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Insulin sensitivity testing

Insulin sensitivity testing

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Insulin sensitivity testing -

Curve c: Decreased insulin sensitivity increased EC50 and reduced insulin responsiveness. Curve d: Leftward shift in the insulin concentration-response response curve.

This represents increased insulin sensitivity decreased EC50 with normal insulin responsiveness. The concept of insulin resistance was proposed as early as to describe diabetic patients requiring high doses of insulin Rigorous evaluation of altered sensitivity and responsiveness therefore requires a comparison of insulin dose-response curves.

The glucose clamp technique, originally developed by Andres and DeFronzo is widely accepted as the reference standard for directly determining metabolic insulin sensitivity in humans This constant insulin infusion results in a new steady-state insulin level that is above the fasting level hyperinsulinemic.

As a consequence, glucose disposal in skeletal muscle and adipose tissue is increased while HGP is suppressed.

An infusion of potassium phosphate is also given to prevent hypokalemia resulting from hyperinsulinemia and increased glucose disposal. After several hours of constant insulin infusion, steady-state conditions are typically achieved for plasma insulin, blood glucose, and the glucose infusion rate GIR.

Assuming that the hyperinsulinemic state is sufficient to completely suppress hepatic glucose production, and since there is no net change in blood glucose concentrations under steady-state clamp conditions, the GIR must be equal to the glucose disposal rate M Fig.

Thus, whole body glucose disposal at a given level of hyperinsulinemia can be directly determined. M is typically normalized to body weight or fat-free mass to generate an estimate of insulin sensitivity. The validity of glucose clamp measurements of insulin sensitivity depends on achieving steady-state conditions.

It is possible to use stable isotope or radio-labeled glucose tracer under clamp conditions to estimate HGP so that appropriate corrections can be made to M in the event HGP is not completely suppressed 14 , 15 , 16 , M is routinely obtained at only a single insulin infusion rate and therefore comparisons between M or SI Clamp among different subjects is valid only if the same insulin infusion rate is used for all subjects.

When glucose tracers are used during a clamp study, the tracer is infused at constant rate throughout the study. HGP estimated during the last 20 or 30 min of the clamp is a measure of insulin-mediated suppression of HGP, an estimate of hepatic insulin sensitivity.

Similarly, lipolytic rates can be assessed at baseline and hyperinsulinemia during clamp by using isotopic tracers e. A single or multistep hyperinsulinemic euglycemic clamp can be used to measure adipose tissue insulin sensitivity. The principal advantage of the glucose clamp in humans is that it directly measures whole body glucose disposal at a given level of insulinemia under steady-state conditions.

Conceptually, the approach is straightforward and there are a limited number of assumptions which are clearly defined. The main limitations of the clamp approach are that it is time-consuming, labor intensive, expensive, and requires an experienced operator to manage technical difficulties.

Thus, for epidemiological studies, large clinical investigations, or routine clinical applications e. in and subsequently modified by Harano et. From the contralateral arm, blood samples for glucose and insulin determinations are taken every 30 min for 2.

The constant infusions of insulin and glucose determine steady-state plasma insulin SSPI and glucose SSPG concentrations. The steady-state period is assumed to be from - min after initiation of the IST.

SSPI concentrations are generally but not always similar among subjects. Therefore, the SSPG concentration will be higher in insulin resistant subjects and lower in insulin sensitive subjects.

That is, SSPG values are inversely related to insulin sensitivity. The IST provides a direct measure SSPG of the ability of exogenous insulin to mediate disposal of an intravenous glucose load under steady-state conditions where endogenous insulin secretion is suppressed.

The SSPG is a highly reproducible direct measure of metabolic actions of insulin that is less labor-intensive and less technically demanding than the glucose clamp. Indeed, since there are no variable infusions with the IST, steady-state conditions are more easily achieved with the IST than with the glucose clamp.

Indeed, SSPG has positive predictive power for cardiovascular disease events and onset of type 2 diabetes 24 , Moreover, the IST can be used for larger populations that may pose difficulties for application of the glucose clamp Many of the limitations of the IST are similar to those described above for the glucose clamp with the exception that the IST is less technically demanding.

