front 1 A healthy adult is 34 hours into fasting. Liver glycogen is depleted.
What now maintains blood glucose? | back 1 C. Hepatic gluconeogenesis |
front 2 Gluconeogenesis is glucose synthesis primarily from: | back 2 A. Noncarbohydrate precursors |
front 3 In humans, gluconeogenesis occurs primarily in: | back 3 D. Liver hepatocytes mainly |
front 4 Which is a major gluconeogenic precursor? | back 4 B. Lactate |
front 5 The amino acid highlighted as a key gluconeogenic precursor
is: | back 5 A. Alanine |
front 6 Relative to glycolysis, gluconeogenesis requires: | back 6 D. Three bypass reactions |
front 7 After stopping food intake, liver glycogen breakdown begins to
support blood glucose after about: | back 7 B. 2–3 hours |
front 8 During an overnight fast, blood glucose is maintained mainly
by: | back 8 C. Glycogenolysis plus gluconeogenesis |
front 9 As glycogen stores fall, adipose triacylglycerol breakdown
provides: | back 9 A. Fatty acids and glycerol |
front 10 During fasting, fatty acids primarily help by: | back 10 B. Providing alternative fuel |
front 11 After ~30 hours of fasting, the only source of blood glucose
is: | back 11 D. Hepatic gluconeogenesis |
front 12 Under extreme starvation, an additional site of gluconeogenesis is
the: | back 12 C. Renal cortex |
front 13 In extreme starvation, glucose produced by the kidney is mainly used
by the: | back 13 B. Renal medulla cells |
front 14 Most gluconeogenic steps mirror glycolysis, but overall: | back 14 D. Carbon flow is reversed |
front 15 Glycerol carbons are gluconeogenic because they form: | back 15 A. Dihydroxyacetone phosphate |
front 16 A hepatocyte uses glycolytic intermediates to generate glycerol
3-phosphate. Its key role is: | back 16 C. Triacylglycerol backbone |
front 17 Liver triacylglycerols are secreted into blood primarily in: | back 17 D. VLDL |
front 18 Measuring ketones in blood and urine can indicate: | back 18 A. Starvation severity or DKA |
front 19 A comatose patient has “fruity” breath. In DKA, the odor is due
to: | back 19 B. Acetone |
front 20 The “acetone” breath odor is linked to breakdown of which ketone
body? | back 20 C. Acetoacetate |
front 21 Deep, relatively rapid respirations in DKA are termed: | back 21 A. Kussmaul respirations |
front 22 Kussmaul respirations occur primarily because: | back 22 D. Acidosis stimulates respiratory center |
front 23 The key gas exhaled more during Kussmaul compensation is: | back 23 B. CO2 |
front 24 Which paired finding most supports DKA coma over hypoglycemic
coma? | back 24 C. Acetone breath, Kussmaul |
front 25 Severe hyperglycemia in DKA causes polyuria mainly via: | back 25 A. Osmotic diuresis |
front 26 Volume depletion from DKA is commonly worsened by: | back 26 D. Vomiting |
front 27 A patient with DKA is volume depleted. Which hemodynamic profile fits
best? | back 27 C. Dehydration, hypotension, tachycardia |
front 28 Why can ethanol carbons not support gluconeogenesis? | back 28 B. Produces only acetyl-CoA |
front 29 In liver, lactate and alanine contribute to gluconeogenesis by
forming: | back 29 A. Pyruvate |
front 30 Which triacylglycerol component contributes carbon to
gluconeogenesis? | back 30 C. Glycerol |
front 31 A patient on a plant-heavy diet oxidizes an odd-chain fatty acid. The
three ω-end carbons produce: | back 31 C. Propionyl-CoA |
front 32 Odd-chain fatty acids are obtained mainly from: | back 32 A. Vegetables |
front 33 Propionyl-CoA is converted first to: | back 33 D. Methylmalonyl-CoA |
front 34 Methylmalonyl-CoA is rearranged to: | back 34 B. Succinyl-CoA |
front 35 In odd-chain fatty acid oxidation, net glucose can be made only
from: | back 35 A. ω-end three carbons |
front 36 Why can acetyl-CoA not generate pyruvate for gluconeogenesis? | back 36 C. PDH reaction is irreversible |
front 37 Which TCA reactions release the two CO2 that prevent net glucose from
acetyl-CoA? | back 37 B. Isocitrate DH, α-KGDH |
front 38 There is no net glucose synthesis from acetyl-CoA because: | back 38 D. Two CO2 lost per turn |
front 39 A 19-carbon fatty acid is oxidized. How many carbons form
propionyl-CoA? | back 39 C. Three |
front 40 In a 19-carbon fatty acid, the remaining 16 carbons primarily
form: | back 40 A. Acetyl-CoA |
front 41 In glycolysis, phosphoenolpyruvate is converted to pyruvate
by: | back 41 B. Pyruvate kinase |
front 42 Pyruvate carboxylase converts pyruvate to: | back 42 D. Oxaloacetate |
front 43 The enzyme that releases CO2 from OAA while generating PEP
is: | back 43 A. PEP carboxykinase |
front 44 Oxaloacetate does not readily cross the: | back 44 C. Mitochondrial membrane |
front 45 Because OAA cannot cross easily, it is often converted to: | back 45 D. Malate or aspartate |
front 46 Glycerol enters gluconeogenesis at the level of: | back 46 B. DHAP |
front 47 During rapid hepatic ethanol oxidation, the redox state shifts
so: | back 47 C. NADH/NAD+ increases |
front 48 Elevated NADH inhibits glycerol use for gluconeogenesis because
