Insulin binding to fat cell receptors

[Burner]

So I understand that insulin will bind to fat cell receptors (as well as other cell receptors) and inhibit fat oxidation, but i want to know if the body has an order or sequence in which cells insulin targets.

So lets say you spike your insulin, it will bind to receptors and pull glucose into the cell, but will the body target cells that need it most or will it bind to everything? Thanks.


EDIT: And if anyone knows a good read on the subject i would love it.

[Burner]

bump

[Nitrox]

Insulin inhibits fat oxidation because insulin is released when you consume food in portions that lead to surplus energy. When you supply your body with extra food energy, it has little need to dip into stores. Insulin is the effect not the cause.

As far as targetting specific cells. Fat deposits are generally larger around the body's center of gravity (mid section). Is that what you mean?

[Jax11]

insulin is signaled when glucose is elevated in the bloodstream (blood sugar levels which depend on either a rapid increase which is bad and steady which is prefered)...as a result, it pulls the glucose to either muscle cells for energy or if energy is not needed, then it is stored as fat

[krogtaar]

think of it in terms of chemical reaction rates...the rate of uptake into muscle cells is proportional to the concentration of glucose in the blood, the amount of "room" in muscles free to be filled, and the anabolic response from exercise pulling glucose into cells.

[Burner]

Insulin inhibits fat oxidation because insulin is released when you consume food in portions that lead to surplus energy. When you supply your body with extra food energy, it has little need to dip into stores. Insulin is the effect not the cause.

As far as targetting specific cells. Fat deposits are generally larger around the body's center of gravity (mid section). Is that what you mean?

insulin is signaled when glucose is elevated in the bloodstream (blood sugar levels which depend on either a rapid increase which is bad and steady which is prefered)...as a result, it pulls the glucose to either muscle cells for energy or if energy is not needed, then it is stored as fat

So are you both saying that glucose will ONLY be stored as fat once all glycogen stores are filled? Which would seem to me that insulin will bind to cells in a specific order (muscle cells then fat cells, just talking about these at the moment) depending on the state of the body. Basically, the body should not store glucose as fat if there are glycogen stores that need to be filled, correct?

[Nitrox]

I have never read any info that is that definitive. Personally, I don't believe that it works that way; that would be a fairly linear response.

Different cells in the body have different 'sensitivities' to insulin. The theory is that after training a muscle, it becomes hungry for energy and becomes more sensitive to insulin. However, if you 'spike' insulin to a high enough level (by consuming more food energy than is necessary for replenishment and maintenance) then theoretically you can 'turn on' all the cells and store fat and replenish glycogen at the same time.

[zaosha]

Muscular contraction causes glucose transporters (GLUT4 to be precise) to transolcate to the outside of the cell membrane and grab glucose molecules out of the bloodstream; this process is completely independent of insulin. This effect tends to diminish rather rapidly post-exercise.

Unless you are doing a lot of endurance work or really high volume lifting you probably aren't even approaching glycogen depletion. But, any level of glycogen depletion should selectively increase skeletal muscle insulin sensitivity.

Also, while protein synthesis is elevated for several hours PWO, so is degradation. Elevated insulin levels mitigate the rate of degradation as do elevated levels of Amino Acids in the bloodstream. What all this means is that we can potentially get a significant partitioning effect by ingesting the bulk of our carbohydrate intake and large amounts of protein in the hour before and several hours after our WO's.

While I am not sold on IF (intermittent fasting) as the most effective nutrient timing strategy for body composition the anecdotal evidence seems to support that it is somewhat effective.

I am currently experiencing excellent recomp effects by limiting my calorie intake to an ~11 hour window with two training sessions in that period. I am sticking with the same caloric intake I would normally consume in a 15-16 hour timeframe and my total volume of training is only slightly elevated from my previous once daily WO's.

I wouldn't suggest this strategy unless your primary goals are fat loss or steady recomp. I couldn't see myself consuming a true bulking diet in this manner.

[russy_russ]

insulin is signaled when glucose is elevated in the bloodstream (blood sugar levels which depend on either a rapid increase which is bad and steady which is prefered)...as a result, it pulls the glucose to either muscle cells for energy or if energy is not needed, then it is stored as fat

Glucose is transported via GLUT4 primarily into skeletal muscle cells. When an abundance is in the cell formation of glycogen begins. Extra is excreted and NOT stored as fat (if this wasn't true then we would have no need for waste being excreted from the body). This is common misconception, because the typical diet is high in fats as well as carbohydrates. When high fats are consumed with high carbohydrates the carbohydrates will drive their own metabolism first then they will fuel the metabolism of fatty acids (they cannot fuel their own metabolism). Since high carbohydrates have been consumed with high fats, the fats do not get utilized, in which case would be stored.

[Cinn]

Glucose is transported via GLUT4 primarily into skeletal muscle cells. When an abundance is in the cell formation of glycogen begins. Extra is excreted and NOT stored as fat (if this wasn't true then we would have no need for waste being excreted from the body). This is common misconception, because the typical diet is high in fats as well as carbohydrates. When high fats are consumed with high carbohydrates the carbohydrates will drive their own metabolism first then they will fuel the metabolism of fatty acids (they cannot fuel their own metabolism). Since high carbohydrates have been consumed with high fats, the fats do not get utilized, in which case would be stored.

A large portion of our carbohydrate intake is synthesized into fatty acids.

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[zaosha]

Extra is excreted and NOT stored as fat (if this wasn't true then we would have no need for waste being excreted from the body).