Thus, it is impractical to apply the IST in large epidemiological studies or in the clinical care setting. SSPG under ideal conditions determines primarily skeletal muscle insulin sensitivity and is not designed to reflect hepatic insulin sensitivity.

After an overnight fast, an intravenous bolus of glucose 0. Some studies use tolbutamide instead of insulin in the modified FSIVGTT to stimulate endogenous insulin secretion 15 , 29 , 31 , 32 , Blood samples are taken for plasma glucose and insulin measurements at , -1, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 14, 16, 20, 22, 23, 24, 25, 27, 30, 40, 50, 60, 70, 80, 90, , , , and min.

These data are then subjected to minimal model analysis using the computer program MINMOD to generate an index of insulin sensitivity S I.

The minimal model is defined by two coupled differential equations with four model parameters Fig. The first equation describes plasma glucose dynamics in a single compartment. The structure of the minimal model allows MINMOD to uniquely identify model parameters that determine a best fit to glucose disappearance during the modified FSIVGTT.

S I is calculated from two of these model parameters and is defined as fractional glucose disappearance per insulin concentration unit.

S G is defined as the ability of glucose per se to promote its own disposal and inhibit HGP in the absence of an incremental insulin effect i. Schematic, equations, and parameters for the minimal model of glucose metabolism. Glucose leaves or enters its space at a rate proportional to the difference between plasma glucose level, G t and the basal fasting level, Gb.

Recently the minimal model has been used to assess free fatty acid FFA insulin sensitivity. Using a one compartment nonlinear model of FFA kinetics during FSIVGTT, showed that the FFA insulin sensitivity parameter correlated well with minimal model indices Furthermore, this model also showed that glucose modulates disposal of FFAs.

Minimal model analysis of the modified FSIVGTT is easier than the glucose clamp method because it is slightly less labor intensive, steady-state conditions are not required, and there are no intravenous infusions that require constant adjustment.

Unlike the glucose clamp or IST, information about insulin sensitivity, glucose effectiveness, and β-cell function can be derived from a single dynamic test. The minimal model generates excellent predictions of glucose disappearance during the FSIVGTT. S I is a strong predictor of the development of diabetes in a prospective study of children of diabetic parents Moreover, the insulin-modified FSIVGT may be used in relatively large-scale population studies Therefore, in research settings where assessing insulin sensitivity along with glucose effectiveness and β-cell function is of interest, minimal model analysis of the insulin-modified FSIVGTT may be appropriate.

The minimal model approach is simpler than direct methods for determining insulin sensitivity. Nevertheless, it still involves intravenous infusions with multiple blood sampling over a 3 h period that is nearly as labor intensive as the glucose clamp or IST. In addition, many limitations of minimal model analysis stem from the fact that the model oversimplifies the physiology of glucose homeostasis and is discussed in detail elsewhere 5.

The oral glucose tolerance test OGTT is a simple test widely used in clinical practice to diagnose glucose intolerance and type 2 diabetes After overnight fast, blood samples for determinations of glucose and insulin concentrations are taken at 0, 30, 60, and min following a standard 75g oral glucose load.

Oral glucose tolerance reflects the efficiency of the body to dispose of glucose after an oral glucose load or meal. The OGTT mimics the glucose and insulin dynamics of physiological conditions more closely than conditions of the glucose clamp, IST, or FSIVGTT.

However, it is important to recognize that glucose tolerance and insulin sensitivity are not equivalent concepts. In addition to metabolic actions of insulin, insulin secretion, incretin effects, and other factors contribute importantly to glucose tolerance. The use of tracers for estimation of insulin sensitivity was first introduced in to overcome the shortcomings of FSIVGTT 37 The minimal model method does not allow segregation of glucose production from liver from exogenously administered glucose during calculations of insulin sensitivity and thus induces error in the insulin sensitivity calculations.

Labeled intravenous glucose can be differentiated from endogenously produced glucose and thus use of labeled glucose during IVGTT provides more precise and accurate measurements 38 , 39 Similarly, labeled glucose has been used in oral glucose tolerance test and insulin sensitivity has been calculated by minimal model technique similar to FSIVGTT Basal hepatic insulin resistance index can then be estimated as the product of HGP rate and the fasting plasma insulin concentration.

