Metabolism

1. What are the changes in Glucose 6 phosphatase, Fructose 1,6 bisphosphate, Pyruvate kinase, and PEP carboxykinase in a person in a fasting state (like lost in the desert for a week)?

*In fasting state you increase Glucagon>Increase cAMP>increase PKA activity>Increase frutose Bisphosphatase 2 and 1 acitivty will be increased Hence we turn Fructose 2,6 bisphosphate and and Fructose 1,6 bisphosphate to create Fructose-6 phosphate thus their concentrations decrease,Hence the Fructose 1,6 bisphosphate concetration will be Decreased,remember that Fructose 1,6 bisphosphate STIMULATES pyruvate kinase(Turns PEP>Pyruvate) but as we Decreased F1,6BP, we thus Decreased activity of Pyruvate kinase.*Now for PEP carboxykinase(in CYTOSOL) and for Glucose 6 phosphatase(In ER) you should just remember that these 2 are IRREVERSIBLE enzymes in Liver that are activated during fasting state to maintain euglycemia(Hence in our case their activity will be increased)*So in summary G6phosphatase,PEP cabroxykinase activity is increased,Pyruvate Kinase activity is decreased while Fructose 1,6 Bisphosphate Concetration will be DOWN(because Fructose 2,6 bisphosphate which would inhibit the Fructose 1,6 bisphosphatASE which turns Fructose 1,6BP>Fructose 6p,is down because During fasting FB2ase increases in activity and thus decreases concentration of its substrate=FB2,6, >Removal of inhibition on F1,6BisphosphatASE>hence the end result is INCREASED F1,6BisphosphatASE activity leading to LOWER concentrations of its Substrate F1,6 BisphosphATE)

PEP carboxykinase activity is decreased in a person in a fasting state due to lower energy demands.

During fasting state, Glucose 6 phosphatase activity is decreased and Fructose 1,6 bisphosphate concentration is increased.

In a fasting state, Pyruvate kinase activity is increased due to higher glucose utilization.

In a fasting state, the body undergoes specific metabolic changes to maintain euglycemia. The correct answer explains how these changes occur in relation to Glucose 6 phosphatase, Fructose 1,6 bisphosphate, Pyruvate kinase, and PEP carboxykinase. The incorrect answers provided do not accurately reflect the metabolic adaptations that occur during fasting.

Explanation

In a fasting state, the body undergoes specific metabolic changes to maintain euglycemia. The correct answer explains how these changes occur in relation to Glucose 6 phosphatase, Fructose 1,6 bisphosphate, Pyruvate kinase, and PEP carboxykinase. The incorrect answers provided do not accurately reflect the metabolic adaptations that occur during fasting.

2. Type IV - Glycogen storage disease-(Andersen's).

Excess production of branching enzyme leading to rapid glycogen breakdown and hypoglycemia.

Defective branching enzymeInability to form branches → long, insoluble glycogen chains accumulate → foreign-body reactions eventually causing organ dysfunction, mainly cirrhosis

Deficiency in glycogen synthase enzyme resulting in decreased glycogen production and muscle weakness.

Defect in glucose-6-phosphatase enzyme leading to impaired glycogen breakdown and hepatomegaly.

In Type IV Glycogen storage disease (Andersen's), the defective branching enzyme causes the inability to form branches leading to the accumulation of long, insoluble glycogen chains. This accumulation results in foreign-body reactions eventually causing organ dysfunction, mainly cirrhosis.

Explanation

In Type IV Glycogen storage disease (Andersen's), the defective branching enzyme causes the inability to form branches leading to the accumulation of long, insoluble glycogen chains. This accumulation results in foreign-body reactions eventually causing organ dysfunction, mainly cirrhosis.

3. Which compound acts as the mediator of TCA that inhibits Glycolysis and stimulates fatty acid synthesis?

*CITRATE*Citrate inhibits PFK1<RATE LIMITING enzyme in Glycolysis, at the same time citrate activates Acetyl Coa Carboxylase<Rate-limiting enzyme of Fatty acid SYNTHESIS.Note that CItrate turns ON gluconeogenesis by inhibition of PFK 1 and stimulation of fructose 1,6 bisphosphatase

Succinate

Oxaloacetate

Malate

Citrate inhibits PFK1, the rate-limiting enzyme in Glycolysis, and activates Acetyl Coa Carboxylase, the rate-limiting enzyme of Fatty acid synthesis. It also turns on gluconeogenesis by inhibiting PFK 1 and stimulating fructose 1,6 bisphosphatase.

