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Insulin is a hormone produced by beta cells of the pancreas. These cells are scattered throughout the pancreas in small clusters known as islets of Langerhans. Insulin produced is released into the blood stream and travels throughout the body. Insulin is an essential hormone that has many actions within the body. Most actions of Insulin are direct to metabolism of carbohydrates, lipids, and proteins. Insulin also regulates the functions of the body's cells, including their growth. Insulin is critical for the body's use of glucose as energy. Insulin Resistance is a condition in which the body's cells become resistant to the effects of Insulin. That is, normal response to the amount of Insulin is reduce. As a result, higher levels of Insulin are needed in order for Insulin to have its proper effects, and the pancreas compensates by trying to produce more Insulin. This resistance occurs in response to the body's own Insulin or when Insulin is administered by injection. With Insulin Resistance, pancreas produces more and more Insulin until the pancreas can no longer produce sufficient Insulin for the body's demands, and then blood sugar rises. Insulin resistance is a risk factor for development of Diabetes and heart disease. Type 2 Diabetes mellitus is a type of Diabetes that occurs later in life or with Obesity at any age. Insulin Resistance precedes development of Type 2 Diabetes, sometimes by years. In individuals who will ultimately develop Type 2 Diabetes, research shows that blood glucose and Insulin levels are normal for many years, until at some point in time, Insulin Resistance develop. High insulin levels are often associated with central Obesity, cholesterol abnormalities, and / or high blood pressure. When these disease processes occur together, it is called metabolic Syndrome. One action of Insulin is to cause the body's cells to remove and use glucose from blood. This is one way by which Insulin controls the level of glucose in the blood. Insulin has this effect on cells by binding to Insulin receptors on the surface of cells. You can think of it as Insulin knocking on doors of muscle and fat cells. Cells hear knock, open up, and let glucose in to be used with Insulin Resistance, muscles don't hear knock. So the pancreas is notified it needs to make more insulin, which increases the level of Insulin in the blood and causes louder knock. Resistance of cells continues to increase over time. As long as the pancreas is able to produce enough Insulin to overcome this resistance, blood glucose levels remain normal. When the pancreas can no longer produce enough Insulin, blood glucose levels begin to rise. Initially, this happens after meals - when glucose levels are at their highest and more insulin is needed eventually while fasting too. When blood sugar rises abnormally above certain levels, Type 2 Diabetes is present.
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You can't tell that you have Insulin resistance by how you feel. You 'll need to get a blood test that checks your blood sugar levels. Likewise, you wonat know if you have most of the other conditions that are part of Insulin resistance syndrome without seeing your doctor. The waistline over 40 inches in men and 35 inches in women. Blood pressure readings of 130 / 80 or higher fasting glucose level over 100 mg / dL fasting triglyceride level over 150 mg / dL HDL cholesterol level over under 40 mg / dL in men and 50 mg / dL in women Skin tags Patches of dark, velvety skin call acanthosis nigricans
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Evaluate patients for comorbid conditions; this is generally feasible on an outpatient basis. Admission for laboratory studies and treatment of acute complications may be warranted for patients whose conditions require urgent or emergent intervention. Metabolic syndrome requires aggressive control of cardiovascular and metabolic risk factors. Tailor therapy for optimal benefits. Weight reduction improves Insulin sensitivity in cases of Obesity and in most Obesity - related Insulin - resistant states. Restriction of caloric intake is indicate. Dietary indiscretion, such as consumption of diet high in cholesterol and sodium, should be avoid. Alcohol use should be limit. Smoking cessation is indicate. Patiends should avoid physical inactivity. Exercise improves Insulin sensitivity via following: in patients with Insulin Resistance, diligent monitoring of metabolic profile, general status, medications, and side effects is indicate. Transfer may be indicated for diagnostic evaluation and for treatment of major primary conditions and complications. Consultation with an endocrinologist indicates Insulin Resistance. Referral to a medical weight management program is usually needed. Consultation with a cardiologist is also usually indicate. Other specialists, such as dermatologist, gynecologist, cardiothoracic surgeon, and ophthalmologist, may need to be consulted based on the nature of the disease and prevailing pathology.
