The Role of Insulin

  • Insulin is a very small protein, technically known as a peptide.
  •  The roles of insulin are many and diverse. It is the primary regulator of fat, carbohydrate, and protein metabolism; it regulates the synthesis of a molecule called glycogen, the form in which glucose is stored in muscle tissue and the liver; it stimulat es the synthesis and storage of fats in fat depots and in the liver, and it inhibits the release of that fat.
  •         Insulin also stimulates the synthesis of proteins and of molecules involved in the function, repair, and growth of cells, and even of RNA and DNA molecules, as well. Insulin, in short, is the one hormone that serves to coordinate and regulate everything having to do with the storage and use of nutrients and thus the maintenance of homeostasis and, in a word, life. It’s all these aspects of homeostatic regulatory systems—in particular, carbohydrate and fat metabolism, and kidney and liver functions—that are malfunctioning in the cluster of metabolic abnormalities associated with metabolic syndrome and with the chronic diseases of civilization.
  •         The more carbs consumed, the more insulin is needed to transport the glucose from the carbs to the cells where it can be used as fuel.  This insulin however, also prompts the liver to synthesise and secrete triglycerides for storage as fat.
  •         Attempts to understand “abnormal metabolic patterns” common to obesity, diabetes, and heart disease. High triglycerides characterized these abnormalities, Albrink said. She proposed that these patterns were caused or exacerbated in susceptible individuals by diets high in either calories or carbohydrates or just “purified carbohydrates.” But she offered no biological mechanism to explain it. The potential explanation arrived in the form of two insulin-related conditions, insulin resistance and chronically elevated levels of insulin in the circulation, hyperinsulinemia—a vitally important focus of our inquiry.
  •         The impact on diabetes research had been immediate. Yalow and Berson showed that those who had developed diabetes as adults had levels of circulating insulin significantly higher than those of healthy individuals—a surprising finding.
  •         The crucial factor, is that, the more carbohydrates consumed, the more insulin is needed to transport the glucose from the carbohydrates into cells where it can be used as fuel. This insulin, however, also prompts the liver to synthesize and secrete triglycerides for storage in the fat tissue.
  •         Researchers have demonstrated that insulin seemed to have a dramatic effect on hunger, that insulin was the primary regulator of fat deposition in the adipose tissue, and that obese patients had chronically high levels of insulin.
  •         The insulin forces the accumulation of fat in the fat tissue, and the animal overeats to compensate.
  •         Elevating insulin even slightly will increase the accumulation of fat in the cells. The longer insulin remains elevated, the longer the fat cells will accumulate fat, and the longer they’ll go without releasing it.
  •         By the mid-1960s, four facts had been established beyond reasonable doubt: (1) carbohydrates are singularly responsible for prompting insulin secretion; (2) insulin is singularly responsible for inducing fat accumulation; (3) dietary carbohydrates are required for excess fat accumulation; and (4) both Type 2 diabetics and the obese have abnormally elevated levels of circulating insulin and a “greatly exaggerated” insulin response to carbohydrates in the diet, as was first described in 1961 by the Johns Hopkins University endocrinologists David Rabinowitz and Kenneth Zierler.
  •         As a result, when insulin is secreted, fat is deposited in the fat tissue, and the muscles have to burn glucose for energy. When insulin levels drop, the LPL activity on the fat cells decreases and the LPL activity on the muscle cells increases—the fat cells release fatty acids, and the muscle cells take them up and burn them.
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