How Does Fat Leave The Body?

Nutrition
41

[quote]schanz_05 wrote:

[quote]bushidobadboy wrote:

[quote]schanz_05 wrote:

[quote]bushidobadboy wrote:

[quote]Med Pro wrote:
This is why marathon runners carb load before a marathon. There bodies can reach a point where they have no glucose for energy or fat stores for lyposis. This is termed, Hitting a wall. This is why many marathon runner look skinny because muscle is cataboized for use in energy.

ALL weight loss occurs through a hypoglycemic state. You can get to this point running on the tread mill for 2hrs, not eat or dramatically reduce food intake or Low Carb it! Eating protein only aids in preventing catabolisum.

[/quote]
Both of these statements are incorrect. Almost no human possesses so little bodyfat that they cannot continue a marathon.

However I wouldn’t expect you to know that GH causes a hyperglycemic state, due to the liberation of FFAs, which contributes to weight loss.

BBB[/quote]

BBB,

So you are saying elevated GH levels can cause the break down of adipose tissue into FFA’s to be used as fuel. As I understand it FFA’s cannot be converted to glucose. So then why would this cause a hyperglycemic state? Whenever there is excess glucose in the blood stream, isn’t that the primary fuel source? So if GH freed up FFA’s to be used as fuel, the body would still preferentially use any excess glucose as the fuel system, not allowing there to be a hyperglycemic state. Anyway, I am interested in your response.
[/quote]
In some users, elevated GH causes a measurable elevation in BG.

Whether or not it comes from the metabolism of FFAs, I can’t be 100% certain, but it makes sense to me.

Anyway, this elevation of BG is what makes GH potentially risky for some users, since chronic BG elevation reduces insulin snsitivity.

But that ‘problem’ is easy to avoid. Simply pulse your GH and you will create an environment where BG is also ‘pulsed’ in a sense. Couple this will long preiods of low/no carb to re-establish insulin sensitivity.

You need to realise that if your body is not using or disposing of BG at a rate equal or greater than the rate at which glucose is hitting the bloodstream, you will be in a state of hyperglycemia.

BBB[/quote]

All of that makes sense to me except for the part where metabolism of FFA’s results an in increase of BG. The only way I could see that is if someone is in a ketogenic state, and their preferred fuel source is FFA’s. So GH causes a breakdown of adipose tissue into FFA’s, and lets say for some reason this individual eats a carbohydrate containing meal that results in an increase of BG. The body’s preferred fuel source is still FFA’s, so instead of using the BG the body uses the circulating FFA’s, leaving the BG, and therefore the GH indirectly leads to elevated BG in the body.

That makes sense in my head, but even then I am not familiar enough with ketosis to know if it would actually work that way.[/quote]

FFA can decrease the use of glucose as a fuel source. Originally presented as the Randle hypothesis, and subsequently revised several times, FFA decrease insulin signaling and/or glycolysis. Though the primary site of this observation is in skeletal muscle and so, can in fact lead to elevations in blood glucose.

42

Lipid particles that aren’t consumed by cells (which releases heat as you stated) or deposited in the various tissues of the body circulate back to the liver to be metabolized and either discarded (out the back end) or recirculated into the blood stream

That is the simple one sentence answer you seek, anything else would require a many page explanation of the entire lifespan and metabolism of a every type of lipid particle you can consume. No point in arguing over or trying to explain a really complex thing that top sciences in this field don’t actually entirely understand let alone everyone in this forum, even with their pedigrees. Like prof X said

43

[quote]OzyNut wrote:

[quote]schanz_05 wrote:

[quote]bushidobadboy wrote:

[quote]schanz_05 wrote:

[quote]bushidobadboy wrote:

[quote]Med Pro wrote:
This is why marathon runners carb load before a marathon. There bodies can reach a point where they have no glucose for energy or fat stores for lyposis. This is termed, Hitting a wall. This is why many marathon runner look skinny because muscle is cataboized for use in energy.