Extra glucose is not excreted - except in the case of diabetics experiencing hyperglycemia. If not burned or stored as muscle/hepatic glycogen it will be converted to fat through DNL (de novo lipogenesis).

[crazyfool405]

Glut 4 pathway goes into adipose AND muscle cells. Not just muscle cells

Posted from my mobile device.

[russy_russ]

Carbohydrates do not turn into fat HUMANS. Studies shown in which carbohydrates turn to fatty acids are not done on humans.

"The daily protein in take is used to maintain existing tissue protein, hormones, and enzymes. If more is taken in than is needed, the "extra" is oxidized for metabolic needs, and fat mass is not increased. The same is true for carbohydrates. Ingested carbohydrates are used to fill liver and muscle glycogen stores; the excess is oxidized and is NOT converted to fat. Carbohydrate intake promotes its own oxidation. This is a relatively new idea that has major ramifications for our understanding of nutrient and energy balance.The evidence seems to be quite convincing that 'de novo' lipogenesis from carbohydrates (the making of new lipids from other nutrients) is of only minor consequence in humans. Simply, carbohydrates are either stored as carbohydrates or oxidized; they do not add directly to adipose tissue mass. This leaves fat.

In contrast to carbohydrate and protein, fat intake is not automatically balanced by fat oxidation. When "extra" fat is added to the diet, the same amounts of carbohydrate, fat, and protein are oxidized as before; the extra fat is stored in adipose tissue. Fat intake does not promote its own oxidation."

Acheson, K. J. 1987. Carbohydrate metabolism and de novo lipogenesis in human obesity. AMERICAN JOURNAL OF CLINICAL NUTRITION 45; 78-85

Powers, Scott and Edward T. Howley. Exercise Physiology: Theory and Applications to
Fitness and Performance. New York: McGraw-Hill, 2009.

[Cinn]

Carbohydrates do not turn into fat HUMANS. Studies shown in which carbohydrates turn to fatty acids are not done on humans.

Yes...they do. In the presence of a caloric surplus, glucose is converted into pyruvic acid and further into Acetyl CoA. That can then be converted into fatty acids(known as lipogenesis). I'm not sure where you think all of that extra glucose goes.

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[russy_russ]

Glut 4 pathway goes into adipose AND muscle cells. Not just muscle cells

Posted from my mobile device.

Wrong, GLUT4 is specifically for glucose. GLUT4 opens a gate on the plasma membrane so that glucose can be shuttled into the cell to form glycogen. Insulin suppressed beta-oxidation (oxidation of fatty acids) by directly inhibiting lipase activity. This stops the metabolism of stored fatty acids, it does NOT store fat.

[russy_russ]

Yes...they do. In the presence of a caloric surplus, glucose is converted into pyruvic acid and further into Acetyl CoA. That can then be converted into fatty acids(known as lipogenesis). I'm not sure where you think all of that extra glucose goes.

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glucose is either converted to pyruvate or lactate (depending on a few physiological reasons) from there the pyruvate or stored as liver glucose or muscle glycogen. Pyruvate is converted to Acetyl-CoA with the enzyme pyruvate kinase. Acetyl-CoA does NOT convert to fat, instead it enters TCA cycle (kreb's cycle, how ever you call it; it has many names). Beta-Oxidation is the pathway for fatty acids to be converted to Acetyl-CoA to enter the TCA cycle for complete oxidation. This process is not reversible in humans.

[Cinn]

glucose is either converted to pyruvate or lactate (depending on a few physiological reasons) from there the pyruvate or stored as liver glucose or muscle glycogen. Pyruvate is converted to Acetyl-CoA with the enzyme pyruvate kinase. Acetyl-CoA does NOT convert to fat, instead it enters TCA cycle (kreb's cycle, how ever you call it; it has many names). Beta-Oxidation is the pathway for fatty acids to be converted to Acetyl-CoA to enter the TCA cycle for complete oxidation. This process is not reversible in humans.

You do realize that you are essentially claiming someone eating an increased kcal, high carb, low fat diet can not gain fat...right? Think about how silly you sound.

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[Mulletsoldier]

glucose is either converted to pyruvate or lactate (depending on a few physiological reasons) from there the pyruvate or stored as liver glucose or muscle glycogen. Pyruvate is converted to Acetyl-CoA with the enzyme pyruvate kinase. Acetyl-CoA does NOT convert to fat, instead it enters TCA cycle (kreb's cycle, how ever you call it; it has many names). Beta-Oxidation is the pathway for fatty acids to be converted to Acetyl-CoA to enter the TCA cycle for complete oxidation. This process is not reversible in humans.

Acetyl-CoA is most certainly not catalyzed to form fatty acids, but it is highly regulated in fatty acid biosynthesis, via its carboxylation to Malonyl-CoA via the aptly named "acetyl-CoA-carboxylase" [ACC].

[russy_russ]

Acetyl-CoA is most certainly not catalyzed to form fatty acids, but it is highly regulated in fatty acid biosynthesis, via its carboxylation to Malonyl-CoA via the aptly named "acetyl-CoA-carboxylase" [ACC].

The beta oxidation process ends with Acetyl-CoA, which then can either enter the TCA cycle or used in biosynthesis of amino acids.

http://www.bgsu.edu/departments/chem...dation_angela/

Which I believe is what you were trying to say. That's why I said the process CANNOT be reversed "acetyl-coa --> fatty acids"

[russy_russ]

I've posted my sources for information. Take what you want from it; I'm out.