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Insulin

Insulin is a hormone that increases when blood glucose rises, and acts to reduce blood glucose by putting it into cells and increasing its usage. It temporarily shifts energy metabolism from fats to carbs, and does not inherently make somebody fat. Its potency is seen as Insulin Sensitivity.

Our evidence-based analysis on insulin features 106 unique references to scientific papers.

Kamal Patel
Research analysis led by Kamal Patel .
Reviewed by
Examine.com Team
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Summary of Insulin

Primary Information, Benefits, Effects, and Important Facts

Insulin is a hormone in the body secreted from the Pancreas, and is known as the Master regulator of carbohydrate metabolism. It works in concert with its sister hormone, Glucagon, and a host of other hormones to regulate blood sugar levels in the body and protect from an excess of blood sugar (hyperglycemia) or too low a level of blood sugar (hypoglycemia).

It is mostly an anabolic hormone, meaning it acts to build molecules and tissues. It has some catabolic properties though (catabolis as in acting to destroy molecules and tissues to provide energy).

When active, insulin and the actions of the proteins under its control can be summed up with having two main actions:

  • Causing a flux of nutrients into the liver, fat, and muscle; to get said nutrients out of the blood

  • Causing a metabolic shift towards carbohydrates, favoring them as fuel, and thus minimizing usage of both fats and proteins for energy

It is increased in response to the diet. Most notably carbohydrates and the a lesser extent proteins. In contrast to many hormones, Insulin is one that is highly responsive to diet and lifestyle; manipulating insulin levels through one's diet and lifestyle is common in diet strategies.

It is essential to survival, and those who do not produce any or insufficient levels of insulin must inject it otherwise (Type I Diabetics).

Insulin has a phenomena known as 'Insulin Sensitivity' which can be summed up as 'The amount of action a single molecule of insulin can exert inside a cell'. The more insulin sensitivity you have, the less overall insulin you need to exert the same effect. A large scale and prolonged state of insulin insensitivity is what is known as Type II diabetes (among other co-morbidities).

Insulin is neither bad nor good from a health and body composition perspective. It has certain roles in the body and activating it may or may not be beneficial for particular individuals, but may also be wondrous for others. Typically sedentary obese persons would be wise to limit insulin secretion while power athletes or relatively lean athletic individuals would be wise to use carbohydrate timing strategies to maximize the effects of insulin.

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Frequently Asked Questions about Insulin

Low-fat vs low-carb? Major study concludes: it doesn’t matter for weight loss
A year-long randomized clinical trial (DIETFITS) has found that a low-fat diet and a low-carb diet produced similar weight loss and improvements in metabolic health markers. Furthermore, insulin production and tested genes had no impact on predicting weight loss success or failure. Thus, evidence to date indicates you should choose your diet based on personal preferences, health goals, and sustainability.
Read full answer to "Low-fat vs low-carb? Major study concludes: it doesn’t matter for weight loss"
How do I increase insulin sensitivity?
Exercise frequently (resistance training and aerobic training are both beneficial), eat better (in this regard, less processed carbohydrates and more vegetables), and lose weight. Supplements can help, but are better when the diet and exercise are in order
Read full answer to "How do I increase insulin sensitivity?"
Does dairy cause acne?
Growth factors can cause acne, either androgens or anything acting on the insulin receptor (including IGF-1) that enhance androgen signaling. Dairy is currently weakly suspected to contribute via the above, but not enough evidence exists to support a strong relationship.
Read full answer to "Does dairy cause acne?"
How are carbohydrates converted into fat deposits?
Read full answer to "How are carbohydrates converted into fat deposits?"
Do artificial sweeteners spike insulin?
Read full answer to "Do artificial sweeteners spike insulin?"

