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Diagnosing Insulin Resistance

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Last Updated: 02 July 2021

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General | Latest Info

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.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

What Is Insulin Resistance?

When you have insulin resistance, your pancreas makes extra insulin to make up for it. For a while, this will work and your blood sugar levels will stay normal. Over time, though, your pancreas wo be able to keep up. If you do make changes in the way you eat and exercise, your blood sugar levels will rise until you have prediabetes. Your doctor will look for these blood test results: fasting Plasma Glucose Test: 100 - 125 oral Glucose Tolerance Test: 140 - 199 after second Test A1C results of 5. 7% to 6. 4% If you are able to manage prediabetes, you will be diagnosed with type 2 diabetes when your test levels reach: fasting Plasma Glucose Test: 126 or higher oral Glucose Tolerance Test: 200 or higher after second Test A1C results of 6. 5% or above

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

RESEARCH DESIGN AND METHODS

Background: Assessing pediatric patients for insulin resistance is one way to identify those who are at high risk of developing type 2 diabetes mellitus. Homoeostasis model assessment is a measure of insulin resistance based on fasting blood glucose and insulin levels. Although this measure is widely used in research, cutoff values for pediatric populations have not been establish. Objective: To assess the validity of HOMA cutoff values used in pediatric studies published in peer - review journals. Methods: Studies published from January 2010 to December 2015 were identified through MEDLINE. Initial screening of abstracts was done to select studies that were conducted in pediatric populations and use HOMA to assess insulin resistance. A subsequent full - text review narrowed the list to only those studies that use specific HOMA score to diagnose insulin resistance. Each study was classified as using a predetermined fix HOMA cutoff value or cutoff that was percentile specific to that population. For studies that use predetermined cutoff value, references cited to provide evidence in support of that cutoff were evaluate. Results: in 298 articles analyze, 51 different HOMA cutoff values were used to classify patients as having insulin resistance. Two hundred fifty - five studies use predetermined fix cutoff value, but only 72 of those studies provide reference that support its use. One hundred ten studies that use fix cutoff either cite studies that do not mention HOMA or provide no reference at all. Tracing of citation history indicates that the most commonly used cutoff values were ultimately based on studies that do not validate their use for defining insulin resistance. Conclusion: Little evidence exists to support HOMA cutoff values commonly used to define insulin resistance in pediatric studies. These findings highlight the importance of validating study design elements when training medical students and novice investigators. Using available data to generate population ranges for HOMA would improve its clinical utility.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

CONCLUSIONS

Predicting Insulin Sensitivity in normoglycemic individuals is important, as diabetes intervention programs are more likely to be successful at this stage rather than after development of impaired Glucose tolerance. Most studies have investigated predictors of Insulin Resistance; however, almost all studies have included people with IGT and diabetes, rather than normoglycemic individuals in the general population. In our study, fasting Insulin alone was as accurate at predicting Insulin Resistance in normoglycemic population as HOMA, Insulin - to - Glucose Ratio, and Bennett Index. Our finding is comparable with that of Laakso, who demonstrated that fasting Insulin alone was less variable and had higher correlation with ISI in individuals with normoglycemia than in individuals with IGT and diabetes. Thus, any method to predict Insulin Sensitivity in normoglycemic individuals should be compared with fasting Insulin. Cross - reactivity with proinsulin is unlikely to alter these findings, because proinsulin levels are low in Insulin - resistant normoglycemic individuals, and the pattern of response is similar to that of specific Insulin. A number of clinical and metabolic abnormalities have been associated with Insulin Resistance. Mykkanen et al. It has been confirmed that Low Insulin Sensitivity is associated with clusters of metabolic disorders and that ISI decreases with increased number of disorders. Metabolic disorders were classified as dyslipidemia, hypertension, and IGT. Howard et al. Compare several alternative methods for measuring Insulin Sensitivity to predict cardiovascular risk. Many methods, including the modified Galvin method and other methods based on frequently sampled IVGTT, are invasive and time - consuming, and they are not appropriate for general population screening. However, they do confirm that the best method was dependent on glucose status. Galvin and HOMA methods were most useful across all glucose levels. In addition, data for individuals with normal Glucose tolerance from these two methods were consistent with our own method, showing that fasting Insulin was as good, if not better, than HOMA, Insulin - to - Glucose Ratio, or Bennett Index. Berglund and Lithell have used BMI and either triglycerides or serum alanine - amino transferase to predict Insulin Resistance in hypertensive patients. They find either combination to be as useful as fasting Insulin, but they do not add fasting Insulin to either combination. However, glucose status was not reported in all of the groups they evaluate. More recently, Strumvoll et al. Assess 104 nondiabetic individuals to determine whether age, BMI, WHR, and Glucose and Insulin levels during oral Glucose tolerance test could predict Insulin Sensitivity. They find that BMI, Insulin at 120 min, and Glucose at 90 min best predict Insulin Sensitivity. These parameters appear robust in individuals with normal Glucose tolerance, as well as in individuals with IGT. Other studies have not found 120 - min Insulin measurement as useful as fasting Insulin measurement. It is worth noting that in Strumvoll et al. Study, correlation coefficient between fasting Insulin and ISI was remarkably similar to that between ISI and 120 - min Insulin, suggesting little difference between fasting Insulin and 120 - min Insulin as predictors.


