🌟 Lipids

Question 1

What happens to excess acetyl-CoA in the fed state?

Answer 1

Converted to fatty acids → stored as triglycerides (TAGs) in adipocytes. Gluconeogenesis is suppressed by insulin.

Question 2

Can acetyl-CoA be used to make glucose?

Answer 2

No! Acetyl-CoA cannot enter gluconeogenesis (irreversibly lost as CO₂ in TCA cycle).

Question 3

What happens to glycerol from TAGs in the fed state?

Answer 3

Recycled back into fat storage (not used for gluconeogenesis due to high insulin).

Question 4

What happens to glycerol from TAGs in the fasting state?

Answer 4

Released during lipolysis → liver converts it to glucose via gluconeogenesis.

Question 5

How does glucagon regulate fat metabolism during fasting?

Answer 5

Activates lipolysis → releases glycerol (for gluconeogenesis) and fatty acids (for β-oxidation/ketones).

Question 6

Why can’t fatty acids contribute to gluconeogenesis?

Answer 6

β-oxidation produces acetyl-CoA, which cannot be converted to glucose (only glycerol can).

Question 7

What inhibits CPT-1 to prevent futile cycles?

Answer 7

Malonyl-CoA (high in fed state) blocks fat oxidation while fatty acids are being synthesized.

Question 8

What is the role of ketones in fasting?

Answer 8

Alternative fuel for brain/heart when glucose is scarce (made from excess acetyl-CoA).

Question 9

How does insulin suppress gluconeogenesis?

Answer 9

Inhibits PEPCK and fructose-1,6-bisphosphatase (key gluconeogenesis enzymes).

Question 10

What signals the liver to switch from fat synthesis to breakdown?

Answer 10

Low insulin + high glucagon (fasting state) activates HSL → lipolysis + gluconeogenesis.