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Human Effect Matrix

The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what supplements affect insulin
Grade Level of Evidence
Robust research conducted with repeated double-blind clinical trials
Multiple studies where at least two are double-blind and placebo controlled
Single double-blind study or multiple cohort studies
Uncontrolled or observational studies only
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Outcome Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
Notes
grade-a
Chromium
- Moderate See all 19 studies
Somewhat similar to the influence on insulin sensitivity, the reductions in fasting insulin concentrations in diabetics appear to exist in some studies but are highly unreliable.
grade-b
Ketogenic diet
Notable High See all 21 studies
While not necessarily more potent than all control diets, studies have generally found a notably larger reduction in fasting insulin, independently of weight loss. The average insulin levels throughout the day tend to be lower on a ketogenic diet as well.
grade-b
Salacia reticulata
Notable Very High See all 3 studies
A decrease in postprandial insulin has been noted with acute supplementation, which is thought to be secondary to the reduction in glucose absorption (as the two correlate highly). There are currently no studies assessing long term changes in fasting insulin

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Research Breakdown on Insulin

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1Background information on the Hormone

1.1Structure

mRNA encodes for a polypeptide chain known as Preproinsulin, which then passively folds into, via amino acid affinity, Insulin.[1]

Insulin is a peptide hormone (hormone made from amino acids) that is composed of two chains, an alpha chain 21 amino acids in length and a beta chain 30 amino acids in length.[2][1] It is connected by sulfide bridges between chains (A7-B7, A20-B19) and in the alpha chain (A6-A11)[1], which give it a hydrophobic core.[3] 

This tertiary protein structure can exist by itself as a monomer[4], together with another as a dimer[5], and as a hexamer.[6]

These forms of insulin are metabolically inert[7] and become active when conformational (structural) changes occur when binding to the insulin receptor.[1]

1.2Roles in the Body

1.3In vivo synthesis, degradation, and regulation

Insulin is synthesized in the Pancreas, in a subset of the Pancreas[8] known as the 'Islets of Langerhans' exists beta-cells which are the sole producers of insulin.[9]

Insulin, after its synthesis, is released into the blood.

Once done its job, it is degraded by Insulin Degrading Enzyme (Insulysin)[10], which is ubiquitously expressed[11] and declines with age[12].

2The insulin receptor signalling cascade

For simplicity, select intermediates that hold a critical spot in the signalling cascade have been bolded.

Insulin stimulation works via insulin acting on the outer side of the insulin receptor (which is embedded in the cell membrane, exposed to both the outside and inside), and causing structural (Conformational) changes that induce a tyrosine kinase on the inside portion of the receptor, and multiple phosphorylations.[13] The compounds that are directly phosphorylated by the inside portion of the insulin receptor include the four denoted substrates (Insulin Receptor Substrate, IRS, 1-4) as well as some other proteins known as Gab1, Shc, Cbl, APD, and SIRPs.[13] Phosphorylation of these intermediates causes structural changes to them that start the post-receptor signalling cascade.

PI3K (activated through the IRS1-4 intermediate) is sometimes seen as the main second tier intermediate[14] and acts through phosphoinositides to activate an intermediate known as Akt, which has its activity highly correlated with GLUT4 translocation.[15] Inhibition of PI3k by wortmannin completely abolishes insulin-mediated glucose uptake, suggesting the criticality of this pathway.[16]

GLUT4 translocation (the ability to take sugars into a cell) seems to be co-dependent on both PI3K activation (as stated above) as well as a CAP/Cbl cascade.[17][18] Activation of PI3K in vitro is not sufficient to explain all of insulin-mediated glucose uptake.[19][20] Activation of the primary intermediate APS recruits both CAP and c-Cbl to the insulin receptor where the form a dimer complex (bind together)[21][22] and then travel via lipid rafts[23] to GLUT4 vesicles, and via a GTP binding protein facilitate their movement to the cell surface.[24]

For a visual representation of the above, please refer to the KEGG metabolic pathway for insulin.