Explanation

Citrate inhibits PFK1, the rate-limiting enzyme in Glycolysis, and activates Acetyl Coa Carboxylase, the rate-limiting enzyme of Fatty acid synthesis. It also turns on gluconeogenesis by inhibiting PFK 1 and stimulating fructose 1,6 bisphosphatase.

4. Black ear Cartilage/Intervertebral discs. Discolored sclerae, urine turns black after standing. They often have trouble with Arthritis due to accumulation of X. What is X, where is it derived from, to what is it metabolized to, and which enzyme is deficient here?

Ochronosis derived from Tyrosine metabolized to Acetoacetyl-CoA deficiency in Tyrosinase enzyme

Gout derived from Uric Acid metabolized to Allantoin deficiency in Xanthine Oxidase enzyme

*ALKAPTONURIA is Autosomal RECESSIVE condition that involves deficiency of HOMOGENTISTATE OXIDASE, so you can't metabolize Homogentistate(derivative of phenylalanine) to maleylacetoacetate(which after few steps would give us Fumarate for TCA)

Hemochromatosis derived from Heme metabolized to Bilirubin deficiency in Hepcidin enzyme

The correct answer is Alkaptonuria, as this condition fits the symptoms described in the question. The incorrect answers provided are conditions that do not match the described symptoms or enzyme deficiencies.

Explanation

The correct answer is Alkaptonuria, as this condition fits the symptoms described in the question. The incorrect answers provided are conditions that do not match the described symptoms or enzyme deficiencies.

5. Why can't hepatocytes use ketones as a source of energy?

Because ketones cannot be transported into hepatocytes.

Because ketones are toxic to hepatocytes.

Because ketones are primarily used by muscle cells for energy production.

*Because they lack succinyl CoA-acetoacetate CoA transferase (thiophorase) - required to convert acetoacetate to acetoacetyl CoA.

Because hepatocytes do not have the necessary enzymes to utilize ketones.

Hepatocytes lack the specific enzyme required to convert a key ketone (acetoacetate) into a form that can be used for energy production.

Explanation

Hepatocytes lack the specific enzyme required to convert a key ketone (acetoacetate) into a form that can be used for energy production.

6. Why might you get cataracts/peripheral neuropathy with diabetes? Why are seminal vesicles/liver least susceptible to this damage?

Due to a lack of blood flow to the lens and nerves caused by diabetes

*Because aldose reductase gives Sorbitol from glucose, sorbitol can't cross membranes and acts creates osmotic gradient...BUT Liver/Seminal vesicles get rid of excess sorbitol by sorbitol dehydrogenase(Converts sorbitol to fructose), while Lens and Schawnn cells(responsible for peirpheral neuropathy) don't have proper activity of this enzyme, just like retina/kidney and other tissues frequently damaged by diabetes.

The liver and seminal vesicles have a higher glucose metabolism which protects them from diabetes-induced damage

Because diabetes causes an increase in insulin levels which directly affects the eyes and nerves

The correct answer explains the role of aldose reductase in converting glucose to sorbitol, leading to cataracts/peripheral neuropathy, and why the liver/seminial vesicles are least susceptible due to the presence of sorbitol dehydrogenase.

Explanation

The correct answer explains the role of aldose reductase in converting glucose to sorbitol, leading to cataracts/peripheral neuropathy, and why the liver/seminial vesicles are least susceptible due to the presence of sorbitol dehydrogenase.

7. Which amino-acids can feed the TCA cycle by increasing Succinyl coa (through increase in Propionyl coa which is eventually transformed into it)?

A - alanineF - phenylalanineC - cysteine

P - prolineG - glycineD - aspartic acid

S - serineE - glutamic acidL - leucine

V - valine
O - odd-chain fatty acids
M - methionine
I - isoleucine
T - Threonine

Amino acids V, O, M, I, and T can increase Succinyl coa by being converted into Propionyl coa, which eventually enters the TCA cycle. The incorrect answers do not contribute to this specific pathway.

Explanation

Amino acids V, O, M, I, and T can increase Succinyl coa by being converted into Propionyl coa, which eventually enters the TCA cycle. The incorrect answers do not contribute to this specific pathway.