Insulin Resistance in Children

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. 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.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Overview

Insulin Resistance is a state in which give concentration of Insulin produces less - than - expected biological effect. Insulin Resistance has also been arbitrarily defined as a requirement of 200 or more units of Insulin per day to attain glycemic control and to prevent ketosis. Syndromes of Insulin Resistance actually make up the broad clinical spectrum, which includes obesity, Glucose intolerance, Diabetes, and Metabolic Syndrome, as well as extreme Insulin - resistant state. Many of these disorders are associated with various endocrine, metabolic, and genetic conditions. These syndromes may also be associated with immunological diseases and may exhibit distinct phenotypic characteristics. Metabolic Syndrome state of Insulin - Resistance that is also know as either Syndrome X or dysmetabolic syndromehas drawn the greatest attention because of its public health importance. Prevalence of hypertension rises with exacerbation of stages of impaired Glucose metabolism;. However, only in early stages of impaired Insulin metabolism do hyperglycemia and hyperinsulinemia appear to be significant contributors to the presence of hypertension. In addition to hypertension, findings can include central obesity, peripheral arterial disease, Type Syndrome, Type B Syndrome, ancanthosis nigricans, polycystic ovary Syndrome, and other Insulin - resistant States. In clinical practice, no single laboratory test is used to diagnose Insulin Resistance Syndrome. Diagnosis is based on clinical findings that corroborate with laboratory tests. Individual patients are screened based on presence of comorbid conditions. Laboratory tests include plasma Glucose level, fasting Insulin level, and lipid profile, among others. Treatment involves pharmacologic therapy to reduce Insulin Resistance, along with surgical management of underlying causes if appropriate. Comorbid conditions should be evaluated and address; this is generally feasible on an outpatient basis, though some patients will require admission. Metabolic Syndrome requires aggressive control of cardiovascular and metabolic risk factors. Modifications to diet and activity are recommend. Medications that reduce Insulin Resistance include metformin and thiazolidinediones. Go to Diabetes Mellitus, Type 1 and Diabetes Mellitus, Type 2 for complete information on these topics.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Fasting blood glucose test

Table

ResultA1C
Normalless than 5.7%
Prediabetes5.7% to 6.4%
Diabetes6.5% or higher

Participants were recruited by voluntary participation through advertising among hospital staff and personnel. Sample selection was performed using a random sampling method. After clinical screening, only healthy subjects with inclusion criteria were randomized into study. A total of 65 subjects, 44 men and 21 women aged 30 - 60 years, were study. Following inclusion criteria were used in this study: normal glucose metabolism, fasting plasma triglyceride level < 2. 25 mmol / l, and general analytical evaluation within normal limits. All subjects were nonsmokers and were not taking any medications. Alcohol consumption was < 35 g per day. Body weight and physical activity habits had been stable for 3 months preceding study. Following exclusion criteria were used in this study: age outside the range of 30 - 60 years, consumption of hypocaloric diet, or weight gain or loss > 10% in 3 months preceding study. Other exclusion criteria include hypothyroidism; liver, kidney, or heart failure; and neoplasia. Clinical history was obtained from all subjects, including age, sex, personal medical history, intake of drugs, smoking and alcohol consumption, levels of physical exercise, previous history of high blood pressure or Diabetes, and symptoms of coronary heart disease, ischemic stroke, or peripheral vascular disease. Family history of high blood pressure, diabetes, coronary heart disease, or dyslipidemia was also ascertain. In all participants, blood pressure was measured after a 10 - min rest period, and readings were recorded at 5 - min intervals. Body weight and height, BMI, and waist circumference were measured using standard methods. Blood samples were collected after 12 - h overnight fast and deposited in dry tubes with EDTA. The plasma was separated immediately using refrigerated centrifugation at 2 500 - 3 000 rpm for a period of 10 min. Samples were processed either immediately or during the first week after conservation at 20C. As previously describe, plasma total cholesterol, triglyceride, free fatty acid, and glucose levels were determined using enzymatic methods; HDL cholesterol was measured after precipitation with polyanions. Apolipoprotein B was determined by immunoturbidimetry and insulin by radioimmunoassay. All tests were performed in the Metabolic Unit near the laboratory with a clinician or nurse in attendance, in accordance with standard procedures. The Intravenous glucose tolerance test, with extraction of multiple blood samples for measurement of glucose and insulin levels, calculation of MMAMG indexes of S i, and use of glucose independent of insulin, was conducted after 12 - h fast and with patient resting supine for at least 15 min before initiation of test. Two baseline venous blood samples for measurement of plasma glucose and insulin levels were collect. At t = 0, bolus of 300 mg glucose / kg body wt in 50% glucose - saline solution was administered over a period of 60 S. At t = 20 min, bolus of 0. 03 units / kg wt of regular insulin was administered intravenously.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