At a symposium on Insulin Resistance, Hypertension, and cardiovascular disease cosponsored by the European Group for Research of Obesity, Hypertension, and Insulin Resistance, Albert P. Rocchini discussed the relationship of Hypertension and Insulin Resistance in Obesity. Potential explanations for the frequency with which Insulin Resistance and Hypertension are associated could be the coincidence of two common abnormalities, causation of one by other, or, intriguingly, existence of common underlying factor. The first explanation appears unlikely, with the preponderance of evidence suggesting that two conditions are relate. It also appears unlikely that Hypertension causes Insulin Resistance, as glucose uptake is not affected in experimental renovascular Hypertension and because lowering blood pressure in individuals with Hypertension does not necessarily improve glucose uptake. There is, however, greater forearm vascular resistance in obese than in nonobese adolescents, with glucose uptake across this tissue inversely related to vascular resistance, suggesting that vascular resistance may play a role in some aspects of Insulin action. Converse, that Insulin Resistance may cause Hypertension, appears more likely to be a factor. Fasting Insulin levels correlate with systolic blood pressure, and drop in blood pressure following weight loss is related to improvement in Insulin sensitivity. Interestingly, in hypertensive obese individuals, somatostatin decreases both insulin level and blood pressure, suggesting the effect of hyperinsulinemia. Insulin can lead to sodium retention and angiotensin II - mediate aldosterone production, can change vascular structure and function, can alter cation flux, and can activate the sympathetic nervous system. In both obese and nonobese individuals during water diuresis, however, sodium excretion decreases with euglycemic - hyperinsulinemic clamp, so Insulin Resistance cannot be proposed as a cause of Hypertension. Furthermore, improvement in Insulin sensitivity need not lower blood pressure, as for example in dogs with high - fat diet - induced Hypertension, where blood pressure is not lower by high - dose aspirin despite Prevention of Insulin Resistance. Rocchini posit common factors related to Obesity, explaining both Insulin Resistance and Hypertension, suggesting activation of the sympathetic nervous system as one such factor. Thus, central and / or peripheral - 2 receptors cause Insulin Resistance, whereas peripheral receptors cause Hypertension. Comparing clonidine with a combination of peripheral - and - blockade, both prevented Hypertension, while only clonidine prevented Insulin Resistance in high - fat - fed dog Model. Arya M. Sharma further discussed the question of the causal relationship between Insulin Resistance and Hypertension, particularly addressing the question of whether angiotensin II blockade can be used both for treatment of Hypertension and Insulin Resistance. He notes that salt - sensitive people, those whose blood pressure increases with increased sodium intake, show Insulin Resistance, which is present on either low - or high - sodium diet. Furthermore, sympathetic nervous system activity is stimulated by Insulin in what appears to be a central effect, suggesting that hyperinsulinemia accompanying Insulin Resistance may be directly deleterious. He also cites a number of studies showing that Insulin sensitizers decrease blood pressure, phenomenon seen both with metformin and thiazolidinediones. Thus, Insulin may stimulate sympathetic activity and sodium Na reabsorption, as Insulin - induced vasodilatation is reduced in individuals who develop Hypertension.
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Medications that reduce insulin resistance include metformin and thiazolidinediones. Metformin is biguanide; it reduces hepatic glucose output and increases uptake in peripheral tissues. Metformin is a major drug in the treatment of patients who are obese and have type 2 Diabetes. The drug enhances weight reduction and improves lipid profile and vascular integrity. Long - term follow - up data from the Diabetes Prevention Program / DPP Outcomes Study find metformin is associated with vitamin B12 deficiency, and routine measurement of vitamin B12 should be considered in patients receiving metaformin. Thiazolidinediones lower plasma insulin levels and treat type 2 Diabetes associated with insulin resistance. In a multicenter, double - blind trial of 3876 insulin - resistant patients who had had recent ischemic stroke or transient ischemic attack, those receiveing pioglitazone had reduced risk of stroke, Myocardial Infarction, and Diabetes compared to those receiving placebo. However, pioglitazone increases the risk of weight gain, edema, and fracture. Successful treatment of severe type B insulin resistance has been reported with rituximab, cyclophosphamide, and prednisone following failure of immunosuppressive therapy and plasmapheresis to control glucose levels or reduce insulin dosage.
Improvement in Insulin resistance occurs after Bariatric Surgery, such as gastric banding, sleeve gastrectomy, and gastric bypass, when carried out in carefully selected morbidly obese patients. Bariatric Surgery may be appropriate for patients with a body mass index greater than 40 kg / m 2 or greater than 35 kg / m 2 in combination with high - risk comorbidities. It is the most effective treatment for obesity that is currently available, but it is reserved for patients who are unable to attain weight reduction after attempting noninvasive or less intense options. In severe cardiovascular disease, procedures such as coronary artery bypass graft and peripheral vascular surgery may be necessary. Cosmetic and palliative treatments may be indicated in the treatment of many patients with Insulin resistance syndrome, depending on the type and severity of physical anomalies.
