NEET MDS Lessons
Biochemistry
FATTY ACIDS
Fatty acids consist of a hydrocarbon chain with a carboxylic acid at one end.
• are usually in esterified form as major components of other lipids
• are often complexed in triacylglycerols (TAGs)
• most have an even number of carbon atoms (usually 14 to 24)
• are synthesized by concatenation of C2 units.
• C16 & C18 FAs are the most common FAs in higher plants and animals
• Are either:
—saturated (all C-C bonds are single bonds) or
—unsaturated (with one or more double bonds in the chain)
—monounsaturated (a single double bond)
1.Example of monounsaturated FA: Oleic acid 18:1(9) (the number in unsaturated FA parentheses indicates that the double bond is between carbons 9 & 10)
2. Double bonds are almost all in the cis conformation
—polyunsaturated (more then one double bond)
Polyunsaturated fatty acids contain 2 or more double bonds. They usually occur at every third carbon atom towards the methyl terminus (-CH3 ) of the molecule. Example of polyunsaturated FA: Linoleic acid 18:2(9,12)
• the number of double bonds in FAs varies from 1 to 4 (usually), but in most bacteria it is rarely more than 1
Saturated FAs are highly flexible molecules that can assume a wide range of conformations because there is relatively free rotation about their C-C bonds.
The Bicarbonate Buffer System
This is the main extracellular buffer system which (also) provides a means for the necessary removal of the CO2 produced by tissue metabolism. The bicarbonate buffer system is the main buffer in blood plasma and consists of carbonic acid as proton donor and bicarbonate as proton acceptor :
H2CO3 = H+ + HCO3–
If there is a change in the ratio in favour of H2CO3, acidosis results.
This change can result from a decrease in [HCO3 − ] or from an increase in [H2CO3 ]
Most common forms of acidosis are metabolic or respiratory
Metabolic acidosis is caused by a decrease in [HCO3 − ] and occurs, for example, in uncontrolled diabetes with ketosis or as a result of starvation.
Respiratory acidosis is brought about when there is an obstruction to respiration (emphysema, asthma or pneumonia) or depression of respiration (toxic doses of morphine or other respiratory depressants)
Alkalosis results when [HCO3 − ] becomes favoured in the bicarbonate/carbonic acid ratio
Metabolic alkalosis occurs when the HCO3 − fraction increases with little or no concomitant change in H2CO3
Severe vomiting (loss of H+ as HCl) or ingestion of excessive amounts of sodium bicarbonate (bicarbonate of soda) can produce this condition
Respiratory alkalosis is induced by hyperventilation because an excessive removal of CO2 from the blood results in a decrease in [H2CO3 ]
Alkalosis can produce convulsive seizures in children and tetany, hysteria, prolonged hot baths or lack of O2 as high altitudes.
The pH of blood is maintained at 7.4 when the buffer ratio [HCO3 − ] / [ H2CO3] becomes 20
Glycogen Metabolism
The formation of glycogen from glucose is called Glycogenesis
Glycogen is a polymer of glucose residues linked mainly by a(1→ 4) glycosidic linkages. There are a(1→6) linkages at branch points. The chains and branches are longer than shown. Glucose is stored as glycogen predominantly in liver and muscle cells
Glycogen Synthesis
Uridine diphosphate glucose (UDP-glucose) is the immediate precursor for glycogen synthesis. As glucose residues are added to glycogen, UDP-glucose is the substrate and UDP is released as a reaction product. Nucleotide diphosphate sugars are precursors also for synthesis of other complex carbohydrates, including oligosaccharide chains of glycoproteins, etc.
UDP-glucose is formed from glucose-1-phosphate and uridine triphosphate (UTP)
glucose-1-phosphate + UTP → UDP-glucose + 2 Pi
Cleavage of PPi is the only energy cost for glycogen synthesis (1P bond per glucose residue)
Glycogenin initiates glycogen synthesis. Glycogenin is an enzyme that catalyzes glycosylation of one of its own tyrosine residues.