ALL weight loss occurs through a hypoglycemic state. You can get to this point running on the tread mill for 2hrs, not eat or dramatically reduce food intake or Low Carb it! Eating protein only aids in preventing catabolisum.

[/quote]
Both of these statements are incorrect. Almost no human possesses so little bodyfat that they cannot continue a marathon.

However I wouldn’t expect you to know that GH causes a hyperglycemic state, due to the liberation of FFAs, which contributes to weight loss.

BBB[/quote]

BBB,

So you are saying elevated GH levels can cause the break down of adipose tissue into FFA’s to be used as fuel. As I understand it FFA’s cannot be converted to glucose. So then why would this cause a hyperglycemic state? Whenever there is excess glucose in the blood stream, isn’t that the primary fuel source? So if GH freed up FFA’s to be used as fuel, the body would still preferentially use any excess glucose as the fuel system, not allowing there to be a hyperglycemic state. Anyway, I am interested in your response.
[/quote]
In some users, elevated GH causes a measurable elevation in BG.

Whether or not it comes from the metabolism of FFAs, I can’t be 100% certain, but it makes sense to me.

Anyway, this elevation of BG is what makes GH potentially risky for some users, since chronic BG elevation reduces insulin snsitivity.

But that ‘problem’ is easy to avoid. Simply pulse your GH and you will create an environment where BG is also ‘pulsed’ in a sense. Couple this will long preiods of low/no carb to re-establish insulin sensitivity.

You need to realise that if your body is not using or disposing of BG at a rate equal or greater than the rate at which glucose is hitting the bloodstream, you will be in a state of hyperglycemia.

BBB[/quote]

All of that makes sense to me except for the part where metabolism of FFA’s results an in increase of BG. The only way I could see that is if someone is in a ketogenic state, and their preferred fuel source is FFA’s. So GH causes a breakdown of adipose tissue into FFA’s, and lets say for some reason this individual eats a carbohydrate containing meal that results in an increase of BG. The body’s preferred fuel source is still FFA’s, so instead of using the BG the body uses the circulating FFA’s, leaving the BG, and therefore the GH indirectly leads to elevated BG in the body.

That makes sense in my head, but even then I am not familiar enough with ketosis to know if it would actually work that way.[/quote]

FFA can decrease the use of glucose as a fuel source. Originally presented as the Randle hypothesis, and subsequently revised several times, FFA decrease insulin signaling and/or glycolysis. Though the primary site of this observation is in skeletal muscle and so, can in fact lead to elevations in blood glucose.[/quote]

So you’re saying in a normal individual that FFA’s can reduce the amount of glucose usage enough to result in hyperglycemia? That just seems counter intuitive to what the body is meant to do in regulating blood glucose levels.

44

[quote]ElevenMag wrote:
Lipid particles that aren’t consumed by cells (which releases heat as you stated) or deposited in the various tissues of the body circulate back to the liver to be metabolized and either discarded (out the back end) or recirculated into the blood stream

That is the simple one sentence answer you seek, anything else would require a many page explanation of the entire lifespan and metabolism of a every type of lipid particle you can consume. No point in arguing over or trying to explain a really complex thing that top sciences in this field don’t actually entirely understand let alone everyone in this forum, even with their pedigrees. Like prof X said[/quote]

I would not consider lipids being discarded out the back end to be of much significance to total lipid homeostasis. Lipids, when oxidised for energy, are systematically broken down to smaller and smaller molecules. Eventually the carbon is released as carbon dioxide.

The body is amazing in that all it really is doing is using the energy stored within the fatty acids and glucose molecules to do mechanical work (think pump), which it recovers and stores in the form of ATP.

45

[quote]schanz_05 wrote:
So you’re saying in a normal individual that FFA’s can reduce the amount of glucose usage enough to result in hyperglycemia? That just seems counter intuitive to what the body is meant to do in regulating blood glucose levels.
[/quote]
Very good point.
Plasma FFA levels do change considerably throughout the day and are quite variable among different people. At what point in a normal person will FFAs cause a clinically relevant difference, I do not know. But, transiently high physiologically relevant levels of plasma FFA (and triglycerides) will reduce insulin sensitivity in resting humans and a decreased rate of glucose disposal in the fed state (highly sensitive measures and by themselves do not indicate a disease state). Constantly high levels can cause hyperglycemia (a la dyslipidemia induced diabetes).

