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An increase in the ratio of insulin to glucagon will increase the activity of which of the following enzymes (+ indicates activity is increased; - indicates activity is not increased by insulin)? - ANS-(-) hormone sensisitve lipase (+) acetyl-CoA carboxylase (+PFK2) (+) Gycogen synthase when insulin is elevated fed state pathways will be persistent. This will include the activation of acetylCoA carboxylase will be activated in fatty acid synthesis. PFK2 in gycolysis (breakdown of glucose) and glycogen synthase will also be active converting excess glucose to glycogen to be stores for later.
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An increase in the ratio of insulin to glucagon will increase the activity of which of the following enzymes (+ indicates activity is increased; - indicates activity is not increased by insulin)? - ANS-(-) hormone sensisitve lipase
(+) acetyl-CoA carboxylase
(+PFK2)
(+) Gycogen synthase
when insulin is elevated fed state pathways will be persistent. This will include the activation of acetyl- CoA carboxylase will be activated in fatty acid synthesis. PFK2 in gycolysis (breakdown of glucose) and glycogen synthase will also be active converting excess glucose to glycogen to be stores for later.
hormone sensitive lipase is active in lipolysis --> in the fasting state
Which of the following is the regulatory enzyme for fatty acid synthesis?
Citrate lyase
Malic enzyme
Fatty acid synthase
Acetyl-CoA carboxylase - ANS-Acetyl-CoA carboxylase
the regulatory step in fatty acid syntehsis is the synthesis of malonyl-coA by acetyl-CoA carboxylase. This reaction uses CO2 and bioton to add carbon to cystolic acteyl-COA
Fatty Acid synthase is used in Beta oxidation!
Insulin stimulates lipogenesis through several mechanisms. Which of the following is not an insulin stimulated process that enhances lipogenesis?
Decreased activity of the pyruvate dehydrogenase complex
Decreased levels of cAMP
Increased glucose transport into the cells
Increased activity of acetyl-CoA carboxylase - ANS-Decreased activity of the pyruvate dehydrogenase complex
Insulin stimulates PDC--> the enzyme that converts pyruvate to Acetyl-CoA which is active during glycolysis (High glucose, high insulin)
Acetyl-CoA Carboxylase- the rate limiting step of fatty acid synthesis(lipogenesis). insulin would increase this.
Increased glucose transport is likely happening with insulin
cAMP- in the glucagon pathway, insulin would inhibit this
An individual consumes a large meal consisting of a cheeseburger and fries. Which of the following intermediates is shuttled out of the TCA cycle to be used as a substrate for fatty acid synthesis?
Isocitrate
Oxaloacetate
VLDL synthesis will increase because this is also a fed state pathway
Under fasting conditions, acetyl-CoA carboxylase will be inhibited by an increase in which of the following compounds?
fatty acyl-CoA
Glucose
Citrate
Malonyl-CoA - ANS-fatty acyl-CoA
In fasting conditions when lipolysis is active, an increase in fatty acyl-CoA in the cell from the process of β-oxidation will decrease citrate efflux from the mitochondria and activity of acetyl-CoA carboxylase.
glucose will Increase acetyl-CoA carboxylase, citrate will also be channeled to fatty acid synthesis
During fatty acid synthesis, after the initial step involving acetyl-CoA, the fatty acid chain is elongated by the addition of which of the following compounds?
Acetyl-CoA
Malonyl-CoA
Succinyl-CoA
Acyl-CoA - ANS-Malonyl-CoA
Initially, acetyl-CoA is bound to the acyl carrier protein (ACP), after this all subsequence 2 carbon units are added via malonyl-CoA.
Which of the following enzymes is correctly paired with its allosteric inhibitor?
Pyruvate kinase: fructose 1,6-bisphosphate
Acetyl-CoA carboxylase: palmitoyl-CoA
Pyruvate dehydrogenase complex: pyruvate
Carnitine palmitoyl transferase I: acetyl-CoA - ANS-Acetyl-CoA carboxylase: palmitoyl-CoA
acteyl-CoA carboxylase will be inhibited by palmitoyl-CoA because palminate is the end product of fatty acid synthesis. Lots of palmitoyl-CoA will inhibit the regulatory enzyme of fatty acid synthesis.
what is the major source of extracellular cholesterol in humans - ANS-LDL
The primary role for LDL is to transport cholesterol to peripheral tissues. HDLs function in reverse cholesterol transport; VLDLs role is to carry newly synthesized triacylglycerols
Nascent chylomicrons interact with HDL particles within circulation. Which of the following Apo proteins are obtained from HDL during this interaction?
