Energy source during starvation

[MudPhud20XX]

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So I had another question from Kaplan asking:

A 4-year-old girl has been unable to eat for 2 days because of a gastrointestinal tract disorder. Which of the following is the major source of fuel being oxidized by her skeletal muscles?

I was debating between two answer choices:
1. Muscle triglycerides
2. serum fatty acids --> This is the answer.

Why not muscle TG? TG can be broken down into fatty acids and muscles can do beta oxidation right?

 

[Myxedema]

They can be used, but in a fasting state, the major source of fatty acids would be from adipose tissue.

 

[ChessMaster3000]

They can be used, but in a fasting state, the major source of fatty acids would be from adipose tissue.

also--do muscle triglycerides get used for systemic consumption? I thought it was analogous to glycogen use which is committed to the muscle (no glucose-6-phosphatase)

 

[MudPhud20XX]

I noticed that it is first the muscle proteins that are used for gluconeogenesis during a starvation less then a week.

And during a prolonged starvation, TG in fat tissue is used for systemic consumption to make ketone bodies.

Thanks for the feedback!

 

[notbobtrustme]

if cells used their own triglycerides, they would destabilize their membranes and die. Adipose cells are specialized cells that store triglycerides for systemic consumption.

 

[sanj238]

also--do muscle triglycerides get used for systemic consumption? I thought it was analogous to glycogen use which is committed to the muscle (no glucose-6-phosphatase)

I never even heard of muscle TG usage..I would suspect this is a pathological state and not for starvation.

 

[Myxedema]

also--do muscle triglycerides get used for systemic consumption? I thought it was analogous to glycogen use which is committed to the muscle (no glucose-6-phosphatase)

Muscle is the "systemic consumption". This is not about the lack of an enzyme, but rather, transfer of an high-energy molecule from a metabolically inactive storage site to active sites (muscle & liver).

I never even heard of muscle TG usage..I would suspect this is a pathological state and not for starvation.

During normal fasting state, fatty acids undergo beta-oxidation in both the liver and muscles to synthesize ATP.

 

[sanj238]

Muscle is the "systemic consumption". This is not about the lack of an enzyme, but rather, transfer of an high-energy molecule from a metabolically inactive storage site to active sites (muscle & liver).

During normal fasting state, fatty acids undergo beta-oxidation in both the liver and muscles to synthesize ATP.

Are you sure its fatty acids in the muscle? I thought it was fatty acids transported in the plasma from adipose tissue...

 

[notbobtrustme]

During normal fasting state, fatty acids undergo beta-oxidation in both the liver and muscles to synthesize ATP.

I think the others are talking about taking out plasma membrane and oxidizing it for energy. That might happen, but you are way past normal "starvation" and into Holocaust territory.

 

[Myxedema]

Are you sure its fatty acids in the muscle? I thought it was fatty acids transported in the plasma from adipose tissue...

It's not either/or. To make it clear, let me say that the muscle tissue can use both intramyocellular lipids and plasma free fatty acids (mainly derived from adipose tissue) for ATP production.

I think the others are talking about taking out plasma membrane and oxidizing it for energy. That might happen, but you are way past normal "starvation" and into Holocaust territory.

Like you've said, even if such a thing were to happen, it is not relevant to normal, physiological metabolism. Muscle tissue normally contains lipids which can be utilized for energy. However, since muscle is not a primary storage tissue, it is logical that adipose tissue would be the primary source of lipids that the muscles and the liver use for beta-oxidation.

 

[sanj238]

It's not either/or. To make it clear, let me say that the muscle tissue can use both intramyocellular lipids and plasma free fatty acids (mainly derived from adipose tissue) for ATP production.

Like you've said, even if such a thing were to happen, it is not relevant to normal, physiological metabolism. Muscle tissue normally contains lipids which can be utilized for energy. However, since muscle is not a primary storage tissue, it is logical that adipose tissue would be the primary source of lipids that the muscles and the liver use for beta-oxidation.

But even if it can- would it do so under 'normal' starvation conditions- someone starving for less than a week? I highly doubt that right? I mean if I were to identify muscle TG usage my first thought would be a genetic pathologic disease... I guess high endurance athletes can be added to that?

 

[Myxedema]

I've done a quick review of textbooks to clarify the issue. I hope this could be of assisstance:

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Boron WF, Boulbpaep EL, Medical Physiology, Updated 2nd Ed., Chapter 58, p. 1215: "...Most of the body’s fat depots exist in the subcutaneous adipose tissue layers, although fat also exists to a small extent in muscle and in visceral (deeper) depots in obese individuals..."