Did that answer your question?

46

[quote]OzyNut wrote:

[quote]schanz_05 wrote:
So you’re saying in a normal individual that FFA’s can reduce the amount of glucose usage enough to result in hyperglycemia? That just seems counter intuitive to what the body is meant to do in regulating blood glucose levels.
[/quote]
Very good point.
Plasma FFA levels do change considerably throughout the day and are quite variable among different people. At what point in a normal person will FFAs cause a clinically relevant difference, I do not know. But, transiently high physiologically relevant levels of plasma FFA (and triglycerides) will reduce insulin sensitivity in resting humans and a decreased rate of glucose disposal in the fed state (highly sensitive measures and by themselves do not indicate a disease state). Constantly high levels can cause hyperglycemia (a la dyslipidemia induced diabetes).

Did that answer your question?[/quote]

So it is an acute drop of insulin sensitivity in an inherently healthy person that could lead to the hyperglycemia, not necessarily a shift in type of fuel usage?

Interesting stuff. May I ask what your background is?

47

[quote]OzyNut wrote:

[quote]ElevenMag wrote:
Lipid particles that aren’t consumed by cells (which releases heat as you stated) or deposited in the various tissues of the body circulate back to the liver to be metabolized and either discarded (out the back end) or recirculated into the blood stream

That is the simple one sentence answer you seek, anything else would require a many page explanation of the entire lifespan and metabolism of a every type of lipid particle you can consume. No point in arguing over or trying to explain a really complex thing that top sciences in this field don’t actually entirely understand let alone everyone in this forum, even with their pedigrees. Like prof X said[/quote]

I would not consider lipids being discarded out the back end to be of much significance to total lipid homeostasis. Lipids, when oxidised for energy, are systematically broken down to smaller and smaller molecules. Eventually the carbon is released as carbon dioxide.

The body is amazing in that all it really is doing is using the energy stored within the fatty acids and glucose molecules to do mechanical work (think pump), which it recovers and stores in the form of ATP.[/quote]

I agree with you I was just answering the OP’s question as simply as possible. Since it asked if they are burnt as heat or released in your excrement. Almost all are recirculated but they could be packaged in the many types of VLDLs (most are in these), IDLs, HDLs, or LDLs. I took a 4 credit class with a leading cardiovascular surgeon and heart disease expert and I still don’t really have a true grasp on it. I actually quoted him exactly in that first one sentence explanation except for the added parentheses so i think its pretty spot on.

48

[quote]HolyMacaroni wrote:
reverse osmosis?[/quote]

Photosynthesis?

49

[quote]schanz_05 wrote:

[quote]OzyNut wrote:

[quote]schanz_05 wrote:
So you’re saying in a normal individual that FFA’s can reduce the amount of glucose usage enough to result in hyperglycemia? That just seems counter intuitive to what the body is meant to do in regulating blood glucose levels.
[/quote]
Very good point.
Plasma FFA levels do change considerably throughout the day and are quite variable among different people. At what point in a normal person will FFAs cause a clinically relevant difference, I do not know. But, transiently high physiologically relevant levels of plasma FFA (and triglycerides) will reduce insulin sensitivity in resting humans and a decreased rate of glucose disposal in the fed state (highly sensitive measures and by themselves do not indicate a disease state). Constantly high levels can cause hyperglycemia (a la dyslipidemia induced diabetes).

Did that answer your question?[/quote]

So it is an acute drop of insulin sensitivity in an inherently healthy person that could lead to the hyperglycemia, not necessarily a shift in type of fuel usage?

Interesting stuff. May I ask what your background is?
[/quote]
In the case of the GH induced FFA release and BG elevation, I would imagine that it would be the GH effects on the liver mediating the BG rise rather than the FFA affecting the muscles.

