• Insulin and Fat - Insulin forces fat cells to take in blood lipids, which are converted to triglycerides. It forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters. Insulin commands the reduction in conversion of fat cell lipid stores into blood fatty acids. The lack of insulin causes the reverse.
• Insulin and Protein - Insulin decreases the breakdown of proteins. It forces cells to absorb circulating amino acids.  The lack of insulin inhibits absorption
• Insulin and Blood Sugar -Insulin decreases the production of glucose from nonsugar substrates, primarily in the liver (the vast majority of endogenous insulin arriving at the liver never leaves the liver). The lack of insulin causes glucose production from assorted substrates in the liver and elsewhere. Insulin forces storage of glucose in liver (and muscle) cells in the form of glycogen, whereas lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood.
• Insulin and Cell Repair - Insulin decreases level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.
  
• Insulin and Electrolytes - Insulin forces cells to absorb serum potassium and lowers potassium levels in blood; lack of insulin inhibits absorption and increases potassium levels. This occurs via insulin-induced translocation of the Na+/K+-ATPase to the surface of skeletal muscle cells. Excess of insulin decreases renal sodium excretion
• Insulin and Blood Pressure - Insulin forces arterial wall muscles to relax and improves vascular compliance, increasing blood flow, especially in microarteries; lack of insulin reduces flow by allowing these muscles to contract. However, excess of  insulin retains sodium
• Insulin and Stomach Acid - Insulin increases secretion of hydrochloric acid by parietal cells in the stomach
• Insulin and Cognition - Insulin enhances learning and memory and benefits verbal memory in particular
• Insulin and Thermoregulation - Insulin enhances the acute thermoregulatory and glucoregulatory response to food intake via central nervous insulin effect of whole-body energy homeostasis

• Type 1 - autoimmune-mediated destruction of insulin-producing β-cells in the pancreas, resulting in absolute insulin deficiency. Patients with type 1 diabetes depend on external insulin for their survival because the hormone is no longer produced internally
  
  
• Type 2 - multi-factorial syndrome with combined influence of genetic susceptibility and influence of environmental factors, the best known being obesity, age, and physical inactivity, resulting in insulin resistance in cells requiring insulin for glucose absorption

Optimizing insulin metabolism is one of the ultimate goals of our treatment protocols as insulin resistance has been shown again and again to be the driving force of chronic inflammation. The latter has been implied to be the ultimate cause of increased risk of heart disease, hypertension, stroke, cancer, kidney failure, dementia, arthritis, and overall aging.