Glucose tolerance test – wikipedia, the free encyclopedia, The glucose tolerance test is a medical test in which glucose is given and blood samples taken afterward to determine how quickly it is cleared from the blood. Glucose tolerance test: learn what the results mean, Glucose tolerance test, was a routine oral glucose tolerance test ordered to diagnose type 2 diabetes, and gestational diabetes.
Glucose tolerance test for gestational and type 2 diabetes, Learn more from webmd about the oral glucose tolerance test, which is used to diagnose prediabetes, diabetes, and gestational diabetes.. Glucose screening and tolerance tests during pregnancy, A glucose screening test is a routine test during pregnancy that checks a pregnant woman’s blood glucose (sugar) level. Hyperglycemia is directly connected with the development of microvascular complications, and also is an important factor of macrovascular complications. It has recently been shown that all these processes are connected with superoxide excess formed by oxidative phosphorylation substrate excess (29).
In healthy individuals, postprandial insulin secretion is biphasic: the first, fast phase is present during the first ten minutes after stimulus, followed by the second, slow phase which can last for several hours (31).
In patients with type I diabetes, absolute insulinopenia is present with dependence on exogenous insulin.
According to the stated facts, postprandial hyperglycemia can be analyzed as a dual problem: postprandial hyperglycemia (still within the reference values of blood glucose in terms of diagnosing diabetes) reflects insulin resistance.
Postprandial hyperglycemia should be treated in patients with diabetes, and especially in pregnant women, as it can be the only sign of inappropriate regulation and a precipitating factor for complications or fetal macrosomy (37-39). A single fasting blood glucose level is of limited value in estimation of long-term glycemic regulation (40). With the development of blood glucose measurement devices, this method of self-control is becoming less popular among patients as well as among physicians. Glycosylated hemoglobin value currently is the standard method of estimating long-term glycemic control. From DCCT it has been established that decreasing the glycosylated hemoglobin value also decreases the progression of chronic complications.
Body weight is one of the general indicators of metabolic regulation for individuals with diabetes. Complying with the basic rules of diabetic diet and intensified insulin therapy remains the crucial principle in the treatment of type I diabetes. Because of defect or absent first phase insulin secretion in type II diabetic patients, certain modifications in their diet are required. Self-control of postprandial glycemia or glycosuria should indicate the critical meals where with additional modification better glycemic control could be achieved. Acarbose is an inhibitor of alpha-glucosidase, an enzyme that breaks down oligosaccharides and disaccharides into monosaccharides. Postprandial glycemia in patients treated with diet and exercise before and after introduction of acarbose. Acarbose is indicated in the treatment of postprandial hyperglycemia in insulin treated patients in whom postprandial hyperglycemia cannot be resolved with adjustment of insulin dose, administration interval, or diet. The disadvantage of these agents is their prolonged action, as they stimulate beta cells permanently, not only after meals when it is required. The main advantage of repaglinide is short duration of action, lasting only for the meal it is taken with.
Insulin treatment in type I diabetes has to substitute for both basal and postprandial insulin secretion. Some individuals with type II diabetes are not able to achieve satisfactory glycemic regulation with diet and oral hypoglycemic agents, or develop secondary failure to oral agents, and insulin treatment becomes necessary. There is only one long acting insulin preparation registered in Croatia (Ultratard), while in EU countries a long acting human insulin analogue (Glargin) is also available.
Another possible strategy in insulin treatment of postprandial glycemia in type II patients is the use of ultrashortacting insulins. They have proven especially useful for the regulation of postprandial hyperglycemia in patients with preserved residual beta cell function (77). Insulin resistance is part of the metabolic syndrome (visceral obesity, hyperlipoproteinemia, and hypertension) that bears a high risk for atherosclerosis and consecutive ischemic diseases. For individuals with type II diabetes and those with impaired glucose tolerance, the primary therapeutic measures are carbohydrate diet with low glycemic index and exercise (especially after the meals, which can decrease postprandial hyperglycemia). There has not yet been enough evidence for the use of medications to decrease postprandial hyperglycemia in patients with impaired glucose tolerance, although there are some implications that suggest a favorable prognostic effect. In individuals with type I diabetes, standard treatment should be basal-bolus insulin administration.