Use of tracer definitely allows for improvement over the FSIVGTT. Use of labeled oral glucose allows for more precise measurements of insulin sensitivity and glucose disposal from a simple OGTT and this can be a useful tool in large studies. The triple tracer method is cumbersome and cannot be employed in large studies.

After an overnight fast, a single blood sample is taken for determination of blood glucose and plasma insulin. In healthy humans, the fasting condition represents a basal steady-state where glucose is homeostatically maintained in the normal range such that insulin levels are not significantly changing and HGP is constant.

In the diabetic state with fasting hyperglycemia, fasting insulin levels are inappropriately low and insufficient to maintain euglycemia.

Therefore, definitions of the more useful surrogate indexes take these considerations into account. Due to lack of a standardized insulin assay, it is not possible to use surrogate indexes to define universal cutoff points for insulin resistance.

If a direct measure of insulin sensitivity is not required, not feasible to obtain, or if insulin sensitivity is of secondary interest, it may be appropriate to use a surrogate index.

The relative merits and limitations of individual surrogate indexes are discussed below. HOMA, developed in , is a model of interactions between glucose and insulin dynamics that is then used to predict fasting steady-state glucose and insulin concentrations for a wide range of possible combinations of insulin resistance and β-cell function The model assumes a feedback loop between the liver and β-cell 43 , 44 , 45 ; glucose concentrations are regulated by insulin-dependent HGP while insulin levels depend on the pancreatic β-cell response to glucose concentrations.

Thus, deficient β-cell function reflects a diminished response to glucose-stimulated insulin secretion. Likewise, insulin resistance is reflected by diminished suppressive effect of insulin on HGP.

HOMA model describes this glucose-insulin homeostasis by a set of empirically derived non-linear equations. The model predicts fasting steady-state levels of plasma glucose and insulin for any given combination of pancreatic β-cell function and insulin sensitivity.

An important caveat for HOMA is that it imputes dynamic β-cell function i. In the absence of dynamic data, it is difficult, if not impossible, to determine the true dynamic function of β-cell insulin secretion.

In practical terms, most studies using HOMA employ an approximation described by a simple equation to determine a surrogate index of insulin resistance. This is defined by the product of the fasting glucose and fasting insulin divided by a constant. HOMA or Log HOMA is extensively used in large epidemiological studies, prospective clinical trials, and clinical research studies 45 , 46 , However, as discussed below, other surrogate indexes have certain advantages over HOMA or Log HOMA in some circumstances.

QUICKI is an empirically-derived mathematical transformation of fasting blood glucose and plasma insulin concentrations that provides a reliable, reproducible, and accurate index of insulin sensitivity with excellent positive predictive power 12 , 48 , 13 , 49 , Since fasting insulin levels have a non-normal skewed distribution, log transformation improves its linear correlation with SI clamp.

To accommodate these clinically important circumstances where fasting glucose is inappropriately high and insulin is inappropriately low, addition of log fasting glucose to log fasting insulin provides a reasonable correction such that the linear correlation with SI Clamp is maintained in both diabetic and non-diabetic subjects.

The reciprocal of this sum results in further transformation of the data generating an insulin sensitivity index that has a positive correlation with SI clamp. Log HOMA is roughly comparable to QUICKI in this regard. Multiple independent studies find excellent linear correlations between QUICKI and glucose clamp estimates either GIR or SI Clamp in healthy subjects, obesity, diabetes, hypertension, and many other insulin-resistant states 49 , 51 , 52 , 53 , 54 , 55 , QUICKI is among the most thoroughly evaluated and validated surrogate index for insulin sensitivity.

As a simple, useful, inexpensive, and minimally invasive surrogate for glucose clamp-derived measures of insulin sensitivity, QUICKI is appropriate and effective for use in large epidemiological or clinical research studies, to follow changes after therapeutic interventions, and for use in studies where evaluation of insulin sensitivity is not of primary interest.