conversion to DHAP requires: | back 48 A. NAD+ |
front 49 High NADH drives lactate dehydrogenase toward producing: | back 49 D. Lactate |
front 50 After heavy alcohol intake, pyruvate generated from alanine is
preferentially converted to: | back 50 B. Lactate |
front 51 A fasting patient binges alcohol and becomes hypoglycemic. Which
precursors are least usable for gluconeogenesis? | back 51 A. Lactate, alanine, glycerol |
front 52 With high NADH, OAA is preferentially converted to: | back 52 C. Malate |
front 53 With high NADH, DHAP is preferentially converted to: | back 53 B. Glycerol 3-phosphate |
front 54 A malnourished patient drinks heavily and then develops confusion and
diaphoresis. Most likely metabolic outcome: | back 54 D. Hypoglycemia |
front 55 Fructose 1,6-bisphosphatase produces: | back 55 B. Fructose 6-phosphate |
front 56 Glucose 6-phosphatase directly generates: | back 56 D. Free glucose |
front 57 Glucose 6-phosphatase is located in the: | back 57 A. Endoplasmic reticulum membrane |
front 58 Which condition does NOT stimulate gluconeogenesis? | back 58 C. High-carbohydrate meal |
front 59 Which conversion is a regulated gluconeogenic “bypass”? | back 59 C. Pyruvate to PEP |
front 60 Which conversion is a regulated gluconeogenic “bypass”? | back 60 A. F1,6BP to F6P |
front 61 Which conversion is a regulated gluconeogenic “bypass”? | back 61 D. G6P to glucose |
front 62 Hepatocytes should funnel PEP toward glucose during fasting. Which
enzyme-state set best fits? | back 62 B. PDH↓ PC↑ PEPCK↑ PK↓ |
front 63 During conditions favoring gluconeogenesis, pyruvate dehydrogenase is
typically: | back 63 A. Inactive |
front 64 A fasting liver increases gluconeogenic capacity by inducing which
enzyme quantity? | back 64 D. PEP carboxykinase |
front 65 A patient receives high-dose prednisone for vasculitis. Which lab
abnormality is most expected? | back 65 B. High blood glucose |
front 66 A fasting liver activates fructose 1,6-bisphosphatase. Which pair
inhibits it allosterically? | back 66 C. F2,6BP and AMP |
front 67 During fasting, hepatic ATP/NADH used for gluconeogenesis comes
mainly from: | back 67 A. β-oxidation |
front 68 An infant with a fatty-acid oxidation defect develops fasting
hypoglycemia. Best mechanistic link? | back 68 D. Low hepatic energy |
front 69 Thirty minutes after a high-carbohydrate meal, glucose rises most
typically to: | back 69 C. 120–140 mg/dL |
front 70 After a typical meal, blood glucose returns to fasting range by
about: | back 70 B. 2 hours |
front 71 A patient with severe hyperglycemia becomes bounded without ketones.
Hyperosmolar coma stems mainly from: | back 71 D. Brain dehydration |
front 72 About 2 hours after a meal, as glucose nears 80–100 mg/dL, the liver
activates: | back 72 A. Glycogenolysis |
front 73 After 5–6 weeks of starvation, blood glucose is closest to: | back 73 B. 65 mg/dL |
front 74 Glucagon signaling in liver most directly raises
intracellular: | back 74 C. cAMP |
front 75 Glucagon raises hepatic cAMP by activating: | back 75 D. Adenylate cyclase |
front 76 By ~4 hours after a meal, hepatic glucose output relies on
glycogenolysis plus: | back 76 A. Gluconeogenesis |
front 77 Glucagon prevents PEP from becoming pyruvate mainly by
inactivating: | back 77 C. Pyruvate kinase |
front 78 With pyruvate kinase inactivated, PEP “runs backward” to
form: | back 78 B. Fructose 1,6-bisP |
front 79 Enzymes unique to gluconeogenesis are most active under: | back 79 A. Fasting conditions |
front 80 In fasting liver, acetyl-CoA from fatty acids directly
activates: | back 80 D. Pyruvate carboxylase |
front 81 Which set is induced during fasting gluconeogenesis? | back 81 B. PEPCK, FBPase, G6Pase |
front 82 Fructose 1,6-bisphosphatase is favored in fasting because: | back 82 C. F2,6BP is low |
front 83 A carbon source explicitly used for gluconeogenesis is: | back 83 A. Glycerol |
front 84 During prolonged fasting, fatty acids are oxidized by tissues
primarily to: | back 84 D. CO2 and H2O |
front 85 After several days without food, the brain decreases glucose use by
increasing: | back 85 C. Ketone body use |
front 86 After ~3–5 days fasting, brain glucose need is roughly: | back 86 B. One-third normal |
front 87 Chronic hyperglycemia narrows microvessels mainly via
protein: | back 87 D. Cross-linking |
front 88 Microvascular narrowing from chronic hyperglycemia classically
targets: | back 88 A. Retina, glomeruli, nerves |
front 89 Narrowed renal glomerular microvessels most directly produce
diabetic: | back 89 B. Nephropathy |
front 90 Narrowed microvessels to peripheral/autonomic nerves most directly
produce diabetic: | back 90 C. Neuropathy |
front 91 Fasting glucose 80–100 mg/dL is approximately: | back 91 B. ~5 mM |
front 92 Post-meal glucose 120–140 mg/dL is approximately: | back 92 D. ~8 mM |
front 93 Hepatic fructose 2,6-bisP levels are regulated by: | back 93 A. Insulin and glucagon |
front 94 After ~3–5 days fasting, brain glucose need is about: | back 94 C. 40 g/day |