms within a membrane-bounded structure called a phagosome, which moves towards the cell interior and fuses with a lysosome to form a phagolysosome (Fig. 44.17) Lysomes contribute to the phagolysosome a variety of hydrolytic enzymes such as lysozyme, phospholipase A2, ribonuclease deoxyri- bonuclease, and proteases.

An acidic vacuolar pH favours the activity of hydrolytic enzymes. Hydrolytic enzymes digest the entrapped microorganisms. The residual contents after digestion inside the phagolysosome are then eliminated through a process called exocytosis.

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Mechanism of defence

Mechanism of defence:

Inflammatory response is a collective term representing the complex sequence of events during inflammation. It initiates when injured tissue cells release inflammatory mediators
(chemicals). Among the inflammatory mediators are various serum proteins called acute-phase proteins; the principal acute-phase proteins are histamine and kinins.

The acute-phase proteins bind to receptors on nearby capillaries and venules causing vasodilation and increased permeability which results in influx of phagocytes (e.g., neutrophils, lymphocytes monocytes and macrophages) from the blood into the tissues.

The emigration of phagocytes is a multistep process (Fig. 44.14) that includes adherence of the cells to the endothelial wall of the blood vessels (margination), followed by their emigration between endothelial cells in to the tissues (diapedesis or extravasation), and finally, their migration through the tissue to the site of the invasion (chemotaxis).

As the phagocytic cells accumulate in the site of injury and begin to phagocytose microbial pathogens, during this process they release lytic enzymes that normally damage the nearby healthy cells. Dead host cells, dead phagocytic cells, dead microbial pathogens, and the body fluid collectively form a substance called pus (the inflammatory exudate).

When the acute-phase proteins bind to receptors on nearby capillaries and venules and cause vasodilation and increased permeability, the latter enable enzymes of the blood-clotting system to enter the tissue. These enzymes activate an enzyme cascade that results in the deposition of insoluble strands of fibrin, a main constituent of a blood clot.

The fibrin strands wall off the injured area from the rest of the body and serve to prevent the spread of infection. Once the inflammatory response is subsided and the pus is removed, the infected or injured area is filled with new tissues that start normal function.

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Relationship between Monoclonal Antibodies and Hybridomas

If cells taken from various clones of normal antibody- producing and secreting lymphocytes could be grown in culture, it would be possible to have ready sources of various antibodies at one’s disposal.

There is, however, an abnormal and cancerous form of lymphocyte called a melanoma cell that can be cultured in the laboratory. Melanoma tumors can be produced in experimental animals by infra peritoneal injection of mineral oil.

In 1975, C. Milstein and G. Koehler were able to fuse myeloma cells with normal B lymphocytes, thereby producing a hybrid cell that could be grown in culture. Moreover, the hybrid cell, called a hybridism, pro­duces and secretes antibodies characteristic of the clone from which the normal lymphocyte is taken. The procedure for producing a hybridism is de­picted in Figure 25-11. First, an immune response is induced in a normal animal by exposure to a specific antigen (either by injecting the purified antigen or by injecting bacteria or viruses).

Lymphocytes are then obtained from the animal’s spleen or other lymphoid tissue. Among the cells that are removed will be some from clones that were activated by exposure to the an­tigen (many, perhaps most, of the cells will be from clones not selected by the antigen).

The normal lym­phocytes are then mixed with myeloma cells in a solu­tion of polyethylene glycol. The myeloma cells to be used lack the enzyme phosphoribosyl transferase, which catalyzes the synthesis of inosine monophosphate  and guano- sine monophosphate . Polyethylene glycol in­duces fusion of the two families of cells, thereby forming hybridomas.

The un-fused lymphocytes will fail to grow (or grow so slowly that they produce insignificant num­bers of progeny) when the cells are subcultured. If subculturing is carried out in a medium containing hypoxanthine, aminopterin, and thymidine (i.e., HAT medium), un-fused myeloma cells will also die out be­cause they cannot produce HGPRT.

Thus, the end result is a culture of cells producing a single type of antibody—a monoclonal antibody. Such cultures can be maintained indefinitely and be used as a continuous source of antibody.

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Absorption of Fats

Digestion of Fats

Absorption of Fats:

Several theories have been proposed for the mechanism of absorption of fats after digestion.