Adipo-IR is a measure similar to HOMA-IR in that it is obtained from a fasting level of FFA and insulin product of FFA and insulin levels. Recent studies have shown that Adipo-IR correlates well with the gold standard measure of adipose tissue insulin sensitivity derived from one-step hyperinsulinemic-euglycemic clamp technique using a palmitate tracer Age and physical fitness were however shown to affect the predictive values.

Thus, Adipo-IR may be suitable for larger population studies, however the multistep pancreatic clamp technique is probably needed for mechanistic studies of adipose tissue insulin action.

Surrogate indexes of insulin sensitivity that use information derived from dynamic tests include OGTT, meal tolerance tests, and IVGTT. Procedures for these tests have been described in a previous section. Specific indexes including Matsuda index 58 , Stumvoll index 59 , Avignon index 60 , oral glucose insulin sensitivity index OGSI 61 , Gutt index 62 , and Belfiore index 63 use particular sampling protocols during the OGTT or the meal.

Glucose disposal of an oral glucose load or a meal is mediated by a complex dynamic process that includes gut absorption, glucose effectiveness, neurohormonal actions, incretin actions, insulin secretion, and metabolic actions of insulin that primarily determine the balance between peripheral glucose utilization and HGP.

Surrogate indexes that depend on dynamic testing take into account both fasting steady-state and dynamic post-glucose load plasma glucose and insulin levels. After an oral glucose challenge, the HGP is maximally suppressed for approximately 60 min and remains suppressed at a constant level for the subsequent 60— min time period.

Therefore, glucose uptake by peripheral tissues e. Recent studies comparing the OGTT-derived, tissue-specific surrogate indices hepatic insulin resistance index HIRI and muscle insulin sensitivity index MISI with clamp measurements showed that surrogate indices derived from an OGTT are accurate in predicting insulin sensitivity, but are not tissue-specific Studies using oral tracers in OGTT, with measurement of insulin sensitivity from OGTT and then comparing these to clamp measurements, would be crucial to ascertain the validity these measures.

Indeed, recent studies have shown that it is possible to measure hepatic insulin sensitivity in healthy volunteers and in prediabetes with the use of single tracer Many surrogate measures derived from dynamic data correlate reasonably well with glucose clamp estimates of insulin sensitivity 58 , 61 , Estimates of insulin sensitivity derived from OGTT predict the development of type 2 diabetes in epidemiologic studies 50 , 68 , The advantage of surrogates based on dynamic testing is that information about insulin secretion can be obtained at the same time as information about insulin action.

The oral route of glucose delivery is more physiological than intravenous glucose infusion. However, poor reproducibility of the OGTT and meal tolerance test due to variable glucose absorption, splanchnic glucose uptake, and additional incretin effects need to be considered.

Thus, distinguishing direct metabolic actions of insulin following oral ingestion of glucose or a mixed meal is more problematic than after FSIVGTT. In addition, as with many other measures of insulin sensitivity, surrogates derived from dynamic testing generally incorporate both peripheral and hepatic insulin sensitivity.

Although OGTT involves considerably less work than FSIVGTT, dynamic testing in general requires more effort and cost than fasting blood sampling. Hispanics, African Americans, and South Asians are highly prone to develop diabetes.

A meta-analysis showed that non-diabetic Africans have lower insulin sensitivity and higher insulin response after an intravenous glucose load compared to Caucasians and East Asians In a study that compared euglycemic hyperinsulinemic clamp derived glucose disposal rates GDR with HOMA-IR, QUICKI, and OGTT-derived indices, fasting insulin levels and HOMA-IR did not correlate with GDR whereas Matsuda index derived from OGTT significantly correlated with GDR in African American men Similarly, in another study in Afro-Caribbean adults, HOMA-IR did not correlate with insulin sensitivity calculated from FSIVGTT and M-value calculated from hyperinsulinemic euglycemic clamp Likewise, IR predictive ability of QUICKI and HOMA-IR was limited in Asian-Indian men Recent studies highlight that minimal model may underestimate insulin sensitivity between groups when acute insulin response AIR is higher in one group African Americans have reduced insulin clearance and higher AIR than Whites, suggesting that the minimal model may underestimate insulin sensitivity in African Americans Metabolomics is an interrogation and quantification of small-molecule metabolites in body fluids and tissues.