8. A 6-month-old male infant has failure to thrive and abdominal enlargement. His parents are concerned that he has shown minimal movement since birth. On physical examination, the infant has marked muscle weakness and hepatosplenomegaly. A chest radiograph shows marked cardiomegaly. He dies of congestive heart failure at age 19 months. A deficiency of which of the following enzymes is most likely to be present in this infant?

Autosomal dominant condition involving lysosomal glucosidase

*This is autosomal recessive condition involving lysosomal glucosidase.*Particularly alpha 1,4 glucosidase with alpha1,6 glucosidase activity(Acid maltase).*Patients are at increased risk of RESTRICTIVE cardiomyopathy, Hypotonia,proximal muscle weakness with hepatosplenomegaly and macroglossia(large tongue) are other common findings.

Lysosomal lipase deficiency

Mitochondrial enzyme deficiency

This condition is characterized by restrictive cardiomyopathy, hypotonia, proximal muscle weakness, hepatosplenomegaly, and macroglossia.

Explanation

This condition is characterized by restrictive cardiomyopathy, hypotonia, proximal muscle weakness, hepatosplenomegaly, and macroglossia.

9. A 9-year-old boy is being evaluated for deafness. Physical examination reveals a child with short stature, coarse facial features (low, flat nose, thick lips, widely spaced teeth, facial fullness), a large tongue, and clear corneas. Laboratory examination reveals increased urinary levels of heparan sulfate and dermatan sulfate. Metachromatic granules (Reilly bodies-due to accumulation of GAGs) are found in leukocytes from a bone marrow biopsy and in Neurons we see Zebra bodies(accumulation of GAGs). These leukocytes are also found to be deficient in iduronosulfate sulfatase. What is the correct diagnosis?

Mucopolysaccharidosis type 4 (MPS IV, Morquio syndrome) - MPS IV is due to a deficiency of galactose-6-sulfatase, leading to deposits of keratan sulfate

*Hunter's syndrome is X-linked recessive def. of Iduronate sulfatase>MPS withOUT corneal clouding(Contrast this with Hurler's where there is corneal clouding)

Mucopolysaccharidosis type 1 (Hurler syndrome) - MPS I is due to a deficiency of alpha-L-iduronidase, leading to accumulation of heparan sulfate and dermatan sulfate

Mucopolysaccharidosis type 2 (MPS II, Hunter syndrome) - MPS II is due to a deficiency of iduronate sulfatase, leading to accumulation of glycosaminoglycans (GAGs)

The correct diagnosis in this case is Hunter's syndrome, a mucopolysaccharidosis (MPS) caused by a deficiency of iduronate sulfatase. The clinical manifestations described in the question, in addition to the laboratory findings, are consistent with Hunter's syndrome. It is important to differentiate between various types of MPS based on the specific enzyme deficiencies and associated clinical features.

Explanation

The correct diagnosis in this case is Hunter's syndrome, a mucopolysaccharidosis (MPS) caused by a deficiency of iduronate sulfatase. The clinical manifestations described in the question, in addition to the laboratory findings, are consistent with Hunter's syndrome. It is important to differentiate between various types of MPS based on the specific enzyme deficiencies and associated clinical features.

10. What metabolic process is true when you wake up and are about to have your first meal?

Protein is converted into carbohydrates during fasting

The brain produces ketone bodies during sleep

*Ketone body synthesis begins 90 Mins after meal, to maintain blood glucose. so first choice is correct(u haven't eaten whole night),however muscles and other tissue rapidly take up ketone bodies and they aren't measured well during first days, however they are MADE by liver even 90 mins after meal.*Glucose can NOT be synthesized by Fatty acids, But glucose can be used to synthesize Fatty acids.(remember FAG<Not trying to be rude, but i promise you won't mess these 2 up)

Glucose is synthesized by fatty acids

Ketone body synthesis begins 90 minutes after a meal to maintain blood glucose levels. While muscles and other tissues take up ketone bodies rapidly, they are primarily produced by the liver. Glucose cannot be synthesized from fatty acids, but fatty acids can be used to synthesize glucose. Additionally, the brain does not produce ketone bodies during sleep, and protein is not converted into carbohydrates during fasting.

