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Pancreas Hormones Insulin and Glucogen Two Important Factors in Fat,Muscle, Energy, and Metabolism. Deeper Understanding for Advanced Bodybuilding Advantages!

Feb 04, 2018 - 12:12 PM - by Presser
Hormones of the pancreas


The vertebrate pancreas contains, in addition to the zymogen cells that secrete digestive enzymes, groups of endocrine cells called the islets of Langerhans. Certain of these cells (the B, or beta, cells) secrete the hormone insulin, inadequate production of which is responsible for the condition called diabetes mellitus. Insulin and the characteristic B cells are present in gnathostomes and in agnathans; in the latter, however, the islet cells are not associated with zymogen cells to form a typical pancreas. Insulin is, as mentioned earlier, a polypeptide molecule composed of two chains of amino acids, an A chain of 21 amino acids containing an intrachain disulfide linkage (−S−S−) and a B chain of 30 amino acids. The two chains are linked by two other disulfide linkages, the destruction of which destroys the activity of the molecule. It is thought that the molecule first appears in the B cell as the single-chain compound proinsulin, which is disrupted by an enzyme-catalyzed reaction to form the two chains of the active hormone. As with other polypeptide hormones, extensive variation in amino acid composition of the molecule occurs among different species, with the differences tending to be greater between the more widely separated species—e.g., between fish and mammal. The variations in amino acid composition have little effect on the biological activity of the molecules but certainly influence their immunological reactions; this suggests that the two properties depend on the amino acid sequences at different parts of the molecule.

Injection of insulin lowers blood sugar (glucose) levels, but this so-called hypoglycemic effect is only one expression of the wide-ranging influence of insulin on storage and mobilization of energy, in which the target tissues of primary importance are muscle, adipose (fat) tissue, and liver. The actions of insulin on these tissues are varied. First, it promotes the use of the sugar glucose as an energy source; at the same time, it encourages the storage of excess carbohydrate as glycogen, the storage carbohydrate of animals. Second, insulin reduces the use of fat as an energy source and promotes its storage. Third, it reduces the use of protein as an energy source and promotes the formation of proteins from amino acids.
Insulin probably acts on carbohydrate metabolism in muscle by increasing the ability of glucose to pass through the muscle cell membranes. This effect depends on a specific interaction between the cell membrane and the hormone; although the same effect occurs in adipose (fat) tissue, it does not occur either in the liver or in the central nervous system, despite the latter’s complete dependence upon glucose for its energy supply. After the entry of glucose into a muscle cell, phosphate is added to the molecule, and two compounds form in succession, first glucose-6-phosphate, then glucose-1-phosphate; after these reactions, the metabolism of glucose is probably aided by two secondary actions of insulin. The hormone stimulates the synthesis of an enzyme (glycogen synthetase), thus promoting the transformation of glucose-1-phosphate into glycogen; it also aids in the breakdown of glucose, thus providing energy to the cell. All of these effects contribute to the hypoglycemic (blood glucose-lowering) action of the hormone. Insulin has other effects on muscle cells: it slows the breakdown of fat and increases the formation of proteins from amino acids. Insulin affects carbohydrate and protein metabolism in adipose tissue much as it does in muscle and also promotes storage of fat.
The action of insulin in liver differs from that in muscle in that it has no direct influence upon the transport of glucose into liver cells; probably, however, insulin promotes the metabolism of glucose within liver cells in much the same way that it does in those of muscle, resulting in increased uptake of glucose from the bloodstream. In addition, insulin decreases gluconeogenesis (the formation of glucose in the liver from amino acids and other noncarbohydrate sources). These various effects cause a decrease in the level of blood glucose. Other actions of the hormone upon the liver include, as in adipose tissue, increases in fat deposition and protein synthesis.
The diverse effects of insulin apparently are adaptively linked to regulating the storage and release of energy, but it is difficult to judge whether or not all of the effects result from a single mode of action of the hormone. The interaction of insulin with the muscle-cell membrane suggests that all of its effects might be produced by similar interactions between it and membranes within cells. The mechanism, however, has not yet been established with certainty.
The B cells of the islets of Langerhans respond directly through negative feedback to the level of glucose in the blood that reaches them; i.e., an increase in blood glucose above the normal level (80 to 100 milligrams per 100 millilitres in humans) brings about increased synthesis and release of insulin with the result that the level of blood glucose falls. As a consequence, the rate of insulin output then decreases. This, however, is only part of the complex hormonal mechanism that regulates carbohydrate metabolism. Another factor is the hormone glucagon, which is secreted in the islets of Langerhans by a second cell type, the A (alpha, or A2) cells.


