After a carbohydrate-rich meal, the liver has more acetyl-CoA than it can immediately oxidize in the citric acid cycle. What happens to the excess, and why?
AIt is exported to muscle as acetyl-CoA for direct oxidation, since the liver cannot store fat
BIt is converted to ketone bodies to supply the brain during the fed state
CIt is channeled into de novo lipogenesis because the cell's energy charge is high and the citric acid cycle slows when ATP is abundant
DIt is transaminated into amino acids to replenish depleted protein stores
In the fed state, the cell's ATP is plentiful, so the citric acid cycle slows (high energy charge inhibits key enzymes). Excess acetyl-CoA cannot simply pile up, so it is redirected into de novo fatty acid synthesis — a biosynthetic pathway that consumes NADPH and runs precisely when there is more fuel than the oxidative pathways can handle. Ketone body production (option B) is a fasted-state response to low glucose; it is suppressed by insulin in the fed state.
Question 2 Multiple Choice
Dietary fat packaged as chylomicrons is released by lipoprotein lipase at adipose capillaries. What happens to the freed fatty acids?
AThey are converted to glucose via gluconeogenesis to maintain blood sugar
BThey are taken up by adipose cells and re-esterified into triglycerides for storage
CThey remain in the bloodstream as free fatty acids until needed by muscle
DThey are transported to the liver for immediate beta-oxidation
In the fed state, insulin suppresses hormone-sensitive lipase (preventing fat breakdown) and promotes re-esterification of fatty acids into triglycerides inside adipocytes. The net result is fat storage: dietary lipids flow from chylomicrons → free fatty acids → triglycerides in adipose. Beta-oxidation (option D) is a fasted-state pathway; gluconeogenesis from fatty acids (option A) is not possible because acetyl-CoA cannot be converted back to pyruvate in animals.
Question 3 True / False
In the fed state, insulin suppresses hormone-sensitive lipase in adipose tissue, ensuring that stored triglycerides are not broken down while dietary nutrients are being absorbed.
TTrue
FFalse
Answer: True
This is a central feature of the fed state's anabolic logic: it would be counterproductive to simultaneously store fat (from dietary lipids) and mobilize fat (via hormone-sensitive lipase). Insulin inhibits hormone-sensitive lipase directly, ensuring the net direction is unidirectionally into storage. In the fasted state, when insulin falls and glucagon rises, this inhibition is removed and lipolysis resumes.
Question 4 True / False
In the fed state, dietary amino acids are primarily converted to glucose via gluconeogenesis to maintain blood glucose levels between meals.
TTrue
FFalse
Answer: False
This reverses the priority: in the fed state, amino acids are primarily directed toward protein synthesis. Insulin activates the mTOR pathway, which is a potent stimulus for translation, and stimulates uptake of amino acids into muscle. Gluconeogenesis from amino acids is a fasted-state response that occurs when glucose is scarce. Excess amino acids beyond what protein synthesis requires are deaminated and their carbon skeletons enter the citric acid cycle or are converted to fat — but this is secondary to protein synthesis in the fed state.
Question 5 Short Answer
Why is the liver's role in the fed state described as 'coordinating,' and what would happen to blood glucose levels if hepatic gluconeogenesis were not suppressed by insulin after a meal?
Think about your answer, then reveal below.
Model answer: The liver coordinates the fed state because it is the central clearinghouse for absorbed nutrients arriving via the portal vein: it takes up glucose (phosphorylating it with glucokinase), synthesizes glycogen and fatty acids, produces VLDL to export lipids, and processes amino acids. If insulin did not suppress hepatic gluconeogenesis after a meal, the liver would continue producing new glucose from amino acids and glycerol even as dietary glucose was pouring in from the intestine, causing blood glucose to rise to hyperglycemic levels. Insulin's suppression of gluconeogenesis (and glycogenolysis) is essential to the homeostatic control of postprandial blood glucose.
This question highlights why the liver requires insulin signaling specifically — the liver normally produces glucose to supply other organs in the fasted state, and this production must be actively turned off after a meal. Type 2 diabetics often have hepatic insulin resistance, meaning the liver fails to suppress gluconeogenesis even in the fed state, contributing to chronic postprandial hyperglycemia. This is why metformin (which inhibits hepatic gluconeogenesis) is a first-line treatment.