It aims at identifying and quantifying small molecules in the sample by either using mass spectrometry MS or nuclear magnetic resonance NMR spectroscopy. The details of the methodology and its application in diabetes research are beyond the scope of this chapter.

In this chapter, we will focus on new markers of insulin resistance that have been discovered using this approach. Using a non-targeted approach, Gall et al. metabolically profiled fasting plasma samples from non-diabetic, clinically healthy subjects Insulin sensitivity was measured using euglycemic hyperinsulinemic clamps.

Individuals in the bottom tertile of the cohort were designated as insulin-resistant. Among the candidate biomarkers identified, plasma α-hydroxybutyrate levels were inversely related to insulin sensitivity and this association was independent of age, sex and BMI.

Other metabolites such as linoleoyl-glycerophosphocholine L-GPC , glycine, and creatine were also highly correlated with insulin sensitivity. Using 26 metabolites from this study, the group went on to develop a model called Quantose algorithm to predict insulin resistance.

Fasting insulin, α-hydroxybutyrate, L-GPC and oleate levels were included in this model. Quantose IR as a fasting surrogate of insulin sensitivity was superior to other simple surrogate measures and was able to predict the progression from normal glucose tolerance to impaired glucose tolerance Branched chain amino acids BCAAs were found to significantly increase in obese compared to lean subjects and a BCAA based index correlated with HOMA The elevation of BCAA in subjects with impaired fasting glucose and diabetes has been confirmed in subsequent studies Lipoprotein insulin resistance score LPIR is a novel metabolomic biomarker based on nuclear magnetic resonance NMR quantification of lipoprotein levels and sizes.

This index has been shown to predict future type 2 diabetes mellitus is some cohorts LPIR is derived from the weighted score of six lipoproteins VLDL, LDL, and HDL sizes and concentrations that are more strongly related to IR than each of its individual subclasses A risk score of between is estimated, with a score of denoting being most insulin resistant.

These metabolomic studies are promising since they can measure hundreds of metabolites in a very small sample. However, the pricing, technology, and access, precludes its use clinically. Further studies using this approach are necessary in larger more heterogeneous cohorts to replicate and validate surrogate insulin resistance markers derived through metabolomics.

View in own window. G mean , mean plasma glucose concentration during OGTT; G o , plasma glucose concentration during fasting; G , plasma glucose concentration at min; G mean , mean plasma glucose concentration during OGTT; I mean , mean insulin concentration during OGTT; I o , plasma insulin concentration during fasting; I , plasma insulin concentration at min.

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Show details Feingold KR, Anawalt B, Blackman MR, et al. Contents www. Search term. Assessing Insulin Sensitivity and Resistance in Humans Ranganath Muniyappa , MD, PhD, Ritu Madan , MBBS, MD, and Ron T. Author Information and Affiliations Ranganath Muniyappa , MD, PhD Diabetes, Endocrinology and Obesity Branch, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD Email: vog.

liam rpayinum. Ritu Madan , MBBS, MD Diabetes, Endocrinology and Obesity Branch, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD Email: moc. liamg utirnaadam. Ron T. Varghese , MBBS Diabetes, Endocrinology and Obesity Branch, National Institutes of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.

Oral Glucose Tolerance Test OGTT The oral glucose tolerance test OGTT is a simple test widely used in clinical practice to diagnose glucose intolerance and type 2 diabetes Intravenous and Oral Tracer Studies The use of tracers for estimation of insulin sensitivity was first introduced in to overcome the shortcomings of FSIVGTT 37 The minimal model method does not allow segregation of glucose production from liver from exogenously administered glucose during calculations of insulin sensitivity and thus induces error in the insulin sensitivity calculations.

