A carnitine deficiency might manifest itself as... O accumulation of long chain fatty acids in the mitochondrial matrix. O an inability to run ß-oxidation on 16-carbon fatty acids. excess medium chain fatty acyl-CoA molecules in the mitochondrial matrix. O ketoacidosis. the inability to synthesize long chain fatty acids.
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- Indicate whether each of the following statements is true or false. If false, correct the statement or provide a brief explanation for why it is false. Malonyl-CoA inhibits carnitine acyltransferase II , thus slowing transport of fatty acyl-CoA into mitochondrial matrix.Indicate whether each of the following B vitamins is involved (as a cofactor) in β-oxidation pathway, ketogenesis, lipogenesis, or conversion of ketone bodies to acetyl CoA. There may be more than one correct response or no correct response for a particular B vitamin.1- Name of the disease/metabolic disorder due to deficiency of propionyl CoA carboxylase enzyme 2-Population affected; gender, age, race ... etc affected by previous disease or disorder 3- Symptoms of the disease/metabolic disorder (maximum 3 - 5 main common symptoms)
- For the mutation of the enzyme, describe the effect it will have on carbohydrate metabolism. Also, make sure to think about the effect it has on muscles versus the liver: Mutation that converted the active site cysteine in glyceraldehyde 3-phosphate dehydrogenase to a serineMetabolic ketoacidosis is a common problem with diabetics, which is caused by which of the following? Excessive oxidation of fatty acids, leading to an accumulation of ketone bodies in the blood. Excessive oxidation of glucose, leading to an accumulation of ketone bodies in the blood. Excessive oxidation of proteins, leading to an accumulation of ammonia in the blood. Hyperglycemia.Which of the following is NOT a fate of pyruvate in metabolism? .. Conversion to alanine as its storage form or for use by peripheral tissues such as skeletal muscles. Conversion to acetyl CoA for complete oxidation in the TCA cycle. Conversion to oxaloacetate in gluconeogenesis Conversion to lactate in a completely anaerobic process. L. Conversion to phophoenolpyruvate for the synthesis of glucose
- Arrange (1-15) the following statements based on their order from lipogenesis, lipolysis, beta-oxidation to ketogenesis. Acetoacetic acid is converted to β-hydroxybutyric acid and acetone Acetyl CoA is transported with oxaloacetate to the cytosol as citrate Palmitic acid is separated from the complex Creation of carbonyl group in the β-carbon Fuelling the different tissues, ketone bodies are transported to the blood Glyceraldehyde-3-PO4 is produced from the conversion of glycerol Unsaturation of the α & β-carbons of the FA chain Acetyl CoA is converted to acetoacetic acid Acetyl CoA and oxaloacetate are produced from citrate Hydolysis of the double bond in the FA acid chain Malonyl CoA is produced from CO2 fixation of acetyl CoA Acetyl CoA enters the Krebs Cycle Separation of the two-carbon product from the fatty acyl CoA Malonyl CoA is converted to saturated FA complexed with protein TG is hydrolyzed to FA and glycerolWhen the acetyl-CoA produced during ß-oxidation in the liver exceeds the capacity of the citric acid cycle, the excess acetyl-CoA forms ketone bodies acetone, acetoacetate, and D-b-hydroxybutyrate. This occurs in severe, uncontrolled diabetes: because the tissues cannot use glucose, they oxidize large amounts of fatty acids instead. Although acetyl-CoA is not toxic, the mitochondrion must divert the acetyl-CoA to ketone bodies. What problem would arise if acetyl-CoA were not converted to ketone bodies? How does the diversion to ketone bodies solve the problem?Carnitine shuttle is used to Transport FA chains from the adipose tissue to the liver. Transport FA chains from the blood-stream to the cytosol. Transport FA chains from the cytosol to the mitochondrial matrix. Transport FA chains from the mitochondrial matrix to the cytosol.
- Deficiencies of carnitine, carnitine acyltransferases, or carnitine/acylcarnitine translocase affect the metabolism of long-chain fatty acids. Many of the symptoms are similar, and include hypoketotic hypoglycemia, low ketone levels and low blood sugar with fasting, and damage to the liver, heart, or muscles due to fatty acid buildup in those tissues. Symptom severity varies with the form of the deficiency. The following abbreviations are used: carnitine acyltransferase (carnitine palmitoyltransferase), CPT and carnitine/acylcarnitine translocase, CACT. Identify each symptom or effect as a deficiency of CPT I, CPT II, or CACT. CPT I deficiency CPT II deficiency CACT deficiency Answer Bank acyl carnitine not transported into mitochondrial matrix long-chain fatty acids not transferred to carnitine long-chain fatty acids remain attached to carnitine in matrixIndicate whether each of the following statements is true or false. If false, correct the statement or provide a brief explanation for why it is false. With high [carbohydrate] levels, excess glucose (after glycogen storage has reached a maximum) is converted to fat, leading to high [malonyl-CoA].The ketogenic diet is now a trend for people who wants to lose weight. Your task is to come up with a report about this diet and assess its efficacy and implication to the health. Here are your guiding questions: 1) What are ketone bodies and ketogenesis? 2) What is a ketogenic diet? What makes it different from other kinds of diet? 3) What are the good and bad effects of this diet? 4)In your personal opinion, is it safe to continue this diet for a long period of time?