Physiological conditions favoring fatty acid synthesis Lipogenesis (de novo fatty acid synthesis) in liver and adipose tissue is most active when:

Introduction / Context:
Fatty acid synthesis is an anabolic pathway that stores excess energy as triacylglycerol. Hormonal and nutrient cues switch the liver and adipose tissue between catabolic (fasted) and anabolic (fed) modes. Understanding these cues clarifies how diet influences lipid metabolism and body composition.

Given Data / Assumptions:

• Fed state: high insulin, low glucagon; abundant glucose.
• Excess carbohydrate provides carbon skeletons via citrate export.
• Sufficient ATP and NADPH are required for synthesis.

Concept / Approach:

In the fed state, glycolysis and the TCA cycle generate citrate that exits mitochondria. ATP citrate lyase produces cytosolic acetyl CoA, which is carboxylated by ACC to malonyl CoA. Fatty acid synthase uses malonyl CoA and NADPH (from pentose phosphate pathway and malic enzyme) to build palmitate. Insulin activates ACC and induces lipogenic gene expression (SREBP 1c), aligning carbon and energy availability with lipogenesis.

Step-by-Step Solution:

Verification / Alternative check:

Postprandial tracer studies show increased lipogenesis; fasting or high glucagon suppresses it and promotes fatty acid oxidation and ketogenesis.

Why Other Options Are Wrong:

Energy scarcity inhibits synthesis despite fatty acid abundance. High carbohydrate without ATP cannot sustain lipogenesis. Prolonged fasting elevates glucagon, which turns off ACC and lipogenesis.

Common Pitfalls:

Assuming substrate abundance alone is enough; hormonal regulation and ATP/NADPH availability are also required.

Final Answer:

Carbohydrate and energy supplies are plentiful (fed state)