I don’t want to set an overly generalized model, so:

  1. Cell energy production is controlled at the level of the mitochondria (so not to overproduce ATP).
  2. Both glucose and FFA oxidation have negative feedback mechanisms to limit abnormal flow through that pathway.
  3. Both glucose and FFA oxidation are controllable (enhanced or decreased both intrinsically and extrinsically).
  4. FFA induced insulin resistance is an evolutionarily consumed mechanism to help protect energy stores in times of stress.
  5. The first observable impact that FFA induced insulin resistance is present would be in insulin mediated glucose disposal (and can be observed after a high fat meal - but everything returns to normal pretty quickly).
  6. When the above gets so bad that FFA impact fasting plasma glucose levels, it is pathological (ie diabetes).

I am a researcher would works in nutritional physiology (mostly lipids) and chronic diseases.

50

[quote]OzyNut wrote:

[quote]schanz_05 wrote:

[quote]OzyNut wrote:

[quote]schanz_05 wrote:
So you’re saying in a normal individual that FFA’s can reduce the amount of glucose usage enough to result in hyperglycemia? That just seems counter intuitive to what the body is meant to do in regulating blood glucose levels.
[/quote]
Very good point.
Plasma FFA levels do change considerably throughout the day and are quite variable among different people. At what point in a normal person will FFAs cause a clinically relevant difference, I do not know. But, transiently high physiologically relevant levels of plasma FFA (and triglycerides) will reduce insulin sensitivity in resting humans and a decreased rate of glucose disposal in the fed state (highly sensitive measures and by themselves do not indicate a disease state). Constantly high levels can cause hyperglycemia (a la dyslipidemia induced diabetes).

Did that answer your question?[/quote]

So it is an acute drop of insulin sensitivity in an inherently healthy person that could lead to the hyperglycemia, not necessarily a shift in type of fuel usage?

Interesting stuff. May I ask what your background is?
[/quote]
In the case of the GH induced FFA release and BG elevation, I would imagine that it would be the GH effects on the liver mediating the BG rise rather than the FFA affecting the muscles.

I don’t want to set an overly generalized model, so:

  1. Cell energy production is controlled at the level of the mitochondria (so not to overproduce ATP).
  2. Both glucose and FFA oxidation have negative feedback mechanisms to limit abnormal flow through that pathway.
  3. Both glucose and FFA oxidation are controllable (enhanced or decreased both intrinsically and extrinsically).
  4. FFA induced insulin resistance is an evolutionarily consumed mechanism to help protect energy stores in times of stress.
  5. The first observable impact that FFA induced insulin resistance is present would be in insulin mediated glucose disposal (and can be observed after a high fat meal - but everything returns to normal pretty quickly).
  6. When the above gets so bad that FFA impact fasting plasma glucose levels, it is pathological (ie diabetes).

I am a researcher would works in nutritional physiology (mostly lipids) and chronic diseases.[/quote]

So would this be an argument against meals that contain both a considerable amount of fat and carbs? The FFA circulation in conjunction with the insulin release from carbohydrates would cause a disruption in glucose disposal via an acute period of increased insulin resistance?

Appreciate your insight!

51

So when a GHRP is used in a fasted state…the muscle using The FFA that were released?

ALso when people use GHRP’s to induce a higher GH spike dont some say they go hypo glycemic not hyper glycemic or does this vary by person as every person in the world has a slightly different metabolism.

52

[quote]schanz_05 wrote:
So would this be an argument against meals that contain both a considerable amount of fat and carbs? The FFA circulation in conjunction with the insulin release from carbohydrates would cause a disruption in glucose disposal via an acute period of increased insulin resistance?

Appreciate your insight!
[/quote]
I wouldn’t go that fat, but you are on the right track and a few points to consider: a majority of carbs will be disposed within 2 hours. In contrast, dietary fat (found in the form of chylomicrons) can still be secreted up to 6 hours after a meal. This would suggest that the dietary fat in one meal would impact glucose disposal more in the next meal than within the same meal. Furthermore, the composition of dietary fat can have substantial impact. While saturated-, mono unsat-, poly unsat- and mixed-fat have all been shown to cause insulin resistance, the molecular pathways do differ. Scientists can determine to ‘blocked’ step in the insulin signalling cascade and have shown where the fats impact. The differences can be explained by the differing affinities to the various pathways of lipid metabolism (glycerolipid, sphingolipid etc.)