The Homeostasis Model Assessment HOMA HOMA, developed in , is a model of interactions between glucose and insulin dynamics that is then used to predict fasting steady-state glucose and insulin concentrations for a wide range of possible combinations of insulin resistance and β-cell function Quantitative Insulin Sensitivity Check Index QUICKI QUICKI is an empirically-derived mathematical transformation of fasting blood glucose and plasma insulin concentrations that provides a reliable, reproducible, and accurate index of insulin sensitivity with excellent positive predictive power 12 , 48 , 13 , 49 , Adipose Tissue Insulin Resistance Index Adipo-IR Adipo-IR is a measure similar to HOMA-IR in that it is obtained from a fasting level of FFA and insulin product of FFA and insulin levels.

Surrogates Derived from Dynamic Tests PROCEDURE Surrogate indexes of insulin sensitivity that use information derived from dynamic tests include OGTT, meal tolerance tests, and IVGTT. Further studies using this approach are necessary in larger more heterogeneous cohorts to replicate and validate surrogate insulin resistance markers derived through metabolomics Table 1.

Methods for Assessing Insulin Sensitivity and Resistance in Humans. S I : fractional glucose disappearance per insulin concentration unit; S G glucose effectiveness : ability of glucose per se to promote its own disposal and inhibit HGP in the absence of an incremental insulin effect i.

Reaven G. The insulin resistance syndrome: definition and dietary approaches to treatment. Annu Rev Nutr. Petersen K. The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome.

Proc Natl Acad Sci U S A. DeFronzo R. Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease.

Diabetes Care. Poirier P. Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism.

Muniyappa R. Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am J Physiol Endocrinol Metab.

Accili D. Lilly lecture the struggle for mastery in insulin action: from triumvirate to republic. Prodi E. Minireview: the brain as a molecular target for diabetic therapy. Cardiovascular actions of insulin. Endocr Rev. Kahn S. Mechanisms linking obesity to insulin resistance and type 2 diabetes.

Himsworth H. Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types. Int J Epidemiol. Glucose clamp technique: a method for quantifying insulin secretion and resistance.

Am J Physiol. Katz A. Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J Clin Endocrinol Metab. Chen H. Assessing the predictive accuracy of QUICKI as a surrogate index for insulin sensitivity using a calibration model.

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: Insulin sensitivity testing

Measuring Insulin Resistance | College of Medicine | MUSC Insulin is a hormone that your pancreas makes. If your healthcare team recommends increasing physical activity and losing weight, adding a mild-moderate exercise to your routine may help your body improve how it balances blood glucose levels and responds to insulin. Thus, distinguishing direct metabolic actions of insulin following oral ingestion of glucose or a mixed meal is more problematic than after FSIVGTT. Back to the Basics — One More Test for Insulin Resistance. Avignon A.
Insulin Test - powy.info Want to know your risk of prediabetes and diabetes? Locations Careers Investors Specialty labs Newsroom Connect With Us. There are available medications such as Metformin and Glucophage. Popular blood test General health blood test Use blood testing insights to improve your recovery time, cardio fitness, and metabolism. Its main function is to control the level of sugar glucose in your blood. Comparison of unlabeled and labeled exogenous glucose infusates.
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The relationship between glucose and insulin is quite complex and involves the interaction of many metabolic and regulatory factors. Normal insulin sensitivity varies widely and is influenced by age, ethnicity, and obesity.

Simply put, not all people with impaired insulin sensitivity are necessarily suffering from a disorder, and pregnancy is a perfect example of this. A World Health Organization consensus group recently concluded that the insulin sensitivity index SI of the lowest 25 percent of a general population can be considered insulin resistant.

The European Group for the Study of Insulin Resistance took a more restricted view, defining insulin resistance as the SI of the lowest 10 percent of a non-obese, nondiabetic, normotensive Caucasian population. Richard Legro and his associates also used the SI of the lowest 10 percent of an obese, non-PCOS population to define insulin resistance.

Ideally, we should be deriving the normal SI range from a population of women who are not obese, have regular menstrual cycles, are not suffering from hirsutism, and have normal circulating androgen levels.

The hyperinsulinemic-euglycemic clamp technique is the most scientifically sound technique for measuring insulin sensitivity, and it's against this standard that all other tests are usually compared. Because this and similar "clamp" techniques are expensive, time consuming, and labor intensive, they are not very practical in an office setting.

