In the grand narrative of life’s chemistry, lipids and amino acids emerge as more than just nutrients. They are energy reserves, structural components, and molecular messengers. Unit 3 explores how the body processes fats and proteins, how imbalances trigger disease, and why understanding these pathways is vital for health and medicine.
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Lipid Metabolism: More Than Just Fat
Lipids serve as dense energy stores, essential membrane components, and precursors of hormones. Their metabolism represents both a powerhouse of energy and a hub of biosynthesis.
β-Oxidation of Fatty Acids
The breakdown of fatty acids begins with β-oxidation, a mitochondrial process that systematically removes two-carbon units as acetyl-CoA.
Example: Palmitic acid, a common saturated fatty acid, generates 8 acetyl-CoA molecules, which then feed into the citric acid cycle.
Energy yield: The complete oxidation of palmitate produces over 100 ATP molecules, underscoring fats as the body’s richest energy source.
Ketone Bodies and Ketoacidosis
When glucose is scarce — during fasting, prolonged exercise, or uncontrolled diabetes — the liver converts acetyl-CoA into ketone bodies (acetoacetate, β-hydroxybutyrate, and acetone).
Utilization: Heart and brain can use ketones as alternative fuels.
Ketoacidosis: Excessive ketone production lowers blood pH, leading to dangerous metabolic acidosis, a hallmark of untreated type 1 diabetes.
Fatty Acid Synthesis
While oxidation breaks down fats, de novo synthesis builds them up. In the cytoplasm, acetyl-CoA is elongated step by step to form palmitic acid. This pathway is crucial when carbohydrate intake exceeds immediate energy needs, storing the surplus as fat.
Cholesterol: A Double-Edged Molecule
Cholesterol, often vilified, plays indispensable roles:
Bile acids: Aid in fat digestion.
Steroid hormones: Serve as precursors for cortisol, aldosterone, and sex hormones.
Vitamin D: Synthesized from cholesterol under UV light, critical for calcium metabolism.
Yet, excessive cholesterol is harmful. Elevated levels contribute to atherosclerosis, narrowing arteries and raising cardiovascular risks.
Disorders of Lipid Metabolism
Imbalances in lipid handling lead to major health burdens:
Hypercholesterolemia: High cholesterol in blood.
Atherosclerosis: Plaque formation in arteries.
Fatty liver: Accumulation of triglycerides in hepatocytes.
Obesity: Excess fat storage linked to metabolic syndrome and diabetes.
Amino Acid Metabolism: Proteins in Motion
Amino acids are constantly recycled, broken down, and repurposed. Their metabolism balances nitrogen disposal and the synthesis of essential biomolecules.
General Reactions of Amino Acids
Transamination: Transfer of amino groups, linking amino acid metabolism with carbohydrate metabolism.
Deamination: Removal of amino groups, releasing ammonia.
Decarboxylation: Produces neurotransmitters like histamine and serotonin.
Urea Cycle: Detoxifying Ammonia
Ammonia, generated during amino acid breakdown, is toxic. The urea cycle in the liver safely converts it into urea for excretion.
Disorders: Enzyme defects can lead to hyperammonemia, causing neurological symptoms.
Catabolism of Phenylalanine and Tyrosine
Phenylalanine is converted to tyrosine, which is further degraded into fumarate and acetoacetate. When these pathways falter, serious disorders arise:
Phenylketonuria (PKU): Defective phenylalanine hydroxylase causes buildup, impairing brain development.
Albinism: Tyrosinase deficiency blocks melanin synthesis, resulting in lack of pigmentation.
Alkaptonuria: Accumulation of homogentisic acid leads to dark urine and connective tissue damage.
Tyrosinemia: A spectrum of disorders with liver and kidney involvement.
Synthesis of Biologically Active Substances
From amino acids arise critical biomolecules:
5-HT (serotonin) and melatonin: Derived from tryptophan, regulating mood and sleep.
Dopamine, noradrenaline, adrenaline: Catecholamines from tyrosine, vital for neural signaling and stress response.
Catabolism of Heme and Jaundice
Heme, from hemoglobin, is broken down into bilirubin. Normally excreted in bile, bilirubin buildup leads to jaundice, a condition visible as yellowing of skin and eyes. Causes range from liver disease to bile duct obstruction and excessive red cell breakdown.