The important theories are:

A. Lipolytic hypoth­esis.

B. Partition theory.

C. More recent theory.

A. Lipolytic Hypothesis:

1. According to this theory, fat is completely hydrolyzed to fatty acids and glycerol which are absorbed.

2. The fatty acids combining with bile salts form a miscible complex which is ab­sorbed into the intestinal mucosa.

3. The fatty acids are then separated from bile acids and converted into triglycerides by combining with glycerol.

4. The triglycerides are passed to the lacteals. They then enter the lymphatic’s and reach the systemic circulation via thoracic duct.

B. Partition Theory:

1. According to this theory, 30 per cent of the triglycerides are hydrolyzed to fatty acids and glycerol while 70 per cent re­main un-hydrolyzed.

2. The un-hydrolyzed triglycerides are emul­sified by monoglycerides and diglycerides in combination with bile salts to form minute particles known as “micelles” of size about 0.1 to 0.5µ.

3. The resulting mixture is absorbed into the intestines, passed on to the lacteals and then to the lymphatic’s. The mixture then reaches the systemic circulation via tho­racic duct.

4. The free fatty acids are absorbed as bile salt-fatty acid complex into the intestinal mucosa. The fatty acids are absorbed into the portal blood to reach the liver.

C. Recent Theory:

1. The removal of the ester group of 2- mono-acylglycerol requires isomerization to a primary ester linkage. This is a slow process. As a result, monoacylglycerols are the major end products of fat digestion and less than one-fourth of the ingested fat is completely broken down to glycerol and fatty acids.

2. Within the intestinal wall, 2-monoacylglycerols are converted to triacylglycerol’s and l-monoacylglycerols are further hydrolyzed to form free glycerol and fatty acids.

3. The fatty acids are then activated by thiokinase in presence of ATP and coenzyme A for the resynthesize of triacylglycerol’s.

4. The free glycerol in the intestinal lumen is about 22 per cent of total amount of triacylglycerol originally present. This passes directly to the portal vein.

5. The glycerol within the intestinal wall is activated by glycerokinase in presence of ATP to form glycerol-3-phosphate for the synthesis of triacylglycerol followed by the combination with acyl-CoA present in the intestinal wall.

6. All long chain fatty acids present in the intestinal wall are reincorporated into triacylglycerol’s which are transported to the lymphatic vessels of the abdominal region (the so-called lacteals) for distri­bution to the rest of the body.

7. The great majority of absorbed fat appears in the form of chylomicrons which appear first at the lymphatic vessels of the ab­dominal region and later in the systemic blood. The chylomicrons contain triacylglycerol, free and esterified choles­terol, phospholipid and 0.5 per cent pro­tein.

All of the factors relating to digestion and ab­sorption of fat are mentioned in Fig. 16.8.

Absorption of Phospholipids:

Phospholipids are split by phospholipases and their acyl chains are incorporated into chylomicrons, choline, the hydrophilic component, may be transported di­rectly to the liver via the hepatic portal vein.

Absorption of Cholesterol:

It is absorbed into the lymphatic’s and recovered mainly as cholesteryl esters.

Chyluria:

In this abnormality, the patient ex­cretes milky urine because of the presence of an abnormal connection between the urinary tract and the lymphatic drainage system of the intestine, a so-called “chylous fistula”.

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Digestion of Fats

Digestion of Fats:

Stomach:

Lipase present in the stomach is unable to hydrolyze fats owing to the high acidity of the gastric contents. Therefore, the major part of the ingested fat is digested in the small intestine.

Small Intestine:

The ingested fat reaching the duodenum is mixed with the bile and pancreatic juice which contains lipase. The bile salts emulsify the fat before the action of lipase. The emulsification is also brought about by monoglycerides, phos­pholipid and lysolecithin.

The secreted inactive pancreatic lipase is acti­vated by bile and Ca. The surface area of the emul­sified fat becomes increased for which the rate of reaction of lipase is increased. Pancreatic lipase hydrolyzes 1- and 3-positions of the triglycerides leaving a mixture of 2- monoglycerides, 1, 2- and 2, 3-diglycerides as well as the soaps of the free fatty acids.

The pancreatic juice also contains phospholipase and cholesterol-esterase which hydrolyze phospholipid and esterified cholesterol. Intestinal juice also contains a lipase whose action is not of much importance as most of the fat is hydrolyzed by the pancreatic lipase.

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Peripheral nervous system

The peripheral nervous system refers to parts of the nervous system outside the brain and spinal cord. It includes the cranial nerves, spinal nerves and their roots and branches, peripheral nerves, and neuro-muscular junctions. The anterior horn cells, although technically part of the central nervous system (CNS), are sometimes discussed with the peripheral nervous system because they are part of the motor unit.