Because the degree of T2DM remission obtained by metabolic surgery is directly related to reduction of contact between food and gut, it seems reasonable to conclude that the effect is due to interruption of diabetogenic signal from the intestine. Two elegant studies by Rubino and colleagues provide support. First, they document that exclusion of the duodenum in overfed, hyperglycemic rats restored euglycemia. 24 in the second study, silicone intestinal liner produced the same result, but the perforating material produced returned to high glucose values. 25 Koehestanie and colleagues report that similar liners in patients with diabetes produce euglycemia. 26 Clinical application of liners, however, is unlikely. Too many patients in the series could tolerate devices only for a brief time. This assessment does not include any consideration of the use of insulin for acute care. Patients with T2DM with sepsis develop severe hyperglycemia that may benefit bacterial growth and hinder protective response. Until separate, appropriate studies evaluate the value of insulin therapy for acute disease, those practices should continue.
When Reaven introduced the concept in 1988, he suggested that Insulin Resistance / hyperinsulinemia was the underlying cause. His suggestion was based on cross - sectional data showing associations between hyperinsulinemia and other aspects of syndrome in patients as well as experimental studies on rodents fed diets high in sucrose or fructose. Support for the role of hyperinsulinemia in Development of Syndrome came in 1992 when Haffner et al. Report 8 years of prospective data from 2217 subjects in San Antonio Heart Study showing that fasting hyperinsulinemia precedes development of other aspects of Syndrome including hypertension, hypertriglyceridemia, and depress HDL - C, as well as development of T2D. After adjusting for baseline obesity and fat distribution, as well as weight gain over the period of observation, significant relationships between Insulin and other factors remain present. Further support for the importance of hyperinsulinemia comes from animal study by Barnard et al. Feeding rodents high - fat sucrose diet results in skeletal muscle Insulin Resistance and hyperinsulinemia within a few weeks before any change in body fat or abdominal fat cell size. Animals subsequently develop hypertriglyceridemia, enhanced clotting and hypertension, that is, MS. Through his Banting Lecture, Reaven suggested some mechanisms to explain how Insulin Resistance / hyperinsulinemia might cause other aspects of MS. He pointed out that hypertension was associated with elevated levels of plasma catecholamines and suggested enhanced sympathetic nervous system activity as contributing mechanism. He also cites studies reporting that Insulin causes the kidney to promote sodium reabsorption and increase plasma volume. For the increase in TG associated with syndrome, he cites study reporting that in perfused rat livers Insulin increases very low density lipoprotein TG production. San Antonio Group provides further support for these mechanisms in two subsequent papers. They point out that although some data has shown that acutely, Insulin could be vasodilator, prolonged Insulin Resistance and hyperinsulinemia was associated with hypertension and could be due to several mechanisms, including overactive sympathetic nervous system, sodium retention, altered membrane ion transport, and proliferation of vascular smooth muscle cells. They also state that hyperinsulinemia would increase liver production of VLDL to increase serum TG, while at the same time reducing high - density lipoprotein production and serum HDL - C. These data all support Reavens suggestion that Insulin Resistance / hyperinsulinemia is the primary factor responsible for MS. Using the Insulin / glucose clamp technique, DeFronzo and Ferrannini demonstrate that cellular resistance to Insulin action subtends hyperinsulinemia. The important question, however, is what causes Insulin Resistance. Reaven suggests that elevated plasma - free fatty acids were involved in the development of Insulin Resistance, as originally suggested by Randle et al., And presented some experimental data to support his claim. Base on the 1947 observation of Vague, women with upper body Obesity were far more likely to get Heart Disease and T2D compared to women with lower body Obesity. Kaplan, in 1989, suggested that obesity, especially abdominal obesity, was the primary factor that induced hyper - insulinemia and subsequently MS.