Explanation

Ketone body synthesis begins 90 minutes after a meal to maintain blood glucose levels. While muscles and other tissues take up ketone bodies rapidly, they are primarily produced by the liver. Glucose cannot be synthesized from fatty acids, but fatty acids can be used to synthesize glucose. Additionally, the brain does not produce ketone bodies during sleep, and protein is not converted into carbohydrates during fasting.

11. Which enzyme catalyzes the esterification of 2/3 of plasma cholesterol from Nascent HDL to Mature HDL?

CETP (Cholesterol Ester Transfer Protein)

HMG-CoA Reductase

ACAT (Acyl-CoA:Cholesterol Acyltransferase)

*LCAT(Lecithin–cholesterol acyltransferase) vs CETP(Cholesterol Ester Transfer Protein)They can describe experiment where Nacent HDL can't be transformed to Mature HDL and ask you defect in enzyme-lCAT.(remember I am Mature CAT)*They can also do the same with transfer of cholesterol esters from MATURE HDL to Other Lipoproteins(VLDL,IDL,LDL)-CETP.

LCAT is responsible for converting cholesterol in nascent HDL to cholesterol esters in mature HDL.

Explanation

LCAT is responsible for converting cholesterol in nascent HDL to cholesterol esters in mature HDL.

12. Does insulin induce Cholesterol synthesis?

*Yes it can as Insulin Induces activity of HMG-CoA reductase(3-hydroxy-3-methyl-glutaryl-coenzyme A reductase)<remember this is the enzyme that is inhibited by STATINS(COMPETITIVE,Reversible inhibition-we increase Km-the amount of substrate to give us the same effect without altering maximal effect Vm, thus dose-response curve is shifted towards right)

Insulin has no effect on Cholesterol synthesis

Insulin only affects glucose metabolism, not Cholesterol synthesis

No, insulin inhibits Cholesterol synthesis

Insulin can induce Cholesterol synthesis by increasing the activity of HMG-CoA reductase, the enzyme involved in this process.

Explanation

Insulin can induce Cholesterol synthesis by increasing the activity of HMG-CoA reductase, the enzyme involved in this process.

13. A 19-year-old patient had a myocardial infarction and has Corneal arcus on physical examination. What other sign would be most likely present and pathognomonic for this disease? Is the patient a homozygote or heterozygote if their cholesterol level is 444? What is the inheritance pattern and defect associated with this condition?

Patient likely has Familial Hypercholesterolemia Type 3, which is an X-linked condition resulting from mutations in the APOB gene. Angina would be pathognomonic for this condition.

*Patient likely has type 2A Familial Hypercholesterolemia which is Autosomal DOMINANT condition that results from absent/defective LDL receptors.*Achilles Tendon xanthoma is pathognomonic finding on physical exam.(For familial Hypercholesterolemia-Type 2 dyslipdemia)*They have accelerated atherosclerosis and can develop MI before age of 20.(otherwise very unusual)*444 is more close to 300 than it is to 700 thus patient is most likely Heterozygote, homozygotes would have levels around 700.*Heterozygote form is wayy more common(1:500) but both have increased risk of MI before age of 20.*Elevated LDL is due to Lack of /defective LDL RECEPTORS, CHOLESTEROL synthesis increases because even though there is BUNCH of LDL out of cells, we can't uptake them inside, so HMG-Coa is not inhibited by negative feedback and Produces MORE cholesterol.<Know that...

Patient likely has Familial Hypercholesterolemia Type 4, which is a Autosomal Recessive condition affecting the ABCG5/G8 transporter. Arcus senilis would be pathognomonic for this condition.

Patient likely has Familial Hypercholesterolemia Type 1, which is an Autosomal Recessive condition resulting from overproduction of LDL in the liver. Xanthelasma would be pathognomonic for this condition.

The correct answer is Type 2A Familial Hypercholesterolemia as described in the answer section. The incorrect answers describe different types of Familial Hypercholesterolemia with corresponding incorrect pathognomonic signs and inheritance patterns.

Explanation

The correct answer is Type 2A Familial Hypercholesterolemia as described in the answer section. The incorrect answers describe different types of Familial Hypercholesterolemia with corresponding incorrect pathognomonic signs and inheritance patterns.

14. Are high levels of HDL good?

High levels of HDL only benefit liver health.

No, high levels of HDL are harmful for vascular health.

HDL has no impact on vascular health.