Glucagon, which is present in gnathostomes but absent from agnathans, is a polypeptide molecule consisting of 29 amino acids. It strongly opposes the action of insulin, primarily through a hyperglycemic (blood glucose-raising) effect that results from its promotion of the breakdown of glycogen (glycogenolysis) in the liver, a process that results in the formation of glucose. Glucagon exerts its action by increasing the availability of the enzyme required for the reaction by which glucose units are released from the glycogen molecule. It also reduces the rate of synthesis of glycogen, promotes the breakdown of protein, promotes the use of fat as an energy source, and evokes increased glucose uptake by muscle cells. The last effect, however, may be a consequence of hyperglycemia induced by the increased secretion of insulin.
Another form of glucagon, called gastrointestinal glucagon, is secreted into the blood when glucose is ingested. Its only action appears to be to stimulate insulin secretion, an effect that may provide information to the islet cells of the pancreas about the entry of glucose into the bloodstream. It is also possible that pancreatic glucagon, which is secreted in the islets by the A cells, may directly stimulate the release of insulin from the adjacent B cells without actually entering the bloodstream.
A number of other hormones also influence the release of insulin, mainly through their own actions upon blood sugar levels. For example, growth hormone, thyroxine, epinephrine, and cortisol may increase insulin release because they can promote a rise in blood sugar through effects on carbohydrate metabolism. Growth hormone and cortisol may also act directly on the B cells.

The complexity and delicacy of the control of metabolism by insulin and other hormones in mammals illustrate again the importance of homeostasis, the control of which may not be as well organized in the lower vertebrates. Some of the responses in mammals, however, do occur in lower forms; for example, removal of pancreatic islet tissue from fishes produces hyperglycemia. Thyroxine induces hyperglycemia in amphibians, and corticosteroids promote gluconeogenesis in them. Far more information is needed, however, before the evolution of these remarkable regulating mechanisms can be determined.

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The Principal Consequence of Growth Hormone is Insulin-like Growth Factor I (IGF-I), aka Somatomedin C

Feb 04, 2018 - 12:03 PM - by Presser
The Dominant Effector of Growth Hormone is Insulin-like Growth Factor I (IGF-1). Now where Bodybuilding and Development is concerned, it is this IGF-1 that exerts the greatest influence on muscle tissue cell proliferation or to put it into layman’s terms........BUILDING MUSCLE!

Insulin-like Growth Factor I (IGF-I), also known as Somatomedin C, is the Prevailing Response of Growth Hormone (GH) and is structurally homologous to Proinsulin. What is Proinsulin you ask, and the answer is intuitively simple in that Pro-Insulin is a substance produced in/and by the pancreas that is converted to Insulin.

Proinsulin is what your body needs in order to turn food into energy.

Human IGF-I is synthesized as two precursor isoforms with N- and alternative C‑terminal propeptides. These isoforms are differentially expressed by various tissues. The 7.6 kDa mature IGF‑I is identical between isoforms and is generated by proteolytic removal of the N- and C-terminal regions. Mature human IGF-I shares 94% and 96% amino acid (aa) sequence identity with the mouse and rat orthologs, respectively.

Growth Hormone (G.H.) stimulates the production of IGF-1 in the majority of tissues. Hepatocytes produce circulating IGF-I, while local IGF-I is produced by many other tissues in which it has paracrine effects.

  • IGF-I induces the proliferation, migration, and differentiation of a wide variety of cell types during development and postnatally.
  • IGF-I regulates glucose, fatty acid, and protein metabolism, steroid hormone activity, and cartilage and bone metabolism .
  • IGF-I plays an important role in muscle regeneration progression.
  • IGF-I binds IGF-I R, IGF-II R, and the Insulin Receptor, although its effects are mediated primarily by IGF-I R .
  • IGF-I also binds with strong affinity to IGF binding proteins (IGFBPs), which regulate the availability and biological activities of IGF-I.

Long R3 IGF-I (LR3 IGF-I) is a 9.2 kDa synthetic analog of IGF-I that is generated by modifying the aa sequence for mature human IGF-I.