ApoCII and ApoE
ApoB48 and ApoE
ApoB48 and ApoCII
ApoCII and ApoB100 - ANS-ApoCII and ApoE
The interaction of chylomicrons and HDLs involves the transfer of the apoproteins CII and E.
Apo E will help the chylomicron enter the liver cells.
ApoC11 will take the triglycerides from the chylomicron and turn them into fatty acids
in this case, both chylomicrons and VLDLs would be present and would contribute to the measured triglyceride levels. The individual would need to fast before a lipid measurement to get a more accurate reading of circulating triglycerides.
Lecithin:cholesterol acyl tranferase (LCAT) is a plasma enzyme associated with HDL particles. Which of the following best describes its role in cholesterol transport?
Esterification of cholesterol is a process needed in increase hydrophobicity to trap cholesterol in the cell or HDL. ACAT is primarily responsible for trapping cholesterol in the cell whereas LCAT is found in circulation associated with HDL.
LCAT needs ApoA
Which of the following is not required for the transport of newly synthesized fatty acids to the adipose?
The carnitine shuttle is required for the process of β-oxidation to transport fatty acyl chains into the mitochondria. This would not be needed for transport and storage of newly synthesized fatty acid chains.
the other processes are used during fatty acid synthesis
A 45-year-old man is found to have an elevated serum cholesterol of 300mg/dL after a 12 hr. fast. Which of the following lipoproteins would be the largest contributors to a measurement of plasma cholesterol in a normal person following a 12 hr. fast?
Both LDL and HDL are the major carriers of cholesterol in circulation. VLDLs would be the best represented of serum triglycerides.
Chylomicrons and VLDLs would be what was measures during a non-fasting blood test after a carb rich meal
What is the primary lipid component of a VLDL particle?
LDLs are characteristic of ApoB100 and this is used for uptake into the cell by the LDL receptor.
APO B48- helps drop the chylomicron from blood stream to lymph
Apo A1- HDL
ApoE- on chylomicrons and VLDLs, used for uptake back into the liver
Apo CII- interacts with LPL to active the enzyme and turn triglycerides into fatty acids
Secondary bile salts lack a hydroxyl (OH) group when compared to primary bile salts. What is the consequence of the loss of this group?
The modification to secondary bile salts renders them less soluble and therefore less likely to be reabsorbed.
Cushing syndrome is caused by an increase in the synthesis of cortisol in the adrenal gland. Which of the following compounds is directly required as a substrate for the synthesis of this hormone?
Cholesterol
Free fatty acids
Amino acids
Glucose - ANS-Cholesterol
Cholesterol is the substrate for steroid hormone synthesis including cortisol and many of the sex hormones
Bile salts are synthesized from cholesterol and are used for the emulsification of dietary lipids. What is the primary fate of bile salts during digestion?
They are digested by pancreatic lipase
They are excreted in the feces
They are reabsorbed in the ileum
They are packaged into chylomicrons - ANS-They are reabsorbed in the ileum
The majority of bile salts are reabsorbed through enterohepatic circulation; secondary bile salts are excreted in the feces.
A 45-year-old man has a mild heart attack and a history of vascular disease. He is placed on a Mediterranean diet and statin drug therapy. Which of the following will be the most likely result of this drug therapy?
NADH, FADH2 and Acetyl-CoA are all produced by β-oxidation. NADPH is required for fatty acid synthesis and can be produced by the pentose phosphate pathway or malic enzyme.
An individual is on a hunger strike and has not eaten in 13 days. Which of the following best describes their metabolic state?
Under conditions of excess fasting (i.e. starvation), the brain will begin to oxidize ketones as a primary fuel source reducing its reliance on glucose.
An 10-year-old boy is brought to the emergency department by his father. He reports his son has recently been very thirsty and needing to make frequent trips to the bathroom. Physical examination revealed a thin boy, in the 30th percentile for height and weight. A rapid dipstick test revealed glucose in his urine. Evaluation of this boy's blood would reveal decreased levels of which of the following compounds or hormones?
Glucose
Insulin
Free Fatty acids
Glutamine
Epinephrine - ANS-Insulin
The description here is of type 1 diabetes which is consistent with a loss of insulin production. Therefore, fasted state metabolic pathways would be highly active contributing to hyperglycemia and ketogenesis.
The process of ketogenesis refers to the conversion of acetyl-CoA to which of the following compounds?
Ketogenesis is the process by which excess acetyl-CoA from β-oxidation is converted to the ketone bodies: D-3-hydroxybutyrate (β-hydroxybutyrate) and acetoacetate.