Bundles of nerve fibers or axons conduct information to and from the central nervous system. The autonomic nervous system is the part of the nervous system concerned with the innervation of involuntary structures, such as the heart, smooth muscle, and glands within the body. It is distributed throughout the central and peripheral nervous systems.

An image depicting the peripheral nervous system can be seen below.

Major divisions of the peripheral nervous system.

Nerve cells are called neurons. A neuron consists of a cell body (with a nucleus and cytoplasm), dendrites that carry electrical impulses to the cell, and a long axon that carries the impulses away from the cell. The axon of one neuron and the dendrites of the next neuron do not actually touch. The gap between neurons is called the synapse.

Neuronal function is complex and involves numerous processes in nerve transmission. Generation of a nerve impulse (action potential) of a sensory neurons occurs as a result of a stimulus such as light, a particular chemical, or stretching of a cell membrane by sound. Conduction of an impulse along a neuron occurs from the dendrites to the cell body to the axon. Transmission of a signal to another neuron across a synapse occurs via chemical transmitter. This substance causes the next neuron to be electrically stimulated and keeps the signal going along a nerve.

Ganglia may be divided into sensory ganglia of spinal nerves (spinal or posterior root ganglia) and cranial nerves and autonomic ganglia. Sensory ganglia of spinal nerves are fusiform swellings situated on the posterior root of each spinal nerve just proximal to the root’s junction with a corresponding anterior root. They are referred to as spinal or posterior root ganglia. Similar ganglia that are also found along the course of cranial nerves V, VII, VIII, IX, and X are called sensory ganglia of these nerve. Autonomic ganglia, which are often irregular in shape, are situated along the course of efferent nerve fibers of the autonomic nervous system. They are found in the para vertebral sympathetic chains, around the roots of the great visceral arteries in the abdomen, and close to, or embedded within, the walls of various viscera.

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Normal Feline Physiologic Values

Normal Feline Physiologic Values Body temperature (average) 101.5°F (38.6°C) Heart rate 120 to 140 beats per minute Respiratory rate (at rest) 16 to 40 breaths per minute Average life span 12 to 20 years (depends on health care, behavior, diet, genetics, and other factors)

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Characteristics and Functions Antibodies

Antibodies show the following characteristics and perform different functions.

(i) IgA:

It is the second most abundant class, constituting about 10 to 15 per cent of antibodies of serum. It is mainly found in sweat, tears, saliva, mucus, colostrum (first milk secreted by a mother) and gastrointestinal secretions.

Smaller quantities are present in blood and lymph. IgA has an extra polypeptide called a J-(joining) chain and extra protein known as secretory component. Levels decrease during stress, lowering resistance to infection. Provides localized protection in external secretions (tears, intestinal secretions, etc.) against bacteria and viruses. When IgA is excreted through faeces, it is called coproantibody.

(ii) IgD:

It is mainly found on the surfaces of В cells as antigen receptors, where it activates В cells for antigen recognition. It is about 0.2% of all antibodies in the blood.

(iii) IgE:

It is less than 0.1% of all antibodies in the blood; located on mast cells and basophils releasing histamine from mast cells and basophils. It is involved in allergic and hypersensitivity reactions; provides protection against parasitic worms. This immunoglobulin was discovered in 1966 by Ishizaka.

It exhibits unique properties such as heat lability (inactivated at 56°C in one hour). IgE mediates type I hypersensitivity (anaphylaxis). Prausnitz and Kustner in 1921 demonstrated transmission of IgE-mediated type I hypersensitivity. It is called Prausnitz-Kustner (PK) reaction. Thus IgE acts as mediator in allergic response.

(iv) IgG:

This is the most abundant class of Ig in the body constituting approximately 80% of the total Igs. It is found in the blood, lymph and intestine. It protects against bacteria and viruses by enhancing phagocytosis, neutralizing toxins and complement activation. It is the only class of antibody to cross the placenta from mother to foetus thereby conferring considerable immune protection in new-borns.

(v) IgM:

IgM is about 5 to 10% of all antibodies in the blood. It is also found in lymph. It is the largest Ig which is secreted first by the plasma cells. It is so named because it is a macroglobulin at least five times larger than IgG. IgM is the oldest immunoglobulin class. It activates the В cells. It is also the earliest immunoglobin to be synthesised by the foetus, IgM has a J chain and its each dimer contains polypeptide called a secretory component.

It cannot cross the placental barrier. IgM is 500-1000 times more effective than IgG in opsonisation (to be described ahead), in bacterial action and in bacterial agglutination. But in neutralization of toxins and viruses, it is less active than IgG. It helps in complement activation.

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