For healthy people, the clinical impact would be very minimal. For those with metabolic disturbances, the effects are exaggerated and likely compounded. Fortunately, there are many ways to antagonize these pathways. Consistent exercise would be very advantageous in this regard.

Overall, there is not enough evidence to say that we should separate carbs and fats. On the otherhand, there isn’t enough evidence to say the spreading the fats out over the day is the best either. Though, as it stands, this doesn’t seem like a bad idea.

53

[quote]ryanbCXG wrote:
So when a GHRP is used in a fasted state…the muscle using The FFA that were released?

ALso when people use GHRP’s to induce a higher GH spike dont some say they go hypo glycemic not hyper glycemic or does this vary by person as every person in the world has a slightly different metabolism.[/quote]
GH has substantial effects on glucose metabolism, the result of which pushes glucose into the blood. I personally have no experience in GH, though my niece (8 years old) does, as she is deficient, and hasn’t had any issues with hypoglycemia. I would imagine the hypoglycemia would be due to some other factor. Perhaps BBB could shed some light on typical practice and BG effects.

Circulating FFA (released from adipose tissue - not talking about circulating triglycerides) can be taken up into just about any cell. FFA can diffuse into cells fairly easily (but at a low rate) where they are metabolically trapped. However, there is some evidence that fatty acid transport proteins play some role in cellular uptake and would likely be most active in organs with high fat needs (skeletal muscle, brain, liver).

If you want to know if more, I would suggest looking whether GH affects skeletal muscle fatty acid uptake; or perhaps indirectly by enhancing fatty acid oxidation.

54

Growth hormone has a lot of different effects upon the body, but in reference to FFA it enhances the release of FFA into circulation, while limiting the effect of insulin and glucose absorption. As per review in a researched paper.

Regulation of Glucose Uptake by Muscle
8. EFFECTS OF FATTY ACIDS, KETONE BODIES AND PYRUVATE, AND OF ALLOXANDIABETES
AND STARVATION, ON THE UPTAKE AND METABOLIC FATE
OF GLUCOSE IN RAT HEART AND DIAPHRAGM MUSCLES
By P. J. RANDLE,* E. A. NEWSHOLMEt AND P. B. GARLAND*
Department of Biochemistry, University of Cambridge

While this may not be the full source of the issue, a lot of this research is still widely controversial and studies go back and forth on which is the correct response. I believe it is still widely affected by the nutritional status of the individuals tested, for everyone is different and depending upon the type of foodstuffs that they are consume, different types of responses are regulated in the body.

Chronic overuse of hGH has been shown to cause diabetes and renal failure, which would make sense if it disrupts insulin actions on skeletal muscle, and perhaps other tissues.

This thread has gone a little off topic, but the OP has stated a too general question that doesn’t take into account of the numerous biochemical pathways that FFA take within the body. It’s not just as simple as you eat fat, you absorb it and burn it as heat or store it.

Adipose tissue is now considered not to be simply inactive tissue that is a fuel source for the body, but also an endocrine organ that releases a variety of hormones that regulate metabolism, such as Interleukin-6 (IL-6), Tumour Necrosis Factor-a (TNFa) Leptin, Resistin, Macrophage and Monocyte Chemoattractant Protein-1 (MPC-1), Plasminogen Activator Inhibitor-1 (PAI-1), Adipsin and Adiponectin. These endocrine functions are largely regulated by insulin and the insulin receptors (ie. GLUT-4, etc) and operate on feedback mechanisms, all highly influenced by what you’re consuming and at what time periods.

With so much activity going on it’s hard to point to exactly what is really affecting the direction of lipid metabolism, unless defined perameters are set.

v/r

Gremster