*Yes as it is protective for vascular health.*It is Happy or Healthy HDL :)*HDL originates from Intestines and Liver and it is "movable fist basically" that hands out cholesterol esters to other lipoproteins(after Nascent HDL>Mature HDL by LCAT), this movable fist also hands out ApoC2(LPL cofactor -to get chylomicron remnants by LPL) and and ApoE(needed for uptake of chylomicron remnants and other lipoproteins by Liver.).*Remember HILL(HDL from Intestine and Liver Liver :) but note that HDL is involved in REVERSE Cholesterol transport from periphery to liver and HDL is what removes Cholesterol from fatty streaks in atherosclerotic plaques, note that HDL synthesis is increased by alcohol.

Having high levels of HDL cholesterol is considered good because it helps in protecting vascular health through reverse cholesterol transport and removing cholesterol from atherosclerotic plaques.

Explanation

Having high levels of HDL cholesterol is considered good because it helps in protecting vascular health through reverse cholesterol transport and removing cholesterol from atherosclerotic plaques.

15. What are lipoproteins?

C) VLDL is larger in size and has a higher TG content compared to chylomicrons.

B) HDL contains more cholesterol than LDL due to its lower density in lipoprotein hierarchy.

*These are amphipathic(has both hydrophobic and hydropilic ends)molecules hat are composed of varying proportions of TGs,Cholesterols,phospholipids.*From low to high density:Chylomicrons<VLDL<LDL<HDL.*Generally,Higher density refers to MORE cholersterol, LESS TG and Smaller size.(Don't get fooled by" LOW" density lipoprotein name, it "Low density" is in reltive to HDL ,otherwise LDL is "More dense" then any other lipoproteins like VLDL and Chylomicrons and here comes important point LDL actually contains The Most amount of cholesterol, more than HDL, HDL has highest density due to its high Protein component ,once again LDL has More cholesterol while HDL has More protein)*Now HDL<LDL<VLDL<Chylomicrons in terms of Size and TG content(Hence you know why TG is increased in Type1(increased Chylomicrons) and in type 4(increased VLDL) dyslipidemias.*All these is meant to give you backrground don't try to memorize these(unless for med school tests) try to imagine,draw them out if you have time, it will make other HY stuff easy to understand and comprehend as we saw with dislipdemias.

A) Lipoproteins are exclusively composed of triglycerides and cholesterol.

Lipoproteins are complex molecules composed of various components, including triglycerides, cholesterol, and phospholipids. The hierarchy of lipoprotein density does not correlate with the amount of cholesterol they contain, with LDL actually having the highest cholesterol content. Understanding the composition and hierarchy of lipoproteins is crucial for grasping lipid metabolism and disorders.

Explanation

Lipoproteins are complex molecules composed of various components, including triglycerides, cholesterol, and phospholipids. The hierarchy of lipoprotein density does not correlate with the amount of cholesterol they contain, with LDL actually having the highest cholesterol content. Understanding the composition and hierarchy of lipoproteins is crucial for grasping lipid metabolism and disorders.

16. Describe key points about chylomicrons

Chylomicrons are secreted by pancreatic cells.

Chylomicrons do not contain any apolipoproteins.

*Dietary(EXOgenous) lipids in enterocytes will combine with newly translated apolipoproteins(Like apo-B45) in ER.*Chylomicrons usually contain other apopliprotiens too like C2 and E.*Now,from intestine Chylomicrons enter lymphatics>Thoracic duct>Blood,in blood they deliver TGs to PERIPHERAL tissues as they are released by LPL, after whichwe are left with Chylomicron remnants which can enter Liver and give our liver some cholesterol.(But not much TGs at they have been stolen by peripheral tissues, contrast this with IDL-degradation product of VLDL which delivers TGs and cholesterol to liver)*Remeber Chylomicrons are secreted by intestinal epithelial cells.

Chylomicrons primarily deliver triglycerides to the liver.

Chylomicrons are mainly secreted by intestinal epithelial cells, deliver triglycerides to peripheral tissues, and do contain apolipoproteins such as apo-B45, C2, and E. Chylomicron remnants contribute cholesterol to the liver.

Explanation

Chylomicrons are mainly secreted by intestinal epithelial cells, deliver triglycerides to peripheral tissues, and do contain apolipoproteins such as apo-B45, C2, and E. Chylomicron remnants contribute cholesterol to the liver.

