Question

1. Even-chain fatty acids and acetyl CoA are not precursors for gluconeogenesis (in humans and other...

1. Even-chain fatty acids and acetyl CoA are not precursors for gluconeogenesis (in humans and other animals). a) how is acetyl CoA is converted into glucose in plants and bacteria? b) If palmitate is labeled with 14C that 14C shows up in glucose, So, carbon atoms from fat end up in glucose. However, I just re-stared that fatty acids are not precursors for gluconeogenesis. How can this be correct?

2. After a meal the ratio of beta-hydroxybutyrate to acetoacetate is about 1, but six hours after fasting it is about 6:1. Why might this be this case?

3. Which will release more energy when broken down, beta-hydroxybutyrate or acetoacetate? Why?

4. Why is liver unable to break down ketone bodies?

Homework Answers

Answer #1

1). Enzymes are present only in tissues, as it maintains only blood and glucohomeostatis which releases glucose into the blood, these are the into liver and into smaller the kidney.

In animals conversion of fatty acids into glucose which is also one of the reason.

2). The ratio between these two depends upon the prevailing redox state, which has major influence on these. This is due to inbalance between acid-base concentration in the body.

3). Both beta-hydroxybutyrate and acetoacetate will produce high energy during break down. More energy released when acetoacetate breaks down

4). Ketone bodies are water soluble particles. Ketone bodies are formed by ketogenesis during the depletion of glycogen in the liver. Ketone bodies generally transferred from liver (released by liver it self) to the body.

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