3Effects on Carbohydrate Metabolism

Insulin is the main metabolic regulator of blood glucose (also known as blood sugar) levels. It acts in concert with its sister hormone Glucagon to balance blood glucose levels in the body. Insulin has both roles that increase and decrease glucose levels in the blood, namely by increasing synthesis of glucose and increasing deposition of glucose into cells; both anabolic (tissue-building) reactions which are generally in opposition to glucagons catabolic (tissue-destroying) actions.

3.1Regulation of Glucose synthesis and degradation

Glucose can be generated from non-glucose sources in the liver and kidneys.[25] The kidneys tend to resorb approximately as much glucose as they synthesis however, indicating that they may be self-sustaining. This is the reason why the liver is seen as the main centre for gluconeogenesis (gluco = glucose, neo = new, genesis = create; to create new glucose).[26]

Insulin is secreted from the pancreas, and does so in response to when beta-cells detect rising glucose levels in the blood.[27] There are also neural sensors which can work vicariously through the pancreas.[28][29] When sugar in the blood rises, insulin (and other factors) mediate a systemic (whole-body) flux of glucose out of the blood and into the liver and other tissues (such as fat and muscle). Sugar can flux into and out of the liver via GLUT2, and is fairly independent of hormonal regulation[30] although some exists in the gut GLUT2.[31] In particular, the sensation of sweetness can upregulate GLUT2 activity in the gut.[32] The flux of glucose into the liver hinders creation of more glucose, and begins to favor production of glycogen via hepatic glycogenesis (glyco = glycogen, genesis = create; to create glycogen).[33][34]

3.2Glucose Uptake into cells

Insulin acts to deliver glucose from the blood into muscle and fat cells via the transport known as GLUT4.[35] There are 6 GLUTs in the body (1-7, in which 6 is a pseudogene) but GLUT4 is the most commonly expressed and significant for muscle and fat tissue[35][13] and GLUT5 responding to fructose.[36]

GLUT4 is not a surface transport, but is contained in small vesicles inside the cell.[37] These vesicles can be moved to the surface of the cell (cytoplasmic membrane) by either insulin stimulation[38] of its receptor or by calcium release from the sarcoplasmic reticulum (muscle contraction).[39]

As mentioned earlier, a synergy of PI3K activation (via insulin signalling) and CAP/Cbl signalling (partially via insulin) is required for effective GLUT4 mobilization and uptake of glucose into fat and muscle cells (where GLUT4 is most commonly expressed).

4Effects on Fat Metabolism

5Effects on Protein Metabolism

6Insulin Sensitivity and Resistance

Insulin resistance is also seen in high-fat diets (typically 60% total calories or greater), which may be due to adverse interactions with the CAP/Cbl signalling cascade required for GLUT4 translocation,[40][41] as the actual insulin receptor phosphorylation is unaffected and the phosphorylation of IRS intermediates only slightly adversed affected.[42]

References

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  2. ^ Bentley G, et al. Structure of insulin in 4-zinc insulin. Nature. (1976)
  3. ^ Thermodynamics of the Hydrophobicity in Crystallization of Insulin.
  4. ^ Bocian W, et al. Structure of human insulin monomer in water/acetonitrile solution. J Biomol NMR. (2008)
  5. ^ Ganim Z, Jones KC, Tokmakoff A. Insulin dimer dissociation and unfolding revealed by amide I two-dimensional infrared spectroscopy. Phys Chem Chem Phys. (2010)
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  11. ^ Insulin-degrading enzyme is differentially expressed and developmentally regulated in various rat tissues.
  12. ^ The effect of age on insulin-degrading activity in rat tissue.
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  14. ^ Phosphoinositide 3-kinase: the key switch mechanism in insulin signalling.
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  16. ^ The Effects of Wortmannin on Rat Skeletal Muscle.
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  19. ^ The inability of phosphatidylinositol 3-kinase activation to stimulate GLUT4 translocation indicates additional signaling pathways are required for insulin-stimulated glucose uptake.
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This page features 106 references. All factual claims are followed by specifically-applicable references. Click here to see the full set of research information and references for Insulin.

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