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Questions and Answers
What type of bond do saturated fatty acids contain?
Which of the following is a key precursor of eicosanoids?
What distinguishes cis fatty acids from trans fatty acids?
What causes the accumulation of homocysteine in the blood and urine?
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What role do phosphoaglycerols play in cell membranes?
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How is homocystinuria primarily treated?
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Which type of lipid is derived from ceramide?
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Which of the following statements about a hypercatabolic state is true?
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How do trans fatty acids affect cholesterol levels in the body?
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What role do amino acids play during infection and wound healing?
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What is a major consequence of elevated purine degradation?
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What is the main structural characteristic of cholesterol?
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Which enzyme is inhibited by allopurinol to treat gout?
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What effect do fish oils, rich in omega-3 fatty acids, have on health?
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Which physiological change occurs in a hypercatabolic state?
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Which of the following describes the metabolic effect of hypercatabolic states?
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What is the active form of folate that can accept carbon atoms from serine and glycine?
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Which of the following conditions can arise from folate deficiency?
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What is the consequence of a vitamin B12 deficiency in relation to folate metabolism?
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Which food sources are primarily associated with vitamin B12?
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Which of the following amino acids provides carbon for folate in metabolism?
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What are the potential effects of low folate levels during early pregnancy?
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Why is vitamin B12 important in the context of folate-dependent metabolism?
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What is the health implication of the folate trap phenomenon?
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What is the primary role of insulin after a high carbohydrate meal?
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What occurs in the body when glucose levels are low?
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Which nutrient's metabolism is directly affected by hormonal regulation during fasting?
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What is the effect of glucagon on liver function during fasting?
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How do insulin and glucagon levels fluctuate in response to glucose presence?
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What happens after a high protein meal with no carbohydrates?
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Which of the following accurately describes the relationship between glucose and insulin?
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What is a key role of adipose tissue in response to glucagon during fasting?
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What is the primary role of NADPH in the Pentose Phosphate Pathway?
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Which phase of the Pentose Phosphate Pathway is irreversible?
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What is the consequence of glucose-6-phosphate dehydrogenase deficiency during oxidative stress?
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How does ribose-5-phosphate contribute to cellular functions?
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What is the importance of transferase enzymes in UDP-sugar metabolism?
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Which of the following substances are synthesized using UDP-glucose?
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What role does ribose-5-phosphate play in rapidly growing cells?
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What is a significant function of the reactive oxygen species (ROS) generated by the Pentose Phosphate Pathway?
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Study Notes
Fatty Acids & Lipids
- Saturated fatty acids: single bonds only
- Monounsaturated fatty acids: one double bond
- Polyunsaturated fatty acids: multiple double bonds
- Essential fatty acids: linoleic acid, α-linolenic acid, and arachidonic acid
- Arachidonic acid: precursor of eicosanoids, which regulate inflammation, muscle contraction, blood pressure
- Cis configuration: virtually all double bonds in naturally occurring polyunsaturated fatty acids are in cis configuration
- Cholesterol: very non-polar, contains a tetracyclic ring, humans cannot degrade the ring structure, can be converted to cholesterol esters
- Phosphoaglycerols: key components of cell membranes, glycerol backbone, play a role in signal transduction and metabolic pathways, contribute to cell membrane fluidity
- Sphingolipids: derived from ceramide, key components of cell membranes, regulate cell death/survival, toxin binding, and cell-cell recognition
- Sphingomyelin: a type of sphingolipid
- Sphingoglycolipid: a type of sphingolipid
- Lipid bilayers: can be formed by phosphoaglycerols and sphingolipids. Cholesterol inserts into these bilayers
- Membrane proteins: include integral and peripheral proteins, carbohydrate moieties on the extracellular side
Trans Fatty Acids
- Trans fatty acids are formed during hydrogenation
- They convert cis bonds to trans bonds
- Cis fatty acids make membrane packing loose, while trans fatty acids make membrane packing tight.
- They increase serum LDL cholesterol, triacylglycerols, and platelet aggregation.
- They decrease HDL cholesterol.
- Fish oils are rich in ω-3 polyunsaturated fatty acids which benefit cardiovascular health.
Pentose Phosphate Pathway
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NADPH is used for:
- biosynthetic reactions
- preventing oxidative damage to cells
- generating reactive oxygen species for phagocytosis
- Ribose is used for nucleotide biosynthesis.
- Oxidative phase: produces 2 NADPH, CO2, and ribose-5-phosphate
- Non-oxidative phase: interconverts 5- and 6- carbon sugars, produces fructose-6-phosphate and glyceraldehyde-3-phosphate.
- Oxidative phase is irreversible, does not generate ATP, G6PDH is the rate-limiting enzyme and is inhibited by NADPH.
- Non-oxidative phase is reversible, ribose-5-phosphate consumed in growing cells, ribose-phosphate can feed into glycolytic intermediates when only NADPH is needed.
Functions of NADPH
- Reductive biosynthesis (anabolism): helps reduce glutathione to scavenge reactive oxygen species.
- Generation of reactive oxygen species in phagocytes.
- Strong reductant.
- Reduced glutathione (GSH): maintains a reducing environment in cells and degrades reactive oxygen species.
Roles of Ribose-5-phosphate
- Sugar component of nucleotides: used in DNA/RNA synthesis, cell growth.
- ATP and cofactors: critical for cell processes.
Pentose Phosphate Pathway in Red Blood Cells
- Scavenges reactive oxygen species.
Pentose Phosphate Pathway in Phagocytosis
- Respiratory burst: provides NADPH for the NADPH oxidase enzyme.
- Phagocytic cells: rapidly consume oxygen to produce reactive oxygen species to kill invading pathogens.