Chronic low - grade inflammation is the central underpinning in development of obesity and insulin resistance and cells of both innate and adaptive immune system are shown to play an important role in the pathogenesis of metabolic disease. In 2003, two seminal papers were published showing accumulation of F4 / 80 - positive immune cells in adipose tissue of obese mice and animals feed diet rich in fat. These F4 / 80 + adipose tissue macrophages obtained from obese animals were found to secrete proinflammatory, insulin resistance - producing factors including TNF, IL6, IL1, serum amyloid A3, and CCL2 to name a few. These two publications sparked a fervent burst of investigation into the role of the immune system in regulation of glucose home - ostasis and adiposity. Subsequent studies have demonstrated that lymphocytes including regulatory T cells, effector T cells, and B cells are recruited during various stages of expansion of adipose tissue as well. Many propose that regulatory T cells, TH2 - polarize T cells as well as alternatively activated anti - inflammatory macrophages are most abundant in adipose tissue from lean rodents, whereas diet - induced adiposity is associated with orchestrated trafficking of B cells, TH1 - polarize T cells, and effector T cells at later stages of adipose tissue expansion showing accumulation of classically activate proinflammatory macrophages and natural killer cells. Despite burgeoning research in this field, metabolic factors regulating immune responses in glucoregulatory tissues including adipose, liver, and skeletal muscle remain poorly define. To date, much of work in this field implicates macrophages as major effectors in pathogenesis of obesity - insulin resistance phenotypes. Early studies clearly show that ablation of genes involved in inflammatory signaling within macrophages is protective against diet - induced obesity and insulin resistance, while conversely, hematopoietic / myeloid - specific ablation of transcription factors involved in inflammation repression promotes diet - induced obesity and whole body insulin resistance as well as accelerates atherosclerotic lesion development. In the latter part of the past decade, theme emerged in which immune cells were rigidly ascribed as either phenotypically anti - inflammatory, alternatively activate M2 or proinflammatory, classically activate, M1. Although the appealingly simplistic binary classification of M1 versus M2 macrophage phenotype has been readily accepted by the obesity / diabetes research community, diversity and complexity of immune cell type and function favors spectral classification taking into account require functionality of immune cell and specificity of chemotactic signal and environmental milieu unique to recruiting tissue. Altering chemotactic signal from give tissue is shown to exert either health benefit or pathogenic repercussions. For instance, there is some suggestion that deletion of MCP1 or its receptor, CCR2, confers protection against adipose tissue macrophage accumulation, insulin resistance, and atherosclerosis during high fat feeding, whereas adipocyte - specific overexpression of MCP1 promotes macrophage infiltration, inflammation, insulin resistance and atherosclerosis. Work over last past decade clearly shows a critical role for the immune system in regulation of glucose homeostasis and pathogenesis of adiposity and atherosclerotic lesion development.
As previously discuss, many studies have documented that AT improved whole body insulin sensitivity. Skeletal muscle, most important target tissue for insulin action, has received most attention for mechanistic studies with emphasis on insulin signaling pathway study from biopsy samples. While effects of AT - induced increases in glucose disposal have been attributed primarily to increases in insulin signaling protein and / or activities, data are not consistent. Studies comparing endurance - trained subjects versus untrained subjects have indicated differences in glycogen storage in response to insulin, insulin signaling proteins, such as increased GS, GLUT4, GLUT4 vesicle - associate protein, and PI3 - K activation, but decreased IRS - 1, IRS - 2, insulin receptor, and no difference in AKT. Using 31P NMR spectroscopy, Perseghin et al. Note that despite lower glucose transport phosphorylation in offspring of T2D patients compared with normal subjects, both exhibited increases in whole body insulin sensitivity after AT by 40% or more and whole body nonoxidative glucose metabolism by 60% to 70%, mediated by increase in glucose transport - phosphorylation. Training - induced improvement in glucose disposal has been attribute, AT least in part, to increased insulin - stimulate glucose storage and GS fractional velocity, which correlate with insulin - stimulate glucose storage. Dela et al. Also note increases in nonoxidative glucose disposal associated with increased GS mRNA and Frosig et al. Note increased GS activity with short - term training. Ferrara et al. Note similar effects on GS fractional activity in response to insulin, with no change in total activity. Dela et al. Note maximum insulin binding and that basal - and insulin - stimulate receptor kinase activity do not change; however, GLUT4 protein concentration increase and training - induced increase in GLUT4 matched increase in maximum insulin - stimulate leg glucose uptake in the same subjects, and individual values of two variables were correlate. In subjects with IGT, independent of changes in body composition, glucose disposal AT high insulin concentration during EHC increased approximately 60% and GLUT4 and glycogen increased after training. Several additional studies have noted increases in GLUT4 content. For example, 60% in middle - age subjects, approximately 80% in nondiabetic men, 38% and 22% in overweight nondiabetic and diabetic men, 40% in healthy men and 23% in men with T2D. Short et al. Noted increases in GLUT4 mRNA and protein content, independent of age, in subjects ranging from age 21 to 87. Furthermore, short - term training increases GLUT4 protein similarly in both younger and older subjects. Frosig et al. Note AT - induced increases in insulin - stimulate glucose uptake of 60% and increase in muscle Akt1 / 2, AS160, GLUT4, HK2 and insulin - responsive aminopeptidase protein content and activities Akt1, GS and AS160 phosphorylation. However, IRS - 1associated PI3K activity was reduce. Short - term training studies report no change in mRNA expression of IR, IRS - 1, IRS - 2 and p85 - subunit of PI3K, but there were noted increases after short - term training in insulin receptor autophosphorylation and PI3K activity in concert with increased insulin sensitivity, and PI3K activity in chronic - trained young men. On other hand, Christ - Roberts et al.