A well, 2-year-old girl presents to the clinic with symptoms of a viral illness. Her parents report she has had bouts of vomiting and diarrhea over the last 24 hours. This morning they could barely wake her from her crib and she was very weak. Laboratory tests show low blood glucose (hypoglycemia) and elevated liver enzymes. There are no ketones present in her urine. The child is hospitalized and glucose is administered by I.V. Additional laboratory analysis showed elevated medium-chain fatty acyl carnitines in blood and 6-8 carbon dicarboxylic acids in the urine. Which of the following abnormalities is the most likely diagnosis for this child?
Carnitine deficiency
Defect of medium-chain fatty acyl synthetase
Mitochondrial defect in the electron transport chain
Mitochondrial defect in fatty acid transport
Defect of medium-chain acyl-dehydrogenase - ANS-Defect of medium-chain acyl-dehydrogenase
Oxaloacetate and pyruvate
Acetone and ethanol
Pyruvate and lactate - ANS-D-3-hydroxybutyrate and acetoacetate
Ketogenesis is the process by which excess acetyl-CoA from β-oxidation is converted to the ketone bodies: β-hydroxybutyrate and acetoacetate.
What is lipolysis? - ANS-process of releasing free fatty acids and glycerol from triacylglycerols stored in the adipose.
occurs in fasted state
Hormone sensitive lipase
What does Acetyl-CoA Carboxylase need in order to function properly?
What is the rate limiting step for Ketoacidosis?
Which enzyme? - ANS-HMG-CoA Synthase
This converts Acetoacetyl-CoA to HMG-CoA (second step in ketogenesis)
What is the rate limiting enzyme in Beta Oxidation?
What inhibits It? - ANS-Carnitine palmitoyl transferase I
CPT 1 is responsible for converting Fatty Acyl-CoA --> Fatty Acyl-Carnitine which can then be shuttle into the mitochondria. This is part of the carnitine transport.
(-) Inhibitors: Malonyl-CoA
What is the rate limiting step to Fatty Acid Synthesis?
What inhibits and activates it? - ANS-Acetyl-CoA Carboxylase
(+) Activators: Insulin, citrate
(-) Inhibitors: Glucagon, palmatoyl-CoA (end product of fatty acid synthesis, if you already have alot then you dont need more)
What is the regulatory step of lipogenesis --AKA fatty acid synthesis? - ANS-Carboxylation of Acetyl-CoA
The regulatory step in fatty acid synthesis is the synthesis of malonyl-Coa by acetyl-CoA carboxylase. This reactions uses CO2 and biotin to add carbon to cytosolic acetyl-CoA.
In case of a deficiency in biotin, which of the following enzymes required for fatty acid metabolism will be impaired?
Fatty acid synthase
Acety-CoA carboxylase
Carnitine palmitoyl transferase I
Triacylglycerol
Free fatty acid
LDL
Cholesteryl-ester - ANS-Cholesteryl-ester
HDL particles interact with VLDL particles to exhange cholesteryl ester for triacylglycerols
HDL particles interact with VLDL particles to exchange cholesterol ester for triacylglyerols. what enzyme is responsible for this process? - ANS-Cholesterol ester transfer protein (CETP)
CETP is responsible for the exchange between the two lipoproteins
Which lipoprotein is responsible for the process of reverse cholesterol transport? (movement of cholesterol from the peripheral tissues back to the liver) - ANS-HDL
A 16 yo woman presents to PCP for F/U. Her initial visit was 3 months ago and her cholesterol was 255 mg/DL (above normal). Today, her triglycerides are reported to be 260 mg/dl(above normal). She finds this very disappointing as she started a strict dietary regime reducing all fats and cholesterol replacing them with a high carb diet. You tell her carb diets can increase serum triglyceride levels in some individuals. this can be attributed to an increase in the synthesis of which of the following lipoproteins?
Increase in dietary carbs can result in increased de novo fatty acid synthesis and therefore increase in VLDL production.
Excess dietary carbs are metabolized to acetyl-CoA that enters the TCA cycle. In the mitochondria, excess citrate will be shuttled out of the organelle and used for fatty acid synthesis.
Dietary cholesterol is primarily transported in the body by which of the following lipoproteins?
Chylomicron - ANS-Chylomicron
Cholesterol and triacylglycerols from the diet are transported from the intestine to the liver via chylomicrons
VLDLs are products of fatty acid synthesis and carry TAG from liver to adipose tissue to be stored.
Which of the following compounds is not synthesized from cholesterol?
Cortisol
Vitamin D
Bile
Guanine - ANS-Guanine
Cholesterol is not a precursor for amino acids
Under cellular conditions when cholesterol is low, what happens to the sterol response element binding protein(SREB)? - ANS-It will be associated with the sterol response element (SRE) in the DNA
Low levels of intarcellular cholesterol will increase translocation of the SReBP:SCAP complex to the golgi where it will be cleaved.