17. Key points about VLDL/IDL/LDL? Contrast VLDL with Chylomicron.

LDL is synthesized in the intestines and delivers hepatic TGs to peripheral tissues. It does not express any apolipoproteins.

Chylomicrons are synthesized in the liver and deliver dietary TGs to peripheral tissues. They are smaller in size and contain less cholesterol compared to VLDL.

*Well it VLDL is synthesized in liVer, its main function is to deliver hepatic/endogenous TGs to PERIPHERAL tissues(Consrast this with Chylomicrons which deliver EXOGENOUS=dietary TGs to PERIPHERAL tissue-so they have similar function), but note that VLDL contains more Cholesterol and delivers it to peripheral tissues too.*VLDL is smaller in size and has less TGs.*Also Chylomicron doesn NOT have ApoB100(it does express B45,A1,C2,E.) contrast this with VLDL which expresses ApoB100,C2,E2 but does NOT express ApoB48,A1(remember functions and it will make sense VLDL doesn't need ApoB48 which is needed for CHYLOMICRON secretion and it also doesn't need A1 which activates LCAT)*Now when LPL acts on VLDL, it eats up TGs and leaves IDL(IDL doesn't have C-II but keeps E and B100), as IDL is metabolized by Hepatic lipase we receive LDL(which looses E and keeps Only B100), now if u know this it is easy to answer the question: by which apolipoproteins LDL receptors recognize and promote receptor mediated endocytosis in peripheral tissue?(Obv only one that LDL has left is ApoB100)-Remember LDL should deliver cholesterol from liver to peripheral tissues.it suckss but apolipoproteins are testable, remember the sequence like it is story.. really know the red stuff...Also remember:*Decreased ApoproteinB synthesis in Kwashiorkor disease due to protein deficiency contributes to fatty liver.

IDL contains more TGs compared to VLDL and expresses ApoB48 and A1.

The correct answer highlights the key differences between VLDL and Chylomicron, their functions, composition, and apolipoprotein expression. The incorrect answers provide inaccurate information to test the understanding of the concepts discussed in the question and correct answer.

Explanation

The correct answer highlights the key differences between VLDL and Chylomicron, their functions, composition, and apolipoprotein expression. The incorrect answers provide inaccurate information to test the understanding of the concepts discussed in the question and correct answer.

18. Why can VLDL and IDL bind LDL receptors?

*Because all 3 express ApoB100<function of which is Binding LDL receptors.*Note that IDL also expresses ApoE while VLDL also expresses C2.

Because VLDL and IDL have a higher density than LDL, making them more likely to bind.

Because VLDL and IDL contain higher levels of cholesterol than LDL, which promotes receptor binding.

Because VLDL and IDL share a similar lipid composition with LDL, increasing their affinity for LDL receptors.

VLDL, IDL, and LDL can bind LDL receptors due to the expression of ApoB100 which is crucial for this interaction. While IDL also expresses ApoE and VLDL expresses C2, the primary factor enabling binding is the presence of ApoB100.

Explanation

VLDL, IDL, and LDL can bind LDL receptors due to the expression of ApoB100 which is crucial for this interaction. While IDL also expresses ApoE and VLDL expresses C2, the primary factor enabling binding is the presence of ApoB100.

19. Why is LDL(Only has ApoB100 delivers cholesterol from liver to peripheral tissue as it interacts with LDL receptors and is uptaken by Receptor mediated endocytosis)?

High levels of LDL are beneficial for cardiovascular health.

Oxidized LDL is cleared from the body without causing any harm.

LDL particles are too large to penetrate the endothelium.

*Small dense LDL particles increases risk of atherosclerosis and CAD as these small particlescan penetrate endothelium easier.*In large arteries LDL can get oxidized and get stuck in Intima layer, Oxidized LDL is endocytosed by macrophages, producing Foam Cells, fatty streaks are formed and smooth muscle migration is induced(under influence of PDGF and FGF), proliferation and extracellular matrix deposition results in formation of fibrous plaque<Pathognomic finding for atherosclerosis.

20. What is the difference between IDL and LDL?

*IDL is product of breakdown of VLDL by LPL and it delivers TGs and Cholesterol TO LIVER.*LDL is formed from IDL under influence of Hepatic lipase and it delivers Cholesterol from liver to peripheral tissues.

LDL is the product of the breakdown of HDL in the bloodstream.