There are several known causes of severe Insulin Resistance, including several rare disorders and genetic conditions. Several medications are known to contribute to Insulin Resistance, including glucocorticoids, protease inhibitors, atypical antipsychotics, and calcineurin inhibitors. In patients with severe Insulin Resistance, effort should be made to discontinue such agents or switch to alternative medications if possible. Poor medication - taking behaviors or pseudoresistance should be ruled out before modifying or intensifying therapy. Pseudoresistance may be the result of nonadherence, poor injection technique, improper Insulin storage, or malingering for secondary gain. Pseudoresistance can be ruled out by conducting a modified Insulin Tolerance Test. During such test, patients are administered witnessed doses of SHORT - acting Insulin in a clinic, and their blood glucose is monitored every 30 minutes for a period of 4 - 8 hours. Patients should be fasting for the test and should have a blood glucose level of > 150 mg / dL. Witnessed Insulin dose approximately equal to what average person with Diabetes might require Insulin dose = Blood Glucose - 100 /] Should be give. If there is not an appropriate drop in Blood Glucose within 4 hours, second dose should be give. If normoglycemia or hypoglycemia is not achieved after either dose, test confirms that the patient likely has severe Insulin Resistance.
This Frontiers article has examined a wide variety of methods currently available for estimating insulin sensitivity / resistance. These range from complex, time - consuming, labor - intensive, invasive procedures to simple tests involving single fasting blood sample. It is important to understand concepts underlying each method so that relative merits and limitations are appropriately matched to proposed applications. The Glucose clamp method is the reference standard for direct measurement of insulin sensitivity. Regarding simple surrogates, QUICKI and log are among the best and most extensively validate. Dynamic tests are useful if information about both insulin secretion and insulin action is needed. As with all measurement techniques, correct interpretation of data from different methods for measuring insulin sensitivity requires complete understanding of technique.
Hec should be the test of first choice in studies where IR is of primary interest. It is a steady - state technique which requires constant insulin infusion. Clearly, this is unphysiological, thus HEC is not appropriate when estimation of insulin action and glucose dynamics under normal physiological conditions is require. Owing to the complexity of HEC, FSIVGTT may be preferred as an alternative option and, as such, can be considered'silver standard. The main FSIVGTT techniques available are standard technique and the more modern insulin - modify version. Simplify short sampling protocols have been described for ease of studying large numbers of subjects. Unlike HEC, FSIVGTT relies on dynamic glucose and insulin data obtained before and following intravenous glucose bolus. It therefore measures IR indirectly. All FSIVGTT techniques require minimal model analysis in order to derive insulin sensitivity index, Si. This can only be done using software packages such as MINMOD. Many different software packages are available but do yield slightly different results. Investigators should endeavour to use the most modern version. In addition to determining Si, differential equations used by the MINMOD program can be used to estimate many other parameters of interest eg. Glucose effectiveness, - cell activity, acute insulin response, disposition index and area under curve. For investigators WHO are interested in these parameters, FSIVGTT will be the test of choice. However, it should be anticipated that for some subjects it may not be possible to derive various parameters from available data. This is a common limitation of technique encountered by authors, including ourselves, which should be taken into account when planning the number of study subjects to be recruit. For investigators interested in assessing hepatic glucose production and IR, stable isotopes of glucose can be used in combination with clamp or FSIVGTT techniques. For further details on this topic, readers are direct to appropriate reference. Other dynamic techniques such as insulin tolerance test and continuous infusion of glucose with model assessment have not been widely benchmarked and only a few groups have used them in their studies. We will not therefore discuss them further here. The number of subjects involved in study is an important determinant of the feasibility of give technique. It is well recognise that reference techniques are generally unsuitable for epidemiological studies involving large numbers of subjects. However, there have been exceptions and, in principle, there is no reason why reference techniques should not be used in epidemiological study provide sufficient resources are available. In the IR atherosclerosis study, large number of subjects were used to examine association between Si derived from insulin - modify FSIVGTT and other cardiovascular risk factors. In general, however, reference techniques have been confined to studies with relatively low numbers of subjects, especially when they are pilot studies investigating new treatment modality or where novel method is being validate. Knowledge of subject glycaemic status influences choice of method.