Op. cit., p. 1225: "Insulin, secreted in response to the carbohydrate or protein components of the meal, has three major effects on lipid metabolism (see Chapter 51). First, insulin stimulates LPL. LPL promotes hydrolysis of TAGs to FAs and glycerol. The breakdown products enter the adipocytes for re-esterification into TAGs. Insulin promotes storage in muscle and adipose tissue of both exogenous TAGs (derived from a meal and carried in chylomicrons) and endogenous TAGs (produced by the liver and carried in VLDLs)."

Op. cit., p. 1231: "...In contrast, oxidative metabolism of FAs is the major mechanism for supporting exercising muscle during prolonged activity, such as running a marathon, which is mostly the work of the slow-twitch type 1 muscle fibers (see Chapter 60)."

Op. cit., p. 1232: "Integrative Metabolism of Fasting [...] In the fed state and early in the fasting state, the brain derives essentially all its energy from oxidation of glucose because ketone bodies are not present and the blood-brain barrier is mostly impermeable to FAs. Most other major organs of the body (liver, skeletal muscle, heart) fill their energy needs at this time by oxidizing FAs... After an overnight fast, the decline in circulating insulin leads to a marked decrease in glucose uptake by insulin-sensitive tissues (e.g., muscle) and a shift toward the use by these tissues of FAs mobilized from fat stores."

Op. cit., p. 1234: "Lipolysis - Finally, the fall in plasma [insulin] after an overnight fast permits the release of FAs and glycerol from fat stores. This response appears to be more pronounced in visceral than peripheral fat depots. The decline in [insulin] and the ensuing lipolysis are sufficient to supply FAs to extracerebral tissues (e.g., muscle, heart, liver) for fuel and glycerol to the liver for gluconeogenesis. However, these changes are not sufficient to stimulate the hepatic conversion of FA to ketone bodies."

Guyton & Hall Textbook of Medical Physiology, 11th Ed., Chapter 68, p. 846: "Probably the most dramatic increase that occurs in fat utilization is that observed during heavy exercise. This results almost entirely from release of epinephrine and norepinephrine by the adrenal medullae during exercise, as a result of sympathetic stimulation. These two hormones directly activate hormone-sensitive triglyceride lipase, which is present in abundance in the fat cells, and this causes rapid breakdown of triglycerides and mobilization of fatty acids.Sometimes the free fatty acid concentration in the blood of an exercising person rises as much as eightfold, and the use of these fatty acids by the muscles for energy is correspondingly increased. Other types of stress that activate the sympathetic nervous system can also increase fatty acid mobilization and utilization in a similar manner."

 

[sanj238]

I've done a quick review of textbooks to clarify the issue. I hope this could be of assisstance:

--------

Boron WF, Boulbpaep EL, Medical Physiology, Updated 2nd Ed., Chapter 58, p. 1215: "...Most of the body’s fat depots exist in the subcutaneous adipose tissue layers, although fat also exists to a small extent in muscle and in visceral (deeper) depots in obese individuals..."

Op. cit., p. 1225: "Insulin, secreted in response to the carbohydrate or protein components of the meal, has three major effects on lipid metabolism (see Chapter 51). First, insulin stimulates LPL. LPL promotes hydrolysis of TAGs to FAs and glycerol. The breakdown products enter the adipocytes for re-esterification into TAGs. Insulin promotes storage in muscle and adipose tissue of both exogenous TAGs (derived from a meal and carried in chylomicrons) and endogenous TAGs (produced by the liver and carried in VLDLs)."

Op. cit., p. 1231: "...In contrast, oxidative metabolism of FAs is the major mechanism for supporting exercising muscle during prolonged activity, such as running a marathon, which is mostly the work of the slow-twitch type 1 muscle fibers (see Chapter 60)."

Op. cit., p. 1232: "Integrative Metabolism of Fasting [...] In the fed state and early in the fasting state, the brain derives essentially all its energy from oxidation of glucose because ketone bodies are not present and the blood-brain barrier is mostly impermeable to FAs. Most other major organs of the body (liver, skeletal muscle, heart) fill their energy needs at this time by oxidizing FAs... After an overnight fast, the decline in circulating insulin leads to a marked decrease in glucose uptake by insulin-sensitive tissues (e.g., muscle) and a shift toward the use by these tissues of FAs mobilized from fat stores."

Op. cit., p. 1234: "Lipolysis - Finally, the fall in plasma [insulin] after an overnight fast permits the release of FAs and glycerol from fat stores. This response appears to be more pronounced in visceral than peripheral fat depots. The decline in [insulin] and the ensuing lipolysis are sufficient to supply FAs to extracerebral tissues (e.g., muscle, heart, liver) for fuel and glycerol to the liver for gluconeogenesis. However, these changes are not sufficient to stimulate the hepatic conversion of FA to ketone bodies."