Glucose-6-Phosphate Dehydrogenase Deficiency
- Hemolysis: occurs during times of oxidative stress.
- Symptoms: revealed by oxidative stress, which can be triggered by antimalarial agents, infections, and fava beans.
- Glutathione defense mechanism: impaired due to deficiency.
UDP-Sugars
- Formation: glucose forms UDP-sugars
- Roles: used in synthesis of lactose, glycoproteins, glycolipids, proteoglycans, and glucuronides
- Metabolic fate of UDP-glucose: donor for glycogen and glycoproteins, epimerization to form UDP-galactose
- Transferase enzymes: utilize UDP-sugars in various metabolic processes, including glycoprotein and galactose metabolism.
- UDP-glucuronate: important for drug detoxification, excretion of bilirubin, and steroid excretion.
Folate (B9) and Vitamin B12 (B12) in Metabolism
- Carbon carriers: crucial in nucleotide biosynthesis.
- Deficiencies: can lead to disease (anemia, etc.).
- Sources of single-carbons in the folate cycle: serine and glycine.
- Nucleotide biosynthesis: Folate is essential.
- Folate-mediated carbon transfer: from serine and glycine to folate.
- Purine nucleotide synthesis: folate transfers carbon to synthesize adenosine and guanosine.
- Deoxythymidine (dTMP) synthesis: folate helps synthesize dTMP.
- Vitamin B12: folate transfers carbon to vitamin B12 for other pathways.
B-Vitamins in Oral Health
- Folate deficiency: leads to megaloblastic anemia.
- Megaloblastic anemia: characterized by decreased mature red blood cells and accumulation of nucleated precursor cells (megaloblasts).
- Neural tube defects: low folate in early pregnancy increases risk of neural tube defects, like spina bifida.
- Vitamin B12 deficiency: also leads to megaloblastic anemia, found exclusively in animal products.
- Folate trap: in absence of B12, FH4 is trapped and cannot be recycled.
- Pernicious anemia: an autoimmune condition preventing vitamin B12 absorption due to parietal cell destruction in the stomach, leads to deficiency.
Homocystinuria (HCU)
- Defect: in cystathionine synthase, leading to homocysteine accumulation.
- Consequences: cardiovascular diseases, thromboembolisms, pectus excavatum, lens dislocation.
- Treatment: high doses of vitamin B6, decreased methionine intake, increased B12 and folate intake.
Gout
- Elevated purine degradation: can lead to gout.
- Uric acid: major purine degradation product, formed by xanthine oxidase.
- Insolubility of uric acid: causes inflammation and gout.
- Allopurinol: inhibits xanthine oxidase, used to treat gout.
Amino Acid Metabolism During Infection and Wound Healing
- Hypercatabolic state: occurs during physical trauma or critical illness, altering amino acid metabolism to support immune cell production.
- Immune system priority: immune system cells receive priority for amino acid utilization.
- Increased fuel utilization: characterized by increased fuel utilization and negative nitrogen balance.
- Cortisol: elevated levels during hypercatabolic state, stimulating glucose/ fatty acid metabolism.
- Mobilization of protein, lipid, and carbohydrates: maintain normal tissue function if dietary intake is insufficient, for immune response and wound healing.
- Negative nitrogen balance: protein breakdown and nitrogen excretion exceed dietary protein intake.
- Amino acid redirection: towards building the immune system.
Amino Acid Metabolism
- Building blocks: required for protein production.
- Cellular energy: some amino acids can be used for energy.
- Neurotransmitters, hormones, and nucleotides: raw materials for synthesis of these molecules.
- Dietary protein: essential source of amino acids.
- Peptidases: digestive enzymes that break down protein.
- Ammonium packaging: ammonia produced from amino acid metabolism is packaged into urea by the urea cycle.
Dietary Needs
- Folate and B12: important for nucleotide biosynthesis which is vital for blood cell production and cell division.
- Vitamin B6: involved in various metabolic processes, including amino acid metabolism.
- Precursors of neurotransmitters: several amino acids serve as precursors.
Fuel Switching
- Storage: when dietary fuel is abundant, we store as much as possible.
- Mobilization: when dietary fuel is scarce, we mobilize fuel stores.
- Insulin and glucagon/catecholamines: control fuel storage, mobilization, and switching.
- Blood glucose levels: regulate insulin and glucagon.
- Insulin: promotes fuel storage after a meal.
- Glucagon: mobilizes fuels and maintains blood glucose levels during fasting.
Insulin and Glucagon Effects
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Insulin effects:
- Stimulates glucose storage as glycogen in muscle and liver.
- Stimulates fatty acid synthesis and storage after a high carbohydrate meal.
- Stimulates amino acid uptake and protein synthesis.
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Glucagon effects:
- Activates gluconeogenesis (making new glucose) and glycogenolysis (breaking down glycogen) in the liver during fasting.
- Activates fatty acid release from adipose tissue.
Time Course of Glucose, Insulin, and Glucagon Levels
- Post-meal glucose/insulin pulse duration: depends on carbohydrate absorption rate in the gut.
- Glucose stimulates insulin release.
- Insulin/glucose inhibits glucagon release.
- Glucagon is stable as long as insulin and glucose levels are above baseline.
- Glucose and insulin parallel each other on time course graphs.
- Glucagon and insulin have opposite effects in blood.
- High protein meal without carbohydrates: small insulin increase for amino acid uptake and protein synthesis, large glucagon increase for glucose and fatty acid metabolism control.
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Description
This quiz provides an in-depth overview of fatty acids and lipids, focusing on their types, structures, and biological roles. Key concepts include saturated, monounsaturated, and polyunsaturated fatty acids, as well as essential fatty acids and their functions in the human body. Test your knowledge on cholesterol and membrane lipids.