During last decades, several studies have defined several and well - characterized risk factors for IR, including ethnicity, puberty, adipose tissue variant depots, polycystic ovary syndrome, gene variants, family history of Diabetes or gestational Diabetes, and fetal growth pattern during pregnancy. The two most important unchangeable risk factors for IR in children are ethnicity and puberty. Several studies have demonstrated that Caucasian children are affected by IR more often than African, American, Hispanic, Pima Indian and Asian children. Puberty is physiologically responsible for IR; in fact, during this period of life, insulin sensitivity undergoes decline of around 25 - 50% and improves when puberty ends. There is a strong association between IR and abdominal obesity, which is known to represent one of the main elements of MS. According to large - population base studies, subcutaneous adipose tissue, and visceral adipose tissue seem to be both related to HOMA - IR. In addition, VAT correlates more strongly to insulin variables than SAT. Pathogenesis on the basis of this evident correlation is still not known exactly but several hypotheses have been consider. Sat and VAT secrete free fatty acids into the blood, and higher plasmatic free fatty acid levels seem to be associated with IR. Moreover, VAT presents strong correlation with endothelial dysfunction and higher blood C - reactive protein values, which may give explanation for inflammation secondary to higher VAT depots. Since adipose tissue acts as an endocrine organ, these two tissues play fundamental role in this field. Vat is more strongly associated with adiponectin levels and release of interleukin - 6 and plasminogen activator inhibitor - 1 to greater extent than SAT. These main factors may be the causes of higher IR in patients with elevated VAT, in fact IL - 6, and PAI - 1 reduce in case of weight loss and properly correlate with parallel improvement of insulin sensitivity. Adolescents affected by PCOS often present IR, whose severity has been observed to be higher in obese patients than in lean ones. Risk factors include genetics, which is considered a great determinant in the incidence of IR. Principal variants which increase the risk of developing type 2 DM, that could represent the final effect of IR, are listed in Table 3. Peroxisome proliferator - activate receptor gamma variant Pro12Ala was one of the first genetic variants found to be related to decreased risk of developing T2D. Gene variants of transcription factor 7 - like 2 are associated to risk of developing Diabetes more than any other gene 7. Rs972283 is located near KLF14. Klf14 gene and protein expression have been observed to be significantly decreased in both muscle and adipose tissue in individuals affected by T2D. Insulin receptor substrate 1 is one of the loci responsible for insulin signaling pathway. Allele C at rs2943641 adjacent to IRS1 was found to be related to IR and hyperinsulinaemia in the European Population, whereas SNP, rs2943650, near IRS1, was found to be related to lower percentage of body fat, higher triglycerides and IR, and decreased HDL - cholesterol.
Diabetes mellitus type 2: tip of iceberg. This simplified schematic presentation illustrates the evolution of type 2 Diabetes mellitus. Diabetes mellitus type 2 represents the end stage of long - lasting metabolic disturbances caused by insulin resistance associated with hyperinsulinemia, obesity, dyslipoproteinemia, arterial hypertension, and consequently premature atherosclerosis. Since this detrimental metabolic milieu is present for many years before plasma glucose levels are elevate, it is not surprising that type 2 diabetic patients have micro - and / or macrovascular complications at the time of initial diagnosis. Subjects in stage I have normal glucose tolerance due to the ability of their cells to compensate for insulin - resistant state. At this stage, elevated triglyceride levels and reduced HDL levels as well as increased waist to hip ratio may indicate insulin resistance and should lead to therapeutic action. In stage II, glucose tolerance after oral glucose load is impaired due to developing insulin - secretory deficiency. To avoid progression to clinically overt type 2 Diabetes, these IGT subjects must receive treatment options to reduce insulin resistance, such as dietary advice and increase in physical activity. The stage model of pathophysiology of type 2 Diabetes has been adapted by Beck - Nielsen and Groop. Diabetes mellitus type 2: tip of iceberg. This simplified schematic presentation illustrates the evolution of type 2 Diabetes mellitus. Diabetes mellitus type 2 represents the end stage of long - lasting metabolic disturbances caused by insulin resistance associated with hyperinsulinemia, obesity, dyslipoproteinemia, arterial hypertension, and consequently premature atherosclerosis. Since this detrimental metabolic milieu is present for many years before plasma glucose levels are elevate, it is not surprising that type 2 diabetic patients have micro - and / or macrovascular complications at the time of initial diagnosis. Subjects in stage I have normal glucose tolerance due to the ability of their cells to compensate for insulin - resistant state. At this stage, elevated triglyceride levels and reduced HDL levels as well as increased waist to hip ratio may indicate insulin resistance and should lead to therapeutic action. In stage II, glucose tolerance after oral glucose load is impaired due to developing insulin - secretory deficiency. To avoid progression to clinically overt type 2 Diabetes, these IGT subjects must receive treatment options to reduce insulin resistance, such as dietary advice and increase in physical activity. The stage model of pathophysiology of type 2 Diabetes has been adapted by Beck - Nielsen and Groop. Troglitazone data is based on references in Table 5. Rosiglitazone data is based on: Patel et al.; Patel et al.; Raskin and Rappaport; raskin et al.; Chabonnel et al.; Mathews et al.; Grunberger et al.; And Salzman and Patel. Pioglitazone data is based on: Mathisen et al.; Rubin et al.; Schneider et al. Troglitazone data is based on references in Table 5. Rosiglitazone data is based on: Patel et al.; Patel et al.; Raskin and Rappaport; raskin et al.; Chabonnel et al.; Mathews et al.
