Short-answers reasoning questions on Fatty acids and Triglycerides synthesis

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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 […]

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Comprehensive Overview of Fatty Acid Metabolism Disorders: Key Enzyme Defects, Clinical Manifestations, and Mnemonics for Easy Recall

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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

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Understanding Organelle Roles in Fatty Acid Metabolism: Synthesis, Elongation, Desaturation, and Oxidation

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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

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Navigating the Fed and Fasting States: Key Pathways, Enzymes, and Memorable Mnemonics

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This table includes a note about the enzyme activity in each state: State Hormone Pathway Enzymes Active Mnemonic Fed State Insulin Glycolysis Hexokinase, PFK-1, Pyruvate Kinase “Hungry Pandas Party” (HPP) Glycogenesis Glycogen Synthase “Glyco Savings” Fatty Acid Synthesis Acetyl-CoA Carboxylase, Fatty Acid Synthase “ACCelerate the Fats” Protein Synthesis Ribosomal enzymes “Ribs Build” Lipogenesis Lipoprotein Lipase

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Fatty acid metabolism – Case-based multiple-choice questions-set 2

Practice questions, USMLE styled question bank /

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,

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“Differentiating Carnitine Deficiency and Enzyme Deficiencies in the Carnitine Shuttle: Clinical and Laboratory Insights”

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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

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Fatty acid and Triglyceride synthesis- Case-based multiple-choice questions

Practice questions, USMLE styled question bank /

1. Which of the following TCA cycle intermediates plays a crucial role in de novo fatty acid synthesis by providing substrate and positively regulating the rate-limiting enzyme involved in fatty acid synthesis? A. Citrate B. Isocitrate C. Malate D. Oxaloacetate E. Succinate   Correct Answer: A. Citrate. Citrate plays a crucial role in de novo

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Glycogen Storage Diseases- Multiple Choice Questions

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1. A 3-month-old male infant presents with poor feeding, hypotonia, and cardiomegaly on physical exam. Blood tests reveal elevated lactate, uric acid, and creatine kinase levels. Echocardiogram demonstrates hypertrophic cardiomyopathy. A muscle biopsy shows excessive glycogen storage in lysosomes. Which enzyme deficiency is most likely responsible for this infant’s condition? A. Glucose-6-phosphatase B. Debranching enzyme

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Glycogen storage diseases with mnemonics to aid memorization

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A table summarizing the main glycogen storage diseases (GSDs) with enzyme defects, key clinical features, and mnemonics to aid memorization: Glycogen Storage Disease Enzyme Defect Key Clinical Features Mnemonic Type I: von Gierke Disease (GSD I) Glucose-6-phosphatase Severe fasting hypoglycemia, hepatomegaly, lactic acidosis, hyperlipidemia, hyperuricemia “von Gierke: ‘G6P’s Gone, Liver Left Low” Type II: Pompe

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