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Инсулин Инсулина е хормон, който се синтезира в панкреаса, орган намиращ се зад стомаха. Панкреаса съдържа групирани клетки, които се наричат островчета. Бета клетките вътре в островчетата правят инсулина и го освобождават в кръвта. Инсулина има огромно роля в метаболизма – начина, по който тялото използва храната за енергия. Трака подпомагащ храносмилането пречупва въглехидратите – захар и скурбялата, която се намира в много храни в глюкоза. Глюкозата е вид захар, която навлиза в кръвта. С помощта на инсулина, клетките успяват да абсорбират глюкозата и да я използват за енергия. Ролята на инсулина с повишаването на кръвната захар. Когато кръвната захар се повиши след хранене, панкреаса освобождава инсулин в кръвта. Инсулина и глюкозата пътуват в кръвта до клетките в тялото. - Инсулина помага на мускулите, мазнините и черния дроб да абсорбират глюкозата от кръвта, понижавайки кръвната захар. - Инсулина стимулира черния дроб и мускулната тъкан да складира глюкоза. Съхраненият вид глюкоза се нарича гликоген. - Инсулина също намалява кръвната захар като намалява продукцията на глюкоза в черния дроб. В здравия човек, тези функции свързани с кръвната захар и инсулина работят в нормални граници. Какво е инсулинова резистентност? Инсулинова резистентност е състояние, при което произведения инсулин не може да се използва ефективно от тялото. Когато хората имат инсулинова резистентност, глюкозата се натрупва в кръвта, вместо да се абсорбира от клетките. Това води до диабет от тип 2. Повечето хора с инсулинова резистентност не знаят, че го притежават от много години, докато не открият, че имат диабет от тип 2. Добрата новина е, че ако хората научат по-рано, те могат да подобрят състоянието си като променят живота си. До какво води инсулиновата резистентност? Чрез инсулиновата резистентност,клетките на мускулите, мазнините и черния дроб не могат да отговорят правилно на инсулина и не могат да абсорбират глюкозата от кръвта. Като резултат, тялото се нуждае от голямо количество инсулин, за да помогне на глюкозата да влезе в клетките. Бета клетките в панкреаса се опитват да увеличат инсулина като произвеждат повече. Колкото по-дълго бета клетките са способни да произвеждат достатъчно инсулин, за да се преодолее инсулиновата резистентност нивата на кръвната захар ще са в здравословни граници. След време инсулиновата резистентност води до диабет от 2 тип, защото бета клетките се провалят с постоянното произвеждане на големи количества инсулин. Каква е причината за инсулиновата резистентност? Все още не са много ясни точните причини за това, но се смята, че голяма вреда имат излишните килограми и стреса. Излишни килограми Смята се, че затлъстяването, особено излишните мазнини в областта на талията и ханша, са причина за инсулиновата резистентност. Стрес Учените смятат, че стреса е причина, особено води до диабет от тип 2. В тялото, голяма част от глюкозата се използва от мускулите. Нормално активните мускули горят запасите си от гликоген за енергия и ги запълват с нова глюкоза, взета от кръвта. По този начин се държи кръвната захар балансирана. След тренировка, мускулите стават по чувствителни към инсулина, предпазвайки от инсулинова резистентност. Упражненията помагат на мускулите да абсорбират повече глюкоза без нуждата от инсулин. Колкото повече мускули имаш, толкова повече глюкоза ще изгаряш за енергия и ще контролираш нивата на кръвната захар. Какви са симптомите за инсулинова резистентност? Инсулиновата резистентност обикновено няма симптоми. Хората могат да го имат от няколко години без да знаят за него. Но дори и без симптоми, той вреди на вашето здраве Хората, които страдат от това могат да имат тъмни торбички по кожата, обикновено по задната част на врата. Понякога имат тъмни кръгове около техните шии. Тъмни места могат да имат и на коленете, лактите, рамена и т.н.. Какво е решението с инсулиновата резистентност? Премахването на стреса и загубата на излишни килограми подобряват чувствителността на инсулина. Стъпките, които помагат, за подобряването на състоянието са: - яжте здравословно храна и се стремете да поддържате здравословни килограми - Увеличете физическата активност - не пушете - взимайте медикаменти Здравословните навици могат да помогнат на хората да изгубят голямо количество излишни килограми и да се отърват от инсулиновата резистентност. Обикновено, хората губят килограми като избират здравословната храна, контролират порциите, ядът по-малко мазнини и увеличат физическата активност. Нормалната физическа активност предпазват от рисковете на много заболявания. Физическата активност помага на тялото да използва по-добре инсулина. Физическата активност помага също за: - сваляне на килограми - контролира кръвната захар - контролира кръвното налягане - контролира холестерола Започнете с тренировки 3 пъти седмично и се старайте да използвате по-често краката си, отколкото колата и автобусите. Хранете се правилно и здравословно, но най-вече си изградете култура за здраве. Статии, които е хубаво да прочетете: - Метаболизъм и действие - Методика за изчистване - Как да се храним, за да отслабнем - Лептин и лептинова резистентност