The Dietary glycemic Index concept supports the role of the rate of carbohydrate digestion in prevention and treatment of chronic disease, including those diseases which have been highlighted in dietary fiber and Insulin - Resistance Syndrome hypotheses. This concept should not be seen as particularly radical at a time when pharmacological approaches to slowing absorption, notably - glycoside hydrolase inhibitors, are now accepted in Management of Diabetes. Further, longer term efficacy studies as well as effectiveness studies are required to better determine the importance of glycemic Index in regulation of Blood Glucose and prevention of diabetic complications, particularly in relations to CHD Risk Factors. The possible role of glycemic Index in decreasing Postprandial oxidative stress and pro - inflammatory process also merits further investigation.
Metabolic complications associated with HIV Disease and its treatment - including insulin resistance and diabetes, abnormal cholesterol and triglyceride levels, and body fat gain or loss - remain a medical mystery and a topic of intense interest for AIDS researchers and people with HIV alike. While these complications have sometimes been collectively referred to as lipodystrophy syndrome, it remains unclear whether or how they are related and what causes them. Scientists are urgently trying to better understand these conditions, which may have a negative impact on quality of life, interfere with adherence to Antiretroviral Therapy, and lead to long - term health problems. High blood glucose levels and dyslipidemia are particular concern because in the population at large they have been linked with increased risk of heart disease. Much research is underway and new clues are steadily emerging, but Daniel Kuritzkes, MD, of Boston's Brigham and Women's Hospital predicts, we 'll need several more years of follow - up to get a better perspective.
Under normal conditions, hormone insulin rises briefly after eating. It stimulates the liver and muscle to take up sugar from blood and convert it into energy. That then causes blood sugar to fall, and then insulin to fall. With normal insulin sensitivity, both sugar and insulin are normal on the fasting blood test. With insulin resistance, blood sugar may be normal, but insulin is high. Why? Because the pancreas has to make more and more insulin to try to get its message through. Too much insulin generates inflammation and causes weight gain. It can also lead to Type 2 diabetes and heart disease. Too much insulin is also an underlying physiological driver of PCOS.
While weight loss can result in better insulin, improving the way you eat can also help to lower your insulin levels. The key is to choose foods that don't raise your insulin even more. Changing your diet to include lots of low glycemic - index fruits, vegetables, and lean proteins can be beneficial. Focus on anti - inflammatory foods which have been shown to improve Insulin resistance. Portion size matters: to best manage insulin levels, keep carbohydrate foods to just one or two servings at meals, or one - quarter of your plate. Carbohydrate foods include grains, fruits, vegetables, beans, legumes, and milk and yogurt. Spread these foods out throughout the day.
Following a fixed diet plan, such as the Mediterranean Diet, can improve insulin sensitivity. The Mediterranean Diet involves eating lots of seasonal, plant - base foods, eating fruit for dessert, and using olive oil as the primary source of fat. People following this diet eat fish, poultry, legumes, and nuts as main protein choices and dairy products in moderation. Mediterranean eaters also limit their intake of red meat and consume little wine during meals. In a recent study, women who follow the Mediterranean Diet reduced their risk of cardiovascular health problems, including factors such as insulin resistance, by around 25 percent. People should base their daily calorie intake on their weight loss goals and body size. The Mediterranean Diet is just one option for healthy eating. Other diet plans, such as DASH and ketogenic diets, also offer ways to improve insulin resistance. These work well when a person combines them with other healthy lifestyle practices, such as stress management, adequate sleep of 7 to 9 hours each night, and regular physical activity.
It is important to know what this study does and does not tell us. To lose weight, all participants followed a calorie restrictive diet consisting of 45% carbohydrates, 30% fat and 25% protein and only participants who achieved weight loss of 12% within that ten - week period were included in the second phase. 1 This was not a weight loss study but rather a study specifically aimed at evaluating the effect of macronutrient partitioning on metabolic function and weight maintenance, said Christopher Gardner, PhD, professor of Medicine at Stanford School of Medicine, and director of nutrition studies at Stanford Prevention Research Center, in Stanford, California. Findings of Dr. Gardners DIETFITS study, 4 in which individuals were evaluated for the amount of weight lost over 12 months, offer evidence that there is no significant difference in the number of pounds lost by participants eating high carbohydrate versus low carbohydrate diet. Maybe a better way to understand the impact of specific food types on weight is that a high fat / low carbohydrate diet is a more effective treatment for people with insulin resistance than dietary prescription for people with normal glucose metabolism, who are trying to manage their weight, say Caroline Apovian, MD, FACP, FACN, professor of Medicine and pediatrics, at Boston University School of Medicine, in Massachusetts. But, dont go running for that stick of butter, just yet.