To overcome these obstacles, alternative tests have been developed, including the frequently sampled IV glucose tolerance test FSIVGTT , insulin tolerance test ITT , insulin sensitivity test IST , and continuous infusion of glucose with model assessment CIGMA.

Unfortunately, all of these methods require IV access and multiple venipunctures, making them relatively impractical for office assessment. The oral glucose tolerance test OGTT does not require IV access but does involve several venipunctures and 2 to 4 hours of patient and technician time.

Each of these tests has been shown to correlate reasonably well with dynamic clamp techniques. Hyperinsulinemic-euglycemic clamp : The gold standard for evaluating insulin sensitivity, this "clamp" technique requires a steady IV infusion of insulin to be administered in one arm.

The serum glucose level is "clamped" at a normal fasting concentration by administering a variable IV glucose infusion in the other arm. Numerous blood samplings are then taken to monitor serum glucose so that a steady "fasting" level can be maintained. In theory, the IV insulin infusion should completely suppress hepatic glucose production and not interfere with the test's ability to determine how sensitive target tissues are to the hormone.

The degree of insulin resistance should be inversely proportional to the glucose uptake by target tissues during the procedure. In other words, the less glucose that's taken up by tissues during the procedure, the more insulin resistant a patient is.

A variation of this technique, the hyperinsulinemic-hyperglycemic clamp provides a better measurement of pancreatic beta cell function but is less physiologic than the euglycemic technique.

Insulin sensitivity test IST : IST involves IV infusion of a defined glucose load and a fixed-rate infusion of insulin over approximately 3 hours.

Somatostatin may be infused simultaneously to prevent insulin secretion, inhibit hepatic gluconeogenesis, and delay secretion of counter-regulatory hormones— particularly glucagon, growth hormone, cortisol, and catecholamines.

Fewer blood samples are required for this test, compared to clamp techniques. The mean plasma glucose concentration over the last 30 minutes of the test reflects insulin sensitivity. Although lengthy, IST is less labor intensive than clamp techniques and the FSIVGTT.

Insulin tolerance test ITT : A simplified version of IST, ITT measures the decline in serum glucose after an IV bolus of regular insulin 0. Several insulin and glucose levels are sampled over the following 15 minutes depending on the protocol used. The ITT primarily measures insulin-stimulated uptake of glucose into skeletal muscle.

Because this test is so brief, there's very little danger of counter-regulatory hormones interfering with its results. When your glucose levels increase — like after you eat or drink — your pancreas responds by releasing a hormone called insulin. Insulin resistance, also known as impaired insulin sensitivity, occurs when your cells have difficulty responding to the hormone.

When this happens, the step-by-step process listed above can go askew and an insulin resistance test is necessary to detect it. If your cells develop an impaired response to insulin, your body may try to compensate by making more insulin. If your pancreas is able to make enough extra insulin to help glucose enter your cells, glucose levels may stay in check.

However, if your pancreas is unable to make enough insulin to keep up with demand, then it can cause:. Insulin resistance is not something that is commonly tested for. However, if prediabetes or type 2 diabetes is suspected, a doctor will perform an insulin resistance test. When you have an annual physical, the standard blood panel includes an FPG test, which makes it the most common type of insulin resistance test.

An OGTT is performed after an overnight fast. A healthcare professional starts by taking a blood sample, and then you are instructed to drink a high-glucose beverage.

Additional blood samples are taken at specific intervals for two to three hours, and the results are compared to analyze how your body processes glucose over time. This test is not used as often as others.

An RBG test measures your blood sugar at any time throughout the day, without the need for fasting. This test is performed when a quick diagnosis is necessary. According to the American Diabetes Association ADA , hemoglobin is a protein in red blood cells that carries oxygen to cells.

Glucose and hemoglobin can join together in the bloodstream, and the A1C test measures the percentage of hemoglobin that is coated with glucose. The CDC classifies the following results for each blood test:.

If this test shows high blood glucose, you will need an OGTT. The target ranges for gestational diabetes are lower than the ranges in the above table.