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Insulin resistance (IR) is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. Insulin resistance in fat cells reduces the effects of insulin and results in elevated hydrolysis of stored triglycerides in the absence of measures which either increase insulin sensitivity or which provide additional insulin. Increased mobilization of stored lipids in these cells elevates free fatty acids in the blood plasma. Insulin resistance in muscle cells reduces glucose uptake (and so local storage of glucose as glycogen), whereas insulin resistance in liver cells results in impaired glycogen synthesis and a failure to suppress glucose production. Elevated blood fatty-acid concentrations (associated with insulin resistance and diabetes mellitus Type 2), reduced muscle glucose uptake, and increased liver glucose production all contribute to elevated blood glucose concentration. High plasma levels of insulin and glucose due to insulin resistance are believed to be the origin of metabolic syndrome and type 2 diabetes, including its complications. Several associated conditions include: Insulin resistance may also be caused by the damage of liver cells having undergone a defect of insulin receptors in hepatocytes. This article is licensed under the Creative Commons Attribution-ShareAlike License. It uses material from the Wikipedia article on "Insulin resistance" All material adapted used from Wikipedia is available under the terms of the Creative Commons Attribution-ShareAlike License. Wikipedia® itself is a registered trademark of the Wikimedia Foundation, Inc. In a person with normal metabolism, insulin is released from the beta (B) cells of the Islets of Langerhans located in the pancreas after eating ("postprandial"), and it signals insulin-sensitive tissues in the body (e.g., muscle, adipose) to absorb glucose. This lowers blood glucose levels. The beta cells reduce their insulin output as blood glucose levels fall, with the result that blood glucose is maintained at approximately 5 mmol/L (mM) (90 mg/dL). In an ''insulin-resistant'' person, normal levels of insulin do not have the same effect on muscle and adipose cells, with the result that glucose levels stay higher than normal. To compensate for this, the pancreas in an insulin-resistant individual is stimulated to release more insulin. The elevated insulin levels have additional effects (see insulin) which cause further biological effects throughout the body. The most common type of insulin resistance is associated with a collection of symptoms known as metabolic syndrome. Insulin resistance can progress to full Type 2 diabetes mellitus (T2DM). This is often seen when hyperglycemia develops after a meal, when pancreatic B-cells are unable to produce sufficient insulin to maintain normal blood sugar levels (euglycemia). The inability of the B-cells to produce sufficient insulin in a condition of hyperglycemia is what characterizes the transition from insulin resistance to Type 2 diabetes mellitus. Various disease states make the body tissues more resistant to the actions of insulin. Examples include infection (mediated by the cytokine TNFa) and acidosis. Recent research is investigating the roles of adipokines (the cytokines produced by adipose tissue) in insulin resistance. Certain drugs may also be associated with insulin resistance (e.g., glucocorticoids). Insulin itself can lead to insulin resistance; every time a cell is exposed to insulin, the production of GLUT4 (type four glucose receptors) on the cell's membrane is decreased. This leads to a greater need for insulin, which again leads to fewer glucose receptors. Exercise reverses this process in muscle tissue, but if left unchecked, it can spiral into insulin resistance. Elevated blood levels of glucose — regardless of cause — leads to increased glycation of proteins with changes (only a few of which are understood in any detail) in protein function throughout the body. Insulin resistance is often found in people with visceral adiposity (i.e., a high degree of fatty tissue underneath the abdominal muscle wall - as distinct from subcutaneous adiposity or fat between the skin and the muscle wall, especially elsewhere on the body, such as hips or thighs), hypertension, hyperglycemia and dyslipidemia involving elevated triglycerides, small dense low-density lipoprotein (sdLDL) particles, and decreased HDL cholesterol levels. With respect to visceral adiposity, a great deal of evidence suggests two strong links with insulin resistance. First, unlike subcutaneous adipose tissue, visceral adipose cells produce significant amounts of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), and Interleukins-1 and -6, etc. In numerous experimental models, these proinfammatory cytokines profoundly disrupt normal insulin action in fat and muscle cells, and may be a major factor in causing the whole-body insulin resistance observed in patients with visceral adiposity. A great deal of attention into the production of proinflammatory cytokines has focused on the IKK-beta/NF-kappa-B pathway, a protein network that enhances transcription of cytokine genes. Second, visceral adiposity is related to an accumulation