“Discover key insights into fatty acid metabolism, ketogenesis, and triglyceride synthesis through clinical scenarios. This guide explains enzyme deficiencies like MCAD, hormonal regulation by insulin, and the role of beta-oxidation and omega oxidation pathways in energy production.”
“Clinical Biochemistry: Fatty Acid Metabolism, Ketogenesis, and Energy Regulation” Read More »
“Dear students,
Assess your understanding of fatty acid and triglyceride metabolism with this 32-question timed quiz. Complete it in one sitting and attempt it multiple times to solidify your knowledge. Explanations for all questions will be available tomorrow. Start your self-assessment journey today!”
Fatty acid and Triglyceride metabolism- a quiz for self-assessment Read More »
“Discover how essential vitamins like B2, B3, B6, B12, folate, and others impact fatty acid, triglyceride, and nucleotide metabolism. This detailed overview explains impaired reactions, enzymes affected, and consequences of deficiencies.”
Question 1: Why are triglycerides a more efficient energy storage form compared to glycogen? Answer: Triglycerides are highly reduced and stored in a nearly anhydrous form, yielding about 9 kcal/g upon complete oxidation. In contrast, the polar nature of glycogen leads to greater hydration, reducing its energy storage capacity to about 1/6th that of fat.
Fatty acid oxidation and TG breakdown- Short-answer questions Read More »
Question 1: Where does fatty acid synthesis primarily occur within the cell? Answer: Fatty acid synthesis occurs in the cytosol of the cell. This is in contrast to fatty acid oxidation, which primarily occurs in the mitochondria. Question 2: What is the primary product of fatty acid synthesis? Answer: The primary product of fatty acid
Short-answers reasoning questions on Fatty acids and Triglycerides synthesis Read More »
Overview of Fatty Acid Metabolism Disorders Disorder Enzyme Defect Impairment Type Clinical Manifestations Mnemonic Medium-Chain Acyl-CoA Dehydrogenase Deficiency (MCAD) Acyl-CoA Dehydrogenase specific for medium-chain fatty acids Impaired beta-oxidation of medium-chain fatty acids Hypoglycemia, lethargy, vomiting, seizures, coma, and sudden infant death MCAD = “Might Collapse And Die” Carnitine Deficiency Carnitine transporter or synthesis defect
Disoder Enzyme Defect Impairment Type Clinical Manifestations Mnemonic Carnitine Deficiency Carnitine transporter or synthesis defect Impaired transport of long-chain fatty acids Muscle weakness, cardiomyopathy, hypoketotic hypoglycemia “Car Can’t Fuel” CPT I Deficiency CPT I (Carnitine Palmitoyltransferase I) Impaired long-chain fatty acid entry into mitochondria Hypoketotic hypoglycemia, liver dysfunction, hyperammonemia “CPT I = Can’t Properly
Table 1: Role of organelles in Fatty Acid Synthesis, Elongation, and Desaturation Process Organelle Function Key Enzymes/Features De Novo Fatty Acid Synthesis Cytoplasm Formation of palmitate (16-carbon saturated fatty acid) from acetyl-CoA and malonyl-CoA. Acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS) Elongation of Fatty Acids Endoplasmic Reticulum (ER), Mitochondria Extends the carbon chain of long-chain
1. A 45-year-old patient presents to the clinic with significant weight loss and fatigue. Blood tests reveal elevated levels of epinephrine and glucagon. Given this clinical context, when these hormones bind to receptors on the adipose cell membrane, which of the following is NOT expected to occur? A. Fatty acids are activated, enter the mitochondria,
Fatty acid metabolism – Case-based multiple-choice questions-set 2 Read More »
Clinical Case: A 6-year-old boy presents to the emergency department with episodes of severe muscle weakness, fatigue, and dark-colored urine after prolonged physical activity. His parents report that he often becomes weak during periods of fasting or intense exercise. Blood tests reveal elevated levels of fatty acylcarnitine and normal levels of free carnitine. Plasma analysis