IDL is responsible for delivering cholesterol from the liver to peripheral tissues.

IDL is formed directly from LDL in the liver.

Understanding the process of lipid metabolism helps differentiate between IDL and LDL and their specific roles in the transport of cholesterol and triglycerides.

Explanation

Understanding the process of lipid metabolism helps differentiate between IDL and LDL and their specific roles in the transport of cholesterol and triglycerides.

21. Which lipoprotein is secreted from the liver and intestine and is involved in Chylomicron/VLDL metabolism, expressing ApoC2 and ApoE?

LDL

IDL

VLDL

*We described HDL which expresses ApoC2 and ApoE and thus is involved in Chylomicron and VLDL metabolism.*Remember ApoC2 is a cofactor of LPL(that converts Chylomicrons to remnants and VLDL to IDL.) while ApoE mediates remnant uptake.*Remember that ApoE is present on All apolipoproteins EXCEPT LDL(So if they describe to you lipoprotein without ApoE you don't need to investigate further you got ur asnwer)

HDL is the correct answer because it expresses ApoC2 and ApoE, which play important roles in Chylomicron and VLDL metabolism. ApoC2 is a cofactor of LPL, while ApoE mediates remnant uptake. It's important to remember that ApoE is present on all apolipoproteins except LDL.

Explanation

HDL is the correct answer because it expresses ApoC2 and ApoE, which play important roles in Chylomicron and VLDL metabolism. ApoC2 is a cofactor of LPL, while ApoE mediates remnant uptake. It's important to remember that ApoE is present on all apolipoproteins except LDL.

22. What is the best video to understand lipoproteins in only 7 minutes?

Https://www.youtube.com/watch?v=zyxwvu98765

Https://www.youtube.com/watch?v=abcdef12345

Https://www.youtube.com/watch?v=qwerty09876

Https://www.youtube.com/watch?v=97uiV4RiSAY

Lipoproteins are complex particles composed of proteins and lipids that transport cholesterol and triglycerides through the bloodstream. Understanding their roles and functions is crucial for maintaining heart health and managing lipid levels.

Explanation

Lipoproteins are complex particles composed of proteins and lipids that transport cholesterol and triglycerides through the bloodstream. Understanding their roles and functions is crucial for maintaining heart health and managing lipid levels.

23. What are the effects of Chronic alcohol on VLDL, HDL, and TG?

Chronic alcohol consumption increases VLDL and TG levels, but decreases HDL levels.

Chronic alcohol consumption has no effect on VLDL, HDL, and TG levels.

*It INCREASES all of them, increase in VLDL and TG contributes to their increased risk of pancreatitis.*Increased HDL actually has protective effects against atherosclerosis.

Chronic alcohol consumption decreases VLDL, HDL, and TG levels.

24. Increased Malonyl-Coa directly inhibits?

Protein Synthesis

*Fatty acid OXIDATION(Not fatty acid synthesis), increased malonyl coa is characteristic finding in resting muscle, generally in anabolic state when you just chill and synthesize everything for future when you might need them(Like running from bear:)***Remember most directly increased Malonyl Coa(One of the mediators of FA synthesis) Inhibits B-oxidation by Preventing transportation of Fatty Acyl Coa from cytosol to MITOCHONDRIA(Which btw needs Carnithine shuttle)<Just btw when you have inherited defect in this carnithine shuttle you can't do B-oxidation of Long-chain fatty acids, because you can't transport Fatty Acyl Coa into the mitochondria, lack of the energy and toxic accumulation of LCFAs leads to classic HYPOketotic Hypoglycemia(HYPOKETOTIC is key here you can't increase ketones because you can't get Fatty-acyl coa in mitochondria you can't B-oxidize it to Acetyl Coa which is needed for Ketone body synthesis)+Weakness and hypotonia are common findings.

Glycolysis

Fatty acid SYNTHESIS

Increased malonyl coa inhibits fatty acid oxidation by preventing transportation of Fatty Acyl Coa from cytosol to mitochondria, leading to a decrease in energy production and accumulation of long-chain fatty acids. This results in hypoketotic hypoglycemia and weakness.

Explanation

Increased malonyl coa inhibits fatty acid oxidation by preventing transportation of Fatty Acyl Coa from cytosol to mitochondria, leading to a decrease in energy production and accumulation of long-chain fatty acids. This results in hypoketotic hypoglycemia and weakness.