Biology: Krebs Cycle Quiz

Carbohydrate Metabolism

• Carbohydrates are digested in the mouth, with salivary amylase acting on cooked starch and glycogen, converting them into dextrin, maltose, and isomaltose. Some starch remains undigested.
• Pancreatic amylase acts on both cooked and uncooked starches at a pH of 7.1, converting them into maltose and isomaltose.
• Final digestion involves intestinal enzymes. Lactose is broken down by lactase into glucose and galactose. Maltose is broken down by maltase into two glucose molecules. Sucrose is broken down by sucrase into glucose and fructose. Isomaltose is broken down by dextrinase into two glucose molecules (bond between carbon 1 and 6).
• Cellulose is not digested due to the lack of the enzyme cellulase, which breaks the β-linkages. It is used in treating constipation.
• Absorbed sugars are taken up by the liver, where galactose and fructose are converted into glucose.
• Sugar utilization follows three pathways: oxidation, storage, and conversion.
• Oxidation: Glycolysis and the Krebs cycle produce energy. The pentose phosphate pathway (HMP shunt) produces ribose, NADPH, and glucuronic acid.
• Storage: Glycogenesis stores glucose as glycogen.
• Conversion: Conversion occurs to fatty acids, or into ribose and deoxyribose for DNA and RNA synthesis. Ribose and deoxyribose also help convert lactose into milk.
• Glucose oxidation occurs in the cytoplasm, except the Krebs cycle which occurs in mitochondria.
• Complete oxidation involves glycolysis (cytoplasm) and the Krebs cycle (mitochondria) to produce CO2 and H2O.
• Glycolysis: Is the anaerobic phase of glucose oxidation, the Embden-Meyerhof pathway, which means the oxidation of glucose into pyruvate. It's most important in muscle during exercise because of O2 lack, and in red blood cells (RBCs) due to the absence of mitochondria.
• Glycolysis produces 8 or 6 ATP in the presence of O2, decreasing Hb's affinity for O2, making O2 easier to reach tissues.
• Glycolysis produces pyruvic acid that initiates the Krebs cycle. DHAP (dihydroxyacetone phosphate) converts to glycerol-3-phosphate, which is important for lipogenesis. Glycolysis also produces 2 amino acids: serine (from 3-phosphoglycerate) and alanine (from pyruvate).
• Mitochondrial Pathway: The Krebs cycle fully oxidizes glucose to CO2 and H2O. The first stage is the oxidative decarboxylation of pyruvate to acetyl CoA. The second stage is the Krebs cycle.
• Oxidative Decarboxylation: This process is catalyzed by the pyruvate dehydrogenase complex (PDC or PDH) and requires 5 coenzymes (TPP, lipoic acid, CoASH, FAD, and NAD).
• Citric Acid Cycle (CAC) / Krebs' cycle / TCA: Occurs in the mitochondria.
• Catabolic Role: Produces 12 ATP for each acetyl CoA. Used in the complete oxidation of carbohydrates, lipids, and proteins.
• Anabolic Role: Synthesizes heme (succinyl CoA + glycine), and certain amino acids (transamination).
• Fatty Acid Synthesis: Acetyl CoA and oxaloacetate form citrate, which then enters the cytoplasm to form fatty acids.
• Gluconeogenesis: The synthesis of glucose from non-carbohydrate sources, uses the Krebs cycle.
• Importance of CO2: Important in several processes including the synthesis of fatty acids (from acetyl CoA and CO2 to malonyl CoA), oxaloacetate formation (from pyruvate and CO2), and urea synthesis (from NH3 and CO2).
• Pentose Phosphate Shunt (HMP Shunt): Occurs in the cytoplasm of the liver. Produces pentoses for DNA and RNA synthesis and NADPH+H for fatty acid, cholesterol, sphingosine, galactolipid, glucuronic acid, and non-essential amino acid synthesis. It also reduces glutathione.
• Favism: A deficiency in glucose-6-phosphate dehydrogenase (G6PD) leads to red blood cell (RBC) hemolysis, especially after eating fava beans. The deficiency affects the production of NADPH, thus affecting the reduction of glutathione, leading to hemolysis.