Table2

ResultFasting Plasma Glucose (FPG)
Normalless than 100 mg/dl
Prediabetes100 mg/dl to 125 mg/dl
Diabetes126 mg/dl or higher

Table3

ResultOral Glucose Tolerance Test (OGTT)
Normalless than 140 mg/dl
Prediabetes140 mg/dl to 199 mg/dl
Diabetes200 mg/dl or higher
* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Lab Studies

Homeostasis model assessment was first developed in 1985 by Matthews et al. It is a method used to quantify insulin resistance and beta - cell function from basal glucose and insulin concentrations. Homa is a model of the relationship of glucose and insulin dynamics that predicts fasting steady - state glucose and insulin concentrations for a wide range of possible combinations of insulin resistance and - cell function. Insulin levels depend on pancreatic - cell response to glucose concentrations while, glucose concentrations are regulated by insulin - mediate glucose production via liver. Thus, deficient - cell function will echo diminished response of - cell to glucose - stimulate insulin secretion. Similarly, insulin resistance is reflected by the diminished suppressive effect of insulin on hepatic glucose production. The HOMA model has proven to be a robust clinical and epidemiological tool for assessment of insulin resistance. Homa describes this glucose - insulin homeostasis by means of a set of simple, mathematically - derive nonlinear equations. Approximating equations for insulin resistance have been simplify; it uses fasting blood sample. It is derived from the use of insulin - glucose product, divided by constant. Product of FPG FPI is INDEX of hepatic insulin resistance. Ir HOMA = I 0 /; girls: Normal weight 1. 21 1. 10 versus overweight 3. 19 2. 02 versus obese 4. 19 2. 52, p < 0. 0001 between all groups.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Other Tests

This test measures the amount of insulin in your blood. Insulin is a hormone that helps move blood sugar, known as glucose, from your bloodstream into your cells. Glucose comes from foods you eat and drink. It is your body's main source of energy. Insulin plays a key role in keeping glucose at the right levels. If glucose levels are too high or too low, it can cause serious health problems. Glucose levels that are not normal are known as: hyperglycemia, blood glucose levels that are too high. It happens when your body doesn't make enough insulin. If there's not enough insulin, glucose can't get into your cells. It stays in the bloodstream instead. Hypoglycemia, blood glucose levels that are too low. If your body sends too much insulin into the blood, too much glucose will go into your cells. This leaves less in the bloodstream. Diabetes is the most common cause of abnormal glucose levels. There are two types of diabetes. Type 1 Diabetes. If you have type 1 Diabetes, your body makes little or no insulin at all. This can cause hyperglycemia. Type 2 Diabetes. If you have type 2 Diabetes, your body may still be able to make insulin, but cells in your body don't respond well to insulin and can't easily take up enough glucose from your blood. This is called insulin resistance. Insulin resistance often develops before type 2 Diabetes. At first, insulin resistance causes the body to make extra insulin, to make up for ineffective insulin. Extra insulin in the bloodstream can cause hypoglycemia. But insulin resistance tends to get worse over time. Eventually, it decreases your body's ability to make insulin. As insulin levels drop, blood sugar levels rise. If levels don't return to normal, you may get type 2 Diabetes. Other names: fasting insulin, insulin serum, total and free insulin

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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