 
 For information on |
Insulin ResistanceBrenda Bryan RD, LDNWhat is Insulin?The first step in understanding insulin resistance is to start with the definition of insulin and expand on its function. Insulin is produced by the beta cells of the pancreas, and is considered the major anabolic hormone of the body. It is a protein that contains 51 amino acids, and plays a vital role in the metabolism of nutrients. Insulin promotes both the storage of fuels and the utilization of fuels for growth (1). Blood insulin levels rise rapidly after a high carbohydrate meal, the glucose that is absorbed into the blood causes rapid secretion of insulin. Insulin works to transport glucose into the cells. It causes rapid uptake, storage, and use of glucose by almost all tissues of the body, but especially by the muscles, adipose tissue, and liver. A number of factors other than the blood glucose concentration can modulate insulin release. The cells of the pancreas are innervated by the autonomic nervous system, including a branch of the vagus nerve, which helps to coordinate insulin release with the act of eating. However, signals from the central nervous system are not required for insulin secretion (1). Certain amino acids can also stimulate insulin secretion, although the amount of insulin released during a high protein meal is very much lower than that released by a high carbohydrate meal. A gut hormone (gastric inhibitory polypeptide) also aids in the onset of insulin release. Another hormone, epinephrine, commonly known as the fight or flight hormone, is secreted in response to fasting, stress, trauma, and vigorous exercise, and it actually decreases the release of insulin (1). Insulin increases glucose transport into and glucose usage by most cells of the body with the exception of the brain cells. The brain is quite different from most other tissues of the body in that it has such a preferential need for glucose, insulin is not required to the same extent to facilitate glucose entry into the brain cells. Therefore, insulin has either little or no effect on uptake or use of glucose. Instead, the brain cells are permeable to glucose without the intermediation of insulin (2). Though not quite as visible as the acute effects of insulin on carbohydrate metabolism, insulin also affects fat metabolism in ways that, in the long run, are equally as important. Insulin has several different effects that lead to fat storage in adipose tissue. Insulin increases the utilization of glucose by most of the body's tissues, which automatically decreases the utilization of fat, therefore functioning as a "fat sparer." However, insulin also promotes fat synthesis or production (2). During the few hours following a meal when excess quantities of nutrients are available in the circulating blood, not only are carbohydrates and fats stored in the tissues, but proteins are as well. Insulin is required for this to occur. The manner in which insulin causes protein storage is not as well understood as the mechanisms for both glucose and fat storage. In summary, insulin promotes protein formation and also prevents the degradation of proteins. Conversely, virtually all protein storage comes to a complete halt when insulin is not available (1). Insulin ResistanceInsulin resistance is the subnormal insulin action on glucose uptake (3). Under normal conditions, the digestive and insulin secreting processes run smoothly, and blood sugar concentrations are maintained within a narrow range while efficiently regulating one's energy needs and usage. In order to keep the processes going, the pancreas must secrete insulin quickly when it is demanded, and the muscle, fat, and liver cells must respond to the insulin (2). Simple feedback loops constantly fine-tune the operation. Food is ingested, a portion of this food is converted into blood sugar, and more insulin is released. Both the quantity and food composition determine the amount of insulin that must be released. Consequently, when there is less blood sugar circulating, less insulin is needed. When everything is working like clockwork, there is always adequate insulin to handle the sugar in the blood, and the body does an excellent job keeping everything nicely balanced. As long as the pancreas has the ability to continually pump out the insulin, everything works efficiently (2). Problems occur when the muscle, fat, and liver cells do not respond appropriately and promptly to the insulin. Insulin signals certain cells to open their doors to blood sugar by attaching to receptors on the cell surface. When the amount of insulin being produced is not enough to unlock or open the doors to certain body cells, they no longer respond to insulin's command to let blood sugar into the cell. As a compensatory mechanism, the pancreas produces additional insulin in an attempt to overcome this obstacle; this results in extra amounts of insulin, which results in hyperinsulinemia (4). Insulin resistance appears to be a defect in the manner in which individual cells process glucose (1). Decreased sensitivity of skeletal muscle to insulin appears to be the first manifestation of insulin resistance. As insulin resistance intensifies, an abnormality in insulin production arises. As the pancreas overcompensates by making more insulin than required, it may soon exhaust itself (5). There is a strong genetic tendency to insulin resistance. Looking at one's ancestry to determine the familial link to insulin resistance is complicated by the fact that insulin resistance is controlled by more than one gene. Although, several forms of insulin resistance have been linked to a single gene alteration. The genetic link is even further complicated by environmental factors such as obesity. One's fat distribution and muscle mass as well, have independent effects on insulin sensitivity (5). Part IIThe article will be continued discussing: the impact of insulin resistance on the PCOS patient, laboratory tests used for measuring insulin resistance, and future health implications for the PCOS patient. References
|
© 2000-2007
|
|