of fat in the liver, a condition known as nonalcoholic fatty liver disease (NAFLD). The result of NAFLD is an excessive release of free fatty acids into the bloodstream (due to increased lipolysis), and an increase in hepatic glucose production, both of which have the effect of exacerbating peripheral insulin resistance and increasing the likelihood of Type 2 diabetes mellitus. Insulin resistance is also often associated with a hypercoagulable state (impaired fibrinolysis) and increased inflammatory cytokine levels. Insulin resistance is also occasionally found in patients who use insulin. In this case, the production of antibodies against insulin leads to lower-than-expected glucose level reductions (glycemia) after a specific dose of insulin. With the development of human insulin and analogues in the 1980s and the decline in the use of animal insulins (e.g., pork, beef), this type of insulin resistance has become uncommon. Magnesium (Mg) is present in living cells and its plasma concentration is remarkably constant in healthy subjects. Plasma and intracellular Mg concentrations are tightly regulated by several factors. Among them, insulin seems to be one of the most important. In vitro and in vivo studies have demonstrated that insulin may modulate the shift of Mg from extracellular to intracellular space. Intracellular Mg concentration has also been shown to be effective in modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli. Poor intracellular Mg concentrations, as found in Type 2 diabetes mellitus and in hypertensive patients, may result in a defective tyrosine-kinase activity at the insulin receptor level and exaggerated intracellular calcium concentration. Both events are responsible for the impairment in insulin action and a worsening of insulin resistance in noninsulin-dependent diabetic and hypertensive patients. By contrast, in T2DM patients daily Mg administration, restoring a more appropriate intracellular Mg concentration, contributes to improve insulin-mediated glucose uptake. The benefits deriving- from daily Mg supplementation in T2DM patients are further supported by epidemiological studies showing that high daily Mg intake are predictive of a lower incidence of T2DM. This article is licensed under the Creative Commons Attribution-ShareAlike License. It uses material from the Wikipedia article on "Insulin resistance" All material adapted used from Wikipedia is available under the terms of the Creative Commons Attribution-ShareAlike License. Wikipedia® itself is a registered trademark of the Wikimedia Foundation, Inc. There are several levels of insulin resistence causation including diet, cellular, molecular, genetic, and disease. Grounds exist for linking insulin resistance to a high-carbohydrate diet. An American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance. Insulin resistance has also been linked to PCOS (polycystic ovary syndrome) as either causing it or being caused by it. Further studies are in progress. Other studies have also linked to the increased amounts of fructose (e.g., in HFCS — high fructose corn syrup, currently the least expensive nutritive sweetener available in industrial quantities); in humans, fructose causes changes in blood lipid profiles, among other things, mostly due to its effects on liver function. The high amounts of ordinary sucrose (i.e., table sugar) in the typical developed-world diet is also suspected of having some causative effect on the development of insulin resistance (sucrose is 1/2 fructose, which may account for the effect, if any). Insulin resistance has certainly risen in step with the increase in sugar consumption and the substantial commercial usage of HFCS since its introduction to the food trades; the effect may also be due to other parallel diet changes however. Further research may distinguish between candidate causes. At the cellular level, excessive circulating insulin appears to be a contributor to insulin resistance via down-regulation of insulin receptors. This occurs due to prolonged and repeated elevations of circulating insulin. Since the usual instances of Type 2 insulin resistance are distinct from pathological over production of insulin, this does not seem to be the typical cause of the insulin resistance leading to Type 2 diabetes mellitus, the largest clinical issue connected with insulin resistance. The presence of insulin resistance typically precedes the diagnosis of Types 2 diabetes mellitus, however, and as elevated blood glucose levels are the primary stimulus for insulin secretion and production, habitually excessive carbohydrate intake is a likely contributor. Additionally, some Type 2 cases require so much external insulin that this down-regulation contributes to total insulin resistance. Inflammation also seems to be implicated in causing insulin resistance. Mice without JNK1-signaling do not develop insulin resistance under dietary conditions that normally produce it. Vitamin D deficiency is also associated with insulin resistance. Some research has shed light on a complex interaction between elevated free fatty acids and inflammatory cytokines seen in obesity activating Protein Kinase C isoform theta. PKC