Guyton & Hall Textbook of Medical Physiology, 11th Ed., Chapter 68, p. 846: "Probably the most dramatic increase that occurs in fat utilization is that observed during heavy exercise. This results almost entirely from release of epinephrine and norepinephrine by the adrenal medullae during exercise, as a result of sympathetic stimulation. These two hormones directly activate hormone-sensitive triglyceride lipase, which is present in abundance in the fat cells, and this causes rapid breakdown of triglycerides and mobilization of fatty acids.Sometimes the free fatty acid concentration in the blood of an exercising person rises as much as eightfold, and the use of these fatty acids by the muscles for energy is correspondingly increased. Other types of stress that activate the sympathetic nervous system can also increase fatty acid mobilization and utilization in a similar manner."

Thank you for posting this.

I've read through it and I am even more confident now that only adipose fat and liver fat is used but not muscle.

After reading I see that it states in many areas that visceral fat (adipose ) is used during starvation periods. The mentions of muscle in these passages merely indicates that muscle is involved in FA breakdown- but no where does it say that this FA comes from muscle. In fact- and in the absence of such a clarifier- the mentioning of the use of visceral fat, adipose fat, and intrinisc liver fat seems to me that the fat from adipose is what is used.

I do not think these passages are implying that FA of muscle is via fat in the muscle- simply that fat stores are used- and fat stores here mean adipose.

Indeed in some of the passages this is quite clear though they were not highlighted (I've bolded what I think is the important points):

Sometimes the free fatty acid concentration in the blood of an exercising person rises as much as eightfold, and the use of these fatty acids by the muscles for energy is correspondingly increased

This response appears to be more pronounced in visceral than peripheral fat depots. The decline in [insulin] and the ensuing lipolysis are sufficient to supply FAs to extracerebral tissues (e.g., muscle, heart, liver) for fuel

Most of the body’s fat depots exist in the subcutaneous adipose tissue layers, although fat also exists to a small extent in muscle and in visceral (deeper) depots in obese individuals


- while it does say that fat is in muscle- I dont think they are referncing this in terms of fat use for starvation or any other physiologic state.

Again- I think the use of fat in the muscle for lipolysis is going to be a pathologic condition or severe and I mean severe- over 10 days - of starvation

 

[Myxedema]

Thank you for posting this.

I've read through it and I am even more confident now that only adipose fat and liver fat is used but not muscle.

After reading I see that it states in many areas that visceral fat (adipose ) is used during starvation periods. The mentions of muscle in these passages merely indicates that muscle is involved in FA breakdown- but no where does it say that this FA comes from muscle. In fact- and in the absence of such a clarifier- the mentioning of the use of visceral fat, adipose fat, and intrinisc liver fat seems to me that the fat from adipose is what is used.

I do not think these passages are implying that FA of muscle is via fat in the muscle- simply that fat stores are used- and fat stores here mean adipose

First of all, starvation is a pathologic process. If you read the quotes I've given you above, they're about fed and fasting states, not starvation. In fact, in the Boron & Boulpaep Medical Physiology textbook, starvation is dealt in a separate subheading from fed & fasting states. That being said, it is clear from the quotes above that during the fed state, insulin stimulates TAG storage in both muscle & adipose tissue. During fasting state, hormone-sensitive lipase breaks down the lipids in these tissues. Since muscle is primarily an active tissue and adipose is primarily a storage tissue, it is not surprising a much greater amount of fatty acids would be stored and released from the adipose tissue. Obviously, the fat used by the muscle tissue is mainly derived from the fatty acids liberated from the adipose tissue, as I've mentioned in my very first post. In short, muscle uses fat for energy. This fat mainly comes from adipose tissue, with some coming from the muscle itself.

 

[sanj238]

First of all, starvation is a pathologic process. If you read the quotes I've given you above, they're about fed and fasting states, not starvation. In fact, in the Boron & Boulpaep Medical Physiology textbook, starvation is dealt in a separate subheading from fed & fasting states. That being said, it is clear from the quotes above that during the fed state, insulin stimulates TAG storage in both muscle & adipose tissue. During fasting state, hormone-sensitive lipase breaks down the lipids in these tissues. Since muscle is primarily an active tissue and adipose is primarily a storage tissue, it is not surprising a much greater amount of fatty acids would be stored and released from the adipose tissue. Obviously, the fat used by the muscle tissue is mainly derived from the fatty acids liberated from the adipose tissue, as I've mentioned in my very first post. In short, muscle uses fat for energy. This fat mainly comes from adipose tissue, with some coming from the muscle itself.

After having looked into this- IMTGs are predominantly used by obese individuals - due to their overall fat levels, and high endurance athletes. I'm still not convinced that IMTGs are used in any clinically significant manner during a fasting state by normal individuals. Its possible that there is some breakdown- but in such a complex system thats not surprising- but for test questions I don't think I would ever pick this outside of starvation, athletes etc.