Insulin is one of the most important hormones in the body governing several critical processes such as…
Introduction to Insulin
Insulin can be fattening. It increases fat synthesis and inhibits the breakdown of fat tissue [R].
In fat tissue, insulin increases uptake of glucose, which makes fat cells bigger [R].
Insulin plays a role in suppressing liver glucose excretion [R].
Insulin is also responsible for the stimulation of protein synthesis in muscles [R].
Insulin: Weight, Fat Tissue, Triglycerides
Insulin has mixed effects with regard to weight – it reduces appetite, but can increase fat mass.
Insulin puts glucose in your liver, muscle and fat cells. (R) Insulin forces fat cells to take up blood fat (lipids) and also converts those fat to other kinds of fat (triglycerides). (R) Insulin decreases the release of fat in your fat cells, so you store more fat. (R)
In healthy men, insulin was shown to decrease levels of triglycerides and cholesterol (VLDL) [R].
It’s also protective by storing fat (higher blood fat is not good).
Insulin has been shown to be important in maintaining levels of an enzyme responsible for breaking down triglycerides in fat tissue [R].
In-vitro, insulin stimulates the creation of fat tissue through the utilization of glucose [R].
In healthy men, elevated insulin levels were associated with greater amounts of fat around the organs (visceral fat) [R]
Hyperinsulinemia may be associated with an increased risk of colon cancer (correlation versus causation is an issue here) [R].
In isolated rat liver cells insulin was shown to inhibit the release of cholesterol (VLDL) and stimulate the release of triglycerides [R].
Insulin is responsible for lowering glucose and storing it into bodily tissues such as fat, muscle, and liver [R].
Lowered levels of insulin cause liver to convert glycogen to glucose and excrete it into the blood. (R) This is one reason why many of my thin clients with low insulin also often have higher blood glucose.
Insulin also decreases the production of glucose from protein. (R)
So we see insulin can be protective in many ways by lowering blood glucose…. It does this by converting glucose to glycogen, increasing glucose uptake (in muscle, liver and fat) and decreasing glucose production from protein.
Nerves and Brain
In a literature review, insulin was shown to enter the brain through the BBB (blood brain barrier) and exert its effects via brain insulin receptors [R].
In a rat model of diabetes, insulin treatment prevented nerve conductance issues and preserved a marker for nerve health (myoinositol) [R].
Insulin is one of many factors that can stimulate nerve growth in test tubes [R].
In test tubes, insulin and the insulin growth factors promote growth of the sciatic nerve in test tubes [R].
In Alzheimer and healthy subjects, insulin was able to enhance memory [R].
However, insulin increased a marker of Alzheimers (AB42) [R].
In isolated bone creating cells (osteoblasts), insulin increased their activity in bone creation [R].
In-vitro, insulin increased the amount of a protein (collagenase-digestible protein) responsible for generating collagen in bone [R].
Insulin inhibits platelet formation via increase of a specific compound (cGMP) [R].
In pig hearts, insulin is able to increase heart muscle contractibility [R].
Insulin forces artery wall muscles to relax, thereby increasing blood flow, especially in micro arteries. A lack of insulin reduces flow. (R) In the thin people I deal with, they often feel cold. One of the many reasons is because of low insulin, which reduces blood flow.
Higher fasting insulin is associated with lower capillary density [R].
Insulin decreases the breakdown of protein from your muscle and also increases uptake of protein/amino acids – hence why bodybuilders like to spike insulin with glucose. (R)
Muscles play a very large role in the utilization and metabolism of glucose mediated by insulin [R]. Diabetics showed much less ability to utilize glucose in muscle tissue due to insulin resistance [R].
Insulin causes increased blood flow (dilation) to muscles through the nitric oxide pathway [R].
The level of triglycerides in a muscle is negatively correlated with that muscles degree of insulin sensitivity (measurement of cellular response to insulin) [R].
Insulin: decreases the protein degradation in muscles, increases protein synthesis in muscle, adipose, and liver tissue, and increases the transport of amino acids into tissues [R].
Insulin increases the secretion of hydrochloric acid by parietal cells in the stomach. (R) In my thin clients, they are more likely to have lower HCL levels. One reason is because of lower insulin.
In-vitro, insulin decreases water, potassium, and sodium secretion by the kidney [R].
In healthy individuals, insulin was able to decrease the amount of sodium secreted in the urine [R].
Insulin lowers blood potassium. It does this by forcing cells to absorb blood potassium. (R)
What Modifies Insulin Release
In a study of men and women, higher alcohol intake was associated with lower fasting insulin levels [R].
When the fiber is taken out of fruit (fruit juice) it causes a greater insulin spike [R].
In women, increased dietary fiber intake was associated with lower levels of fasting insulin [R].
- Insulin increases heparin-releasable and LPL activity [R]
- Insulin suppresses VLDL1 apo B production [R]
- Insulin inhibits CYP2E1 [R]
- Insulin increases glucokinase gene transcription [R]
- In PCOS insulin shows increased serine phosphorylation [R]
- Insulin inhibits VLDL secretion and increases triglyceride secretion [R]
- Insulin in diabetics preserves motor nerve conduction velocity [R]
- Insulin stimulated cell proliferation in septal cholinergic, pontine cholinergic, and mesencephalic dopaminergic neurons (independent of NGF) [R]
- Insulin increased Schwann cells around myelinated and unmyelinated nerves [R]
- IGF-2 stimulated motor nerve axon regeneration [R]
- Insulin increases CSF AB42 levels in healthy older adults [R]
- Insulin increases VEGF via the PI3-K, MAPK, and Nitric oxide pathway [R]
- Insulin inhibits platelet formation via activation of guanylate cyclase and subsequent production of cGMP [R]
- TNF-a inhibits insulin-stimulated tyrosine phosphorylations and insulin receptor substrate-1 at the insulin receptor [R]
- IKKB/NF-Kb activation stimulates insulin resistance [R]
- Il-6 blunts insulin’s ability to suppress liver glucose secretion and insulin-stimulated IRS-2 PI3-K activity in the liver [R]
- Il-6 inhibits muscle glucose uptake via disruption of insulin-stimulated IRS-1 PI3-K activity [R]
- IL-10 inhibited the negative effects of IL-6 on liver and muscle insulin signaling, these effects were associated with decreased levels of acyl-CoA [R]
- Insulin stimulates MCP-1 secretion [R]
- GDR (glucose disposal rate a marker for insulin resistance, lower in insulin resistant individuals) was found to be correlated with creatinine clearance, APO A-1/B, acidosis, and a negative correlation with creatinine levels [R]
- Insulin decreases secretion of sodium, potassium and water by kidney [R]
- Insulin stimulates osteocalcin release in osteoblasts which promotes glucose metabolism [R]
- Insulin stimulated the release of collagenase-digestible protein (CDP) and to a lesser extent non-collagen protein (NCP) [R]
- Leptin increased insulin sensitivity and decreased fasting insulin levels (although this did not reach significance) [R]