If you are diagnosed with prediabetes, the ADA recommends being checked for type 2 diabetes every years. The CDC reports that an excess amount of glucose in the bloodstream can be very damaging to the body. This can also lead to an increase in insulin, which signals to the liver and muscles that they should start storing glucose.

The liver sends excess glucose to fat cells, which can lead to weight gain. Prediabetes is considered a precursor for type 2 diabetes, where glucose levels are elevated above normal but not considered high enough for a diabetes diagnosis. Prediabetes develops in people who already have a resistance to insulin and also increases your risk of type 2 diabetes, cardiovascular disease, and stroke.

Just because you may have prediabetes does not mean you will develop type 2 diabetes. Type 2 diabetes develops from prediabetes, as insulin resistance is sustained. Type 2 diabetes often develops over years, but some people can manage their glucose levels through diet and lifestyle changes, preventing or delaying the need for glucose-lowering medications.

There are also other contributing factors to developing type 2 diabetes, including genetics, activity levels, and weight. Most commonly, type 2 diabetes develops in people over the age of However, the number of children, teenagers, and young adults who develop type 2 diabetes has been increasing in recent years.

The liver releases it when blood sugar levels are low, or when a person needs more energy. Insulin is essential for regulating blood sugar, ensuring that levels remain within certain limits, and stopping them from rising too high or falling too low. In the past , type 1 diabetes was a fatal condition.

After scientists discovered how to use insulin to treat diabetes , it became possible for people with diabetes to live full and productive lives. However, the person needs the right amount of additional insulin for the best effect.

The amount can vary over time and between individuals. The American Diabetes Association ADA note that careful blood glucose management may reduce the risk of complications for people with type 1 diabetes.

This article looks at ways of assessing how much additional insulin a person with type 1 diabetes needs in order to adjust their insulin dose to stay healthy. It also looks at ways of managing blood glucose levels when a person has type 2 diabetes. A person with diabetes needs to keep their blood sugar levels within a target range to stay healthy.

Insulin can stop blood sugar levels from rising to dangerously high levels. When a person takes insulin, their blood sugar levels fall. However, if blood sugar levels fall too far, this can be dangerous, too. A person with type 1 diabetes can use this number when deciding how much insulin they need to keep their blood sugar levels within the target range.

They will usually add this amount to their existing premeal insulin dose. According to the ADA, the target level should be as close as possible to the levels that a person without diabetes would have. Some people use an insulin pump. The pump delivers an amount of fast-acting insulin throughout the day and night and another amount of insulin for mealtimes.

People who use this type of pump can use a calculation to find out how much rapid-acting insulin they need to reduce blood sugar by a certain amount. The ADA give full instructions for deciding how much insulin a person needs when using an insulin pump. The individual should calculate this with the help of their healthcare provider.

Finally, the person should discuss the results with their healthcare provider before making any changes, especially for a child or a person with a recent diagnosis. For example, if a person is taking a total of 30 units of rapid-acting insulin through the day, they would calculate like this:.

The person will calculate like this:. For regular insulin, the person would divide into 1, instead of 1, However, most people do not use this type of insulin nowadays. If it is out of this range on two or more occasions, they may need to change their correction factor. The person should speak to their doctor about this.

They may need further testing to confirm the results. Anyone who believes they need to adjust their insulin sensitivity factor should speak to a healthcare provider before taking any action. Many things can affect insulin sensitivity factor during the day, so it is important to choose the right time of day to test.

The body of a person with type 1 diabetes cannot produce the insulin the person needs to regulate their blood sugar levels. According to the ADA, around 5 percent of people with diabetes have type 1 diabetes.

An insulin test is Healthy weight supplements blood test Insulin sensitivity testing helps evaluate insulin production by the beta cells in Healthy weight supplements Enhancing digestive function. An insulin test senitivity a blood test used to measure the sensitivit levels being produced sensitivjty your body. It is primarily used in one of the following ways:. Testing for insulin may be ordered with glucose and C-peptide tests. Insulin levels are also sometimes used with the glucose tolerance test GTT. In this situation, blood glucose and insulin levels are measured at pre-established intervals to evaluate insulin resistance. This test measures the amount of insulin in the blood — a hormone produced and stored in the beta cells of the pancreas.

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