• Blood Glucose: Fasting blood glucose level is 70-110 mg/dl. One-hour after meal it reaches 120-150 mg/dl. Insulin decreases blood glucose by transferring glucose to cells, stimulating glycolysis and glycogenesis, inhibiting glycogenolysis and gluconeogenesis, stimulating lipogenesis, and stimulating protein synthesis.
• Anti-insulin Hormones: Glucagon, catecholamines, corticosteroids (glucocorticoid), growth hormone, and thyroid hormones all increase blood glucose by stimulating or inhibiting processes.
• Hepatic Regulation: During fasting, glycogenolysis and gluconeogenesis increase blood glucose. After a meal, glycogenesis and lipogenesis increase.
• Renal Regulation: Renal threshold is the blood glucose level above which glucose appears in urine (180 mg/dl). Abnormal low renal threshold (100 mg/dl) is called diabetes innocense.
• Variation in Blood Glucose (Hyperglycemia): Blood glucose above normal. Fasting levels >126 mg/dl, postprandial levels >200 mg/dl Causes include: ↓ insulin (diabetes mellitus, pancreas removal); ↑ anti-insulin hormones (adrenaline, cortisone, growth hormone, and thyroid problems).
• Hypoglycemia: Blood glucose below 40 mg/dl. It's dangerous as the brain depends on glucose. Symptoms include confusion, dizziness, tremors, weakness, tachycardia, and ultimately coma.
• Causes of hypoglycemia: Excessive insulin dose, missed meals during insulin therapy, insulinoma (tumor secreting excess insulin), ↓ anti-insulin hormones (Addison's disease, hypothyroidism, etc.), glycogen storage diseases (Von Gierke's disease), fructosemia/galactosemia.
• Diabetes Mellitus (DM): Symptoms include polyphagia (excessive eating), polydipsia (excessive drinking), polyuria (excessive urination), glucosuria (glucose in urine), and excessive loss of water-soluble vitamins. Type I DM is insulin-dependent, typically occurring during childhood, and is autoimmune. Type II DM is non-insulin-dependent, usually occurring after 35, and is often linked to obesity.
• Protein Metabolism in DM: Insulin ↓ protein catabolism → ↓ levels of glucose → Muscle wasting happens; Antibody formation → Resistance & ↑ Infection; Poor wound healing.
• Lipid Metabolism in DM: ↓ insulin → ↑ lipolysis → Loss of weight, Fatty liver, ↑ Free Fatty acid→ Hypercholesterolemia, atherosclerosis.
• Microangiopathy: Damage to small blood vessels. Retinopathy affects the retina → blindness; Nephropathy affects the kidneys → renal failure.
• Diagnosis of DM: Oral glucose tolerance test (OGTT) measures glucose tolerance (body utilizing glucose without appearing in urine).
• Glycosylated Hemoglobin (HbA1c): A measure of average blood glucose over 2-3 months. Normal is 4-8%; >8% indicates diabetes.
• Difference between DM and Renal Glucosuria: In DM, high glucose and diseased pancreas, treating with insulin. Renal glucosuria is due to a ↓ renal threshold, normal glucose, a diseased kidney, treating with glucose.
• Diabetic Coma: A severe complication of diabetes. Hyperglycemic (ketotic) coma is due to high ketone bodies and lactic acidosis. Hyperglycemic hyperosmolar coma is a non-ketotic coma due to severe dehydration. Hypoglycemic coma is due to insulin overdose.
• Glucosuria: Glucose in urine. Hyperglycemic glucosuria is due to high blood glucose. Normoglycemic glucosuria is due to a lower than normal renal threshold, or an experimental condition (after phlorizin injection, which inhibits glucose absoption).

Test your knowledge of the Krebs cycle with this quiz! Explore the primary functions, produced substances, and crucial coenzymes involved in this vital metabolic pathway. Perfect for biology students and enthusiasts looking to enhance their understanding of cellular respiration.