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. […]
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Question 1: Explain why gluconeogenesis is not simply the reverse of glycolysis. Answer: Gluconeogenesis is not simply the reverse of glycolysis because there are three irreversible reactions in glycolysis that must be bypassed in gluconeogenesis. These irreversible reactions are catalyzed by hexokinase, phosphofructokinase, and pyruvate kinase. Gluconeogenesis uses different enzymes to bypass these steps, making
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Here’s a table showing the amino acids associated with each intermediate and helpful mnemonics to aid memorization: Intermediate Amino Acids Associated Mnemonic for Amino Acid Entry Points Pyruvate Glycine, Alanine, Serine, Cysteine, Threonine, Tryptophan, Hydroxyproline G – Glycine A – Alanine S – Serine C – Cysteine T – Threonine T – Tryptophan H – Hydroxyproline
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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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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
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
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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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
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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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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