All About Insulin

Bone

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From Dr.Juice at CJM

[font="verdana, arial, helvetica"]What is Insulin?
Insulin is a small polypeptide produced by the pancreatic beta cells. Insulin is crucial for the transport of glucose into the cell. The hormone binds receptor sites on the cell membrane, which promotes movement of glucose- transport proteins from the interior to the surface of the cell. These proteins, in turn, bind glucose and carry it into the cell. As you can see insulin is highly anabolic.

Insulin is a key player in the control of intermediary metabolism. It has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism.

Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane.

The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response.

Insulin facilitates entry of glucose into muscle, adipose and several other tissues. The only mechanism by which cells can take up glucose is by facilitated diffusion through a family of hexose transporters. In many tissues - muscle being a prime example - the major transporter used for uptake of glucose (called GLUT4) is made available in the plasma membrane through the action of insulin. In the absence of insulin, GLUT4 glucose transporters are present in cytoplasmic vesicles, where they useless for transporting glucose. Binding of insulin to receptors on such cells leads rapidly to fusion of those vesicles with the plasma membrane and insertion of the glucose transporters, thereby giving the cell an ability to efficiently take up glucose. When blood levels of insulin decrease and insulin receptors are no longer occupied, the glucose transporters are recycled back into the cytoplasm.

It should be noted here that there are some tissues that do not require insulin for efficient uptake of glucose: important examples are brain and the liver. This is because these cells don't use GLUT4 for importing glucose, but rather, another transporter that is not insulin-dependent.

Insulin stimulates the liver to store glucose in the form of glycogen. A large fraction of glucose absorbed from the small intestine is immediately taken up by hepatocytes, which convert it into the storage polymer glycogen.

A well-known effect of insulin is to decrease the concentration of glucose in blood, which should make sense considering the mechanisms described above. Another important consideration is that, as blood glucose concentrations fall, insulin secretion ceases. In the absence of insulin, a bulk of the cells in the body become unable to take up glucose, and begin a switch to using alternative fuels like fatty acids for energy. Neurons, however, require a constant supply of glucose, which in the short term, is provided from glycogen reserves.

In the absence of insulin, glycogen synthesis in the liver ceases and enzymes responsible for breakdown of glycogen become active. Glycogen breakdown is stimulated not only by the absence of insulin, but by the presence of glucagon, which is secreted when blood glucose levels fall below the normal range.

All of the above was covered in more simplistic terms in Part 3 of the Animalbolics series located elsewhere on this site, so it should be well known to most of you. The writer of those articles has a bit more skill at simplifying terms than I do, so if you are lost, read that article.

Insulin also effects lipid storage as well. Insulin is stimulatory to synthesis of glycogen in the liver. However, as glycogen accumulates to high levels (roughly 5% of liver mass), further synthesis is strongly suppressed.

When the liver is saturated with glycogen, any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids, which are exported from the liver as lipoproteins. The lipoproteins are ripped apart in the circulation, providing free fatty acids for use in other tissues, including adipocytes, which use them to synthesize triglycerides.

Insulin inhibits breakdown of fat in adipose tissue by inhibiting the intracellular lipase that hydrolyzes triglycerides to release fatty acids.

Insulin facilitates entry of glucose into adipocytes, and within those cells, glucose can be used to synthesize glycerol. This glycerol, along with the fatty acids delivered from the liver, is used to synthesize triglyceride within the adipocyte. By these mechanisms, insulin is involved in further accumulation of triglyceride in fat cells. This is why high insulin levels leads to the storage of adipose tissue.

Now for the good news. In addition to insulin's effect on entry of glucose into cells, it also stimulates the uptake of amino acids. This is the reason bodybuilders use insulin.