Some foods and nutrients can reduce insulin resistance. Certain others, though they may not directly reduce insulin resistance, have been linked to lower risk for developing type 2 Diabetes. These foods may be helpful for preventing or delaying diabetes. Whole grains, such as oatmeal, whole - wheat bread and pasta, brown rice, quinoa, shredded wheat, and bulgur. Fatty fish, such as salmon, tuna, and herring. Non - starchy vegetables, such as greens, broccoli, cauliflower, bell peppers, mushrooms, eggplant, zucchini, onions, tomatoes, carrots, beets, green beans, and Brussels sprouts. Olive oil Avocado Nuts and peanuts Legumes, such as lentils, split peas, soybeans, and garbanzo, navy, black, pinto, and other beans. Fresh fruit, such as berries, oranges, apples, pears, cantaloupe, and watermelon.
A diet alone isnt enough to properly manage PCOS. Because they have higher testosterone levels, women with PCOS tend to build muscle more easily than those without the condition. More muscle mass increases the metabolic rate so you burn calories more effectively, and it helps you to use Glucose better, resulting in less Insulin needing to be secrete. Try to get at least two days of weight training each week to build and maintain muscle mass. Adding more activity to your day by taking stairs instead of elevator, parking your car further from the door, or taking short walks at lunch or breaks can make a difference in your health and help you to produce less Insulin. Some people find use of fitness trackers helpful to increase their steps each day and even have competitions with co - workers or friends.
Generally speaking, T2D involves a combination of IR and inadequate insulin secretion to adequately compensate. Progression to T2D has been suggested to comprise five definitive stages with IR initiating pathological decline that requires years or even decades to complete. The critical role of IR in this sequence IS exemplified by the fact that it underpins strong genetic predisposition for T2D with FH + demonstrating mark IR long before Glucose Tolerance becomes impaired. Indeed, in accordance with this genetic link, IR has been advanced as a significant contributor to T2D progression. In stage 1, IR begins when insulin - sensitive target tissues begin to demonstrate decreased response to regulatory prowess of circulating hormone. Particularly relevant in this regard is skeletal muscle, which represents the predominant site of insulin - stimulate glucose disposal in the body. At this early stage of disease progression, measurement of C - peptide concentration in blood or urine might provide a useful way to identify the need for prophylactic exercise intervention. Fortunately, in this initial compensation stage, increased insulin secretion secondary to an increase in pancreatic - cell mass / productivity allows for maintenance of homeostatic levels of plasma Glucose. Leave unaddressed, however, chronic overload associated with this quick fix takes its toll and - cells become dysfunctional with Glucose - stimulate insulin secretion ultimately reduce. Resultant hyperglycemia continues pathological progression and allows for diagnosis of prediabetes via measurement of fasting plasma Glucose and / or hemoglobin A1c. With the passage of time, cell function continues to decline with increasing IR, causing a cascade of events that ultimately culminate in T2D.
One of the main functions of insulin is to lower blood glucose levels by enabling glucose to enter cells of the body, where it is used for energy or stored for future use. A person who is insulin - sensitive needs only a relatively small amount of insulin to keep blood glucose levels in normal range and to keep body cells supplied with glucose they need. Person who are insulin - resistant, on the other hand, need a lot more insulin to get the same blood - glucose - lowering effects. Insulin resistance is associated with numerous health risks. For one thing, it causes hyperinsulinemia, or high circulating insulin levels, which may be directly damaging to blood vessels. Hyperinsulinemia is also associated with high blood pressure, heart disease and heart failure, obesity, osteoporosis, and certain types of cancer, such as colon, breast, and prostate cancer. In contrast, having low circulating insulin levels is associated with greater longevity; most centenarians without diabetes have low circulating insulin levels.
If dietary changes are not sufficient and insulin resistance has been confirmed through testing, you may want to discuss adding insulin - altering medication with your physician. Many women have found great success in weight loss by combining medication with lifestyle changes. It is important to know, however, that these drugs have not been approved by FDA for use in treating PCOS. Metformin is usually the first choice of most doctors, assuming that a woman is a candidate for taking medication. It works by increasing the cell's sensitivity to insulin and also suppressing production of glucose in the liver. For many women, taking this medication can help restore regular ovulation and periods. Glitazones are another class of drug that is sometimes used either alone or in conjunction with metformin. These medications directly decrease insulin insensitivity and often have fewer gastrointestinal side effects than metformin. Also, women taking glitazones may actually gain weight instead of losing it. Victoza and other injectable medications have also been studied in women with PCOS and show good results in combination with metformin and a healthy lifestyle.
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