Theta inhibits Insulin Receptor Substrate (IRS) activation and hence prevents glucose up-take in response to insulin. Insulin resistance has been proposed at a molecular level to be a reaction to excess nutrition by superoxide dismutase in cell mitochondria that acts as a antioxidant defense mechanism. This link seems to exist under diverse causes of insulin resistance. It is also based on the finding that insulin resistance can be rapidly reversed by exposing cells to mitochondrial uncouplers, electron transport chain inhibitors, or mitochondrial superoxide dismutase mimetics. Individual variability is a cause with an inherited component, as sharply increased rates of insulin resistance and Type 2 diabetes are found in those with close relatives who have developed Type 2 diabetes. Sub-clinical Cushing's syndrome and hypogonadism (low testosterone levels) seem to be the major insulin resistance causes . Recent research and experimentation has uncovered a non-obesity related connection to insulin resistance and Type 2 diabetes. It has long been observed that patients who have had some kinds of bariatric surgery have increased insulin sensitivity and even remission of Type 2 diabetes. It was discovered that diabetic / insulin resistant non obese rats whose proximal small intestine and duodenum has been surgically removed also experienced increased insulin sensitivity and remission of Type 2 diabetes. This suggested similar surgery in humans, and early reports in prominent medical journals (January 8) are that the same effect is seen in humans, at least the small number who have participated in the experimental surgical program. The speculation is that some substance is produced in that portion of the small intestine which signals body cells to become insulin resistant. If the producing tissue is removed, the signal ceases and body cells revert to normal insulin sensitivity. No such substance has been found as yet, so its existence remains speculation. This article is licensed under the Creative Commons Attribution-ShareAlike License. It uses material from the Wikipedia article on "Insulin resistance" All material adapted used from Wikipedia is available under the terms of the Creative Commons Attribution-ShareAlike License. Wikipedia® itself is a registered trademark of the Wikimedia Foundation, Inc. The primary treatment for insulin resistance is exercise and weight loss. Low-glycemic index or low-carbohydrate diets have also been shown to help. Both metformin and the thiazolidinediones improve insulin resistance, but are only approved therapies for type 2 diabetes, not insulin resistance, ''per se''. By contrast, growth hormone replacement therapy may be associated with increased insulin resistance. Metformin has become one of the more commonly prescribed medications for insulin resistance, and currently a newer drug, exenatide (marketed as Byetta), is being used. Exenatide has not been approved except for use in diabetics, but often improves insulin resistance by the same mechanism as it does diabetes. It also has been used to aid in weight loss for diabetics and those with insulin resistance, and is being studied for this use as well as for weight loss in people who have gained weight while on antidepressants. The ''Diabetes Prevention Program'' showed that exercise and diet were nearly twice as effective as metformin at reducing the risk of progressing to type 2 diabetes. Many people with insulin resistance currently follow the lead of some diabetics, and add cinnamon in therapeutic doses to their diet to help control blood sugar. This has the danger of increasing the risk of bleeding, since most commercial cinnamon preparations are actually from Cassia (''Cinnamomum aromaticum''), which also contains anticoagulants; whereas "true cinnamon" (''Cinnamomum zeylanicum'' or ''sp. verum'') does not. Some types of Monounsaturated fatty acids and saturated fats appear to promote insulin resistance, whereas some types of polyunsaturated fatty acids (omega-3) can increase insulin sensitivity. There are scientific studies showing that vanadium (e.g., as vanadyl sulfate) and chromium (e.g., in chromium picolinate and GTF formulations) in reasonable doses have reportedly also shown some efficacy in improving IR sensitivity, but these effects are controversial. Naturopathic approaches to insulin resistance have been advocated including supplementation of vanadium (but see preceding paragraph), bitter melon (Momordica, but reportedly dangerous if not used with care), and Gymnema sylvestre. One study found that chromium is necessary for maintaining normal glucose tolerance. Daily Mg administration, restoring an appropriate intracellular Mg concentration, contributes to improve insulin-mediated glucose uptake. High daily Mg intake are predictive of a lower incidence of NIDDM. This article is licensed under the Creative Commons Attribution-ShareAlike License. It uses material from the Wikipedia article on "Insulin resistance" All material adapted used from Wikipedia is available under the terms of the Creative Commons Attribution-ShareAlike License. Wikipedia® itself is a registered trademark of the Wikimedia Foundation, Inc.