Insulin exerts its dramatic anabolic effect by inhibiting muscle breakdown/degradation. This process is believed to occur by the inhibition of the ubqitin-proteasome pathway (one of three major muscle degradation pathways in muscle cells), but once again, little is known about the cellular mechanisms by which insulin exerts this anti-catabolic action. Research does show that the introduction of insulin stops proteolysis (muscle breakdown) and while insulin is driving amino acids and glucose into muscle cells, it appears it also prevents the leakage of these nutrients from the muscle cells that usually occur in response to training. Absence of insulin or allowing insulin levels to drop is the fastest, easiest way to induce muscle protein breakdown (catabolism).

So why supplement with insulin? Many bodybuilders (especially "natural" bodybuilders) choose to use external sources of insulin. Exogenous insulin is completely undetectable by current drug testing procedures.



The Basics of Injectable Insulin
Insulin is described and subdivided by concentration strength, source, and time of onset/peak. This last category is most critical, but an understanding of all three criteria is needed.

Concentration Strength
All insulins sold in the United States today are of U-100strength, 100 units of insulin per cc of fluid. (Since most of our readers are American, I'll use American standards throughout this series) But there are other dilutions in other countries, and if you were to encounter one of these (all perfectly usable), and inject your usual volume of insulin, you'd get a different amount of insulin. You'd get the wrong dosage.

Sources
At one time, all insulin was produced by laboratory animals, most often cows and pigs. In the last decade, however, American insulin manufacturers have almost completely shifted to use of "recombinant DNA" technology, enabling laboratory production of a close analog to real human insulin. This "human" insulin is said to more closely match our endogenous (pancreatic) insulin. Although labeled much like "animal source" insulins, recombinant DNA insulins are not quite the same, either in time-of-onset or in amount of insulin required. Experience shows that any switch between the one and the other must be done with care, and under your doctor's supervision--the types might be different enough to cause you trouble otherwise.

Time of Onset/Peak
The different insulin types: Humalog, Regular, NPH, Lente, Ultralente, and the pre-mixes: 70/30 and 50/50, divided and distinguished by their time of onset and duration. As shown in the chart below, critical questions that you MUST know are:

1. When does this insulin begin to act in my body?
2. When does it reach its peak?
3. When does it fade to insignificance?

NOTE: Each human body is different. Charts reflect averages -- you may well find a given insulin is different for you. Below is a general approximation, derived from data furnished by both U.S. insulin manufacturers, Eli Lilly and Company and Novo Nordisk Pharmaceuticals Inc.

Usual Action Times:

(Table Key)
1. Onset
2. Peak Action
3. Duration

Humalog
1. 15 min.
2. 1/2 -1 1/2 hrs
3. 3-5 hrs

Regular
1. 1/2 hr
2. 2-4 hrs
3. 6-8 hrs

NPH, Lente
1. 1-3 hrs
2. 6-12 hrs
3. 18-26 hrs

Ultralente
1. approx. 4-8 hrs
2. 12-18 hrs
3. approx. 24-28 hrs
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raybravo

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good read :) , insulin is the maker of beasts !! bump !!!:) .
 

Jstrong20

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Good read! Insulin is so underated IMO.
 

Bone

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Be careful though Dave. I hope you read alot about it. It can be dangerous if not properly used. Oh yeah WB man ;)

Peace

Bone
 

BigPoppaThrilla

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thanks bro for your concern,
i have been reading about it, i will start at 3 iu and work my way up to 1o iu post workout:}
by the way what is wb?
 

Hal

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BigPoppaThrilla, keep some glucose tabs around if you're gonna take insulin. It's not that hard to drop into a coma or kill yourself with it. Be careful!
 

semmer

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Yeah, make sure you're well read on it, I got great results from it and using it post cycle to help maintain gains. My personal recommendation would be to shoot in the morning after a workout, I felt safer that way and was able to modify carbs to the minimum to keep the fat gain down without worrying about falling asleep at home. You can get really tired quickly on it, so watch out.
 

ironviking

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alright here is a question:

how can a diabetic tailor his insulin regimine to better suit his bodybuilding goals

I've researched this for quite some time and I still cant find a decent answer. Any help from the dark side would be appreciated.
 

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