Physiological regulation of glycogen metabolism
Both synthesis and breakdown of glycogen are spontaneous. If glycogen synthesis and phosphorolysis were active simultaneously in a cell, there would be a futile cycle with cleavage of 1 P bond per cycle
To prevent such a futile cycle, Glycogen Synthase and Glycogen Phosphorylase are reciprocally regulated, both by allosteric effectors and by covalent modification (phosphorylation)
Glycogen catabolism (breakdown)
Glycogen Phosphorylase catalyzes phosphorolytic cleavage of the →(1→4) glycosidic linkages of glycogen, releasing glucose-1-phosphate as the reaction product.
Glycogen (n residues) + Pi → glycogen (n-1 residues) + glucose-1-phosphate
The Major product of glycogen breakdown is glucose -1-phosphate
Fate of glucose-1-phosphate in relation to other pathways:
Phosphoglucomutase catalyzes the reversible reaction:
Glucose-1-phosphate → Glucose-6-phosphate
The Hemoglobin Buffer Systems
These buffer systems are involved in buffering CO2 inside erythrocytes. The buffering capacity of hemoglobin depends on its oxygenation and deoxygenation. Inside the erythrocytes, CO2 combines with H2O to form carbonic acid (H2CO3) under the action of carbonic anhydrase.
At the blood pH 7.4, H2CO3 dissociates into H+ and HCO3 − and needs immediate buffering.
Niacin: Vitamin B3, Nicotinamide, Nicotinic Acid Niacin, or vitamin B3,
is involved in energy production, normal enzyme function, digestion, promoting normal appetite, healthy skin, and nerves.
RDA Males: 16 mg/day; Females: 14 mg/day
Niacin Deficiency : Pellagra is the disease state that occurs as a result of severe niacin deficiency. Symptoms include cramps, nausea, mental confusion, and skin problems.
Growth hormone
Growth hormone (GH or HGH), also known as somatotropin or somatropin, is a peptide hormone that stimulates growth, cell reproduction and regeneration in humans.
Growth hormone is a single-chain polypeptide that is synthesized, stored, and secreted by somatotropic cells within the lateral wings of the anterior pituitary gland.
Regulation of growth hormone secretion
Secretion of growth hormone (GH) in the pituitary is regulated by the neurosecretory nuclei of the hypothalamus. These cells release the peptides Growth hormone-releasing hormone (GHRH or somatocrinin) and Growth hormone-inhibiting hormone (GHIH or somatostatin) into the hypophyseal portal venous blood surrounding the pituitary.
GH release in the pituitary is primarily determined by the balance of these two peptides, which in turn is affected by many physiological stimulators (e.g., exercise, nutrition, sleep) and inhibitors (e.g., free fatty acids) of GH secretion.
Regulation
Stimulators of growth hormone (GH) secretion include peptide hormones, ghrelin, sex hormones, hypoglycemia, deep sleep, niacin, fasting, and vigorous exercise.
Inhibitors of GH secretion include somatostatin, circulating concentrations of GH and IGF-1 (negative feedback on the pituitary and hypothalamus), hyperglycemia, glucocorticoids, and dihydrotestosterone.
Clinical significance
The most common disease of GH excess is a pituitary tumor composed of somatotroph cells of the anterior pituitary. These somatotroph adenomas are benign and grow slowly, gradually producing more and more GH excess. The adenoma may become large enough to cause headaches, impair vision by pressure on the optic nerves, or cause deficiency of other pituitary hormones by displacement.
Biotin
Biotin helps release energy from carbohydrates and aids in the metabolism of fats, proteins and carbohydrates from food.
RDA The Adequate Intake (AI) for Biotin is 30 mcg/day for adult males and females
Biotin Deficiency Biotin deficiency is uncommon under normal circumstances, but symptoms include fatigue, loss of appetite, nausea, vomiting, depression, muscle pains, heart abnormalities and anemia.