These modifications include the substitution of an Arg for Glu at position 3 of the mature IGF-1 sequence and the addition of a thirteen aa N-terminal extension, which is derived from methionyl porcine Growth Hormone.

These aa changes generate a protein that is still capable of binding to IGF-I and Insulin receptors, but shows considerably lower affinity binding to IGFBPs compared to wild-type IGF-I.

As a result, LR3 IGF-I has an increased half-life and displays increased biological potency compared to IGF-I.

  • Oh Now I Know:

    1. Arg being Arginine (when referenced in differences between IGF-1 & IGF-1 LongR3)
    2. Glu being Glutamic acid ( (when referenced in differences between IGF-1 & IGF-1 LongR3)
    3. Growth Hormone can be thought of as a Precursor to IGF-1, and IGF-1 LongR3.

  • Proper Name:
    Insulin-like Growth Factor I

  • Gene Identifications:
    3479 (Human); 16000 (Mouse); 24482 (Rat)

  • Alternate Names:
    IBP1; IGF1; IGF-1; IGF1A; IGFI; IGF-I; IGF-IA; IGF-IB; insulin-like growth factor 1 (somatomedin C); insulin-like growth factor 1; insulin-like growth factor I; insulin-like growth factor IA; insulin-like growth factor IB; Mechano growth factor; MGF; Somatomedin A; Somatomedin C; somatomedin-C

Peptide Sciences or MuscleChemistry Abbreviation Guide Can Be Found Below When Referencing Amino Acid Sequences. Know How You Grow! Amino Acid BodyBuilding Blocks .

Amino Acids

[COLOR=rgba(0, 0, 0, 0.792157)]

Proteinogenic Amino Acids
Ala Alanine A
Arg Arginine R
Asn Asparagine N
Asp Aspartic acid D
Asx Asn or Asp
Cys Cysteine C
Gln Glutamine Q
Glu Glutamic acid E
Glx Gln or Glu
Gly Glycine G
His Histidine H
Ile Isoleucine I
Leu Leucine L
Lys Lysine K
Met Methionine M
Phe Phenylalanine F
Pro Proline P
Ser Serine S
Thr Threonine T
Trp Tryptophan W
Tyr Tyrosine Y
Val Valine V
  0 Replies | 168 Views

Which Synthetek product do you want for FREE? MuscleChemistry Sponsor Offer!

Jan 11, 2018 - 6:56 PM - by Presser

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Powder Conversion Instructions

Jun 15, 2004 - 4:22 AM - by Flexmaster
Most of these recipes can be done with less than the recommended amounts of ba and bb, but you will need to change the amount of oil in the recipe if you do. Use the powder converter sticky to find the appropriate amounts.

Test Enanthate 5 gram conversion

5... [Read More]
  93 Replies | 80,511 Views

Clomid therapy and detection times for you guys Read!

Jun 24, 2004 - 7:40 PM - by strider
here ya go guys I pulled this up for ya, should asnwer most questions as to when to start clomid and such and how long it stays active and detection times.

Detection times for AAS

Anavar 3 weeks
Anadrol 2 months
Andriol 1 week
Clenbuterol 4-5 Days
Deca Durabolin (Nandrolone Decanoate) 18 months
Dianabol 5 weeks
Durabolin... [Read More]
  22 Replies | 40,681 Views

Understanding IGF-1

Oct 29, 2004 - 2:22 PM - by Cordoba
Understanding IGF-1
By Bryan Haycock

To understand how IGF-1 works you have to understand how muscles grow. The ability of muscle tissue to constantly regenerate in response to activity makes it unique. It’s ability to respond to physical/mechanical stimuli depends greatly on what are called satellite cells. Satellite cells are muscle precursor cells. You might think... [Read More]
  55 Replies | 30,375 Views

Oral Liquid Recipes

May 02, 2005 - 5:03 AM - by Bignick
For each hormone I listed ingredients needed. For the procedure scroll down.

Highest concentration made - 50mg/ml
Per 1 gram of Oxymetholone you will need:
8.4 ml's of PEG 300
10.5 ml's 190 Proof Grain Alcohol

Highest concentration made - 20mg/ml
Per 1 gram of Oxandrolone powder you will need:
... [Read More]
  95 Replies | 72,363 Views

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