In individuals with type II diabetes and secondary failure to oral agents, two strategies of insulin therapy are possible. Figures 7 and 8 show schematically the approach to the problem of postprandial hyperglycemia. Stratton IM, Adler AI, Neil HAW, Matthews DR, Manley SE, Cull CA, Hadden D, Turner RC, Holman RR on behalf of the UK Prospective Diabetes Study Group. Hanefeld M, Fischer S, Julius U, Schulze J, Schwanebeck U, Schmechel H, Ziegelasch HJ, Lindner J.
Polonsky KS, Given BD, Hirsch LJ, Tillil H, Shapiro ET, Beebe C, Frank BH, Galloway JA, Van Cauter E. Chiasson JL, Josse RG, Hunt JA, Palmason C, Rodger NW, Ross SA, Ryan EA, Tan MH, Wolever TM. Moses R, Slobodniuk R, Boyages S, Colagiuri S, Kidson W, Carter J, Donnelly T, Moffitt P, Hopkins H. Del Sindaco P, Ciofetta M, Lalli C, Perriello G, Pampanelli S, Torlone E, Brunetti P, Bolli GB.
Pampanelli S, Torlone E, Ialli C, Del Sindaco P, Ciofetta M, Lepore M, Bartocci L, Brunetti P, Bolli GB. Maintaining glycemia within certain levels can prevent the development of chronic complications. The risk of developing microvascular complications is already present at glycosylated hemoglobin values slightly above the normal range and progressively increases with hyperglycemia (4).
This process could be connected with the previous finding of postprandial free radical excess (30), and provide a biochemical basis for the role of postprandial hyperglycemia control in preventing endothelial damage. The first, fast phase is accomplished by insulin release from the secretory granula adjacent to the cell membrane, whereas insulin from the second phase comes from the more internal granula, and partly from the newly synthesized insulin.
Availability of simple and precise methods for self-control of blood glucose has allowed for an increased and more active role of the patient in taking care of himself. While a single blood glucose value reflects only the actual blood glucose level, urine glucose can reflect blood glucose values between two voidings. Nonenzymatic glycosylation is dependent of blood glucose concentration and duration of exposure, so glycosylated hemoglobin value confirms the average glycemic regulation during the lifetime of erythrocytes (100-120 days). Diurnal correlation of HbA1c and glycemia in 100 persons with type II diabetes (the best correlation between Hb1c and postprandial glycemia, i.e.
The limiting factor in achieving good regulation are hypoglycemic episodes, so target values for glycosylated hemoglobin in diabetes patients are slightly higher than the reference values in the healthy population, which implies tolerating higher glycemic values occasionally. Moderate body weight loss may have beneficial effect on glycemic regulation by lowering the peripheral insulin resistance and insulin demand, at the same time improving the beta cell function. As endogenous insulin production is practically absent, it is necessary to adjust the time of meal and time of insulin application as well as calorie intake with insulin doses. Omitting concentrated carbohydrates and dividing daily caloric requirements into several small meals are aimed at lowering insulin demand in the first phase.
Additional exercise after the critical meal is also an option to decrease postprandial hyperglycemia (44).


By delaying digestion, the resorption of carbohydrates is delayed as well, and consequently the postprandial glycemia decreases. It can also be used as monotherapy in newly detected patients with type II diabetes who still have satisfactory fasting glycemia but high postprandial values, or as adjuvant to sulphonylurea, metformin or insulin in patients with mild fasting but significant postprandial hyperglycemia and high values of glycosylated hemoglobin.
It has no direct effect on beta cells, but compensates for peripheral insulin resistance, primarily in muscles (52-54). About 25% of patients treated with metformin as monotherapy achieved satisfying glycemic regulation (56). Upon receptor activation, cell membrane depolarization follows and calcium enters the cell, which causes translocation of secretory granula to the membrane and insulin secretion (61). A high secondary failure rate is present in patients treated with sulphonylureas: 5%-7% each year, and after 10 years practically all patients need addition of another oral agent or insulin (66,67). Repaglinide permits more liberty in timing the meals, and probably induces less beta-cell exhaustion. The need to distinguish between the basal and postprandial insulin requirements has been known for more than twenty years now (70). A certain level of endogenous insulin production is preserved in a major proportion of patients, however, it is inadequate to overcome insulin resistance.
One evening dose is sufficient to maintain basal insulinemia during the night and part of the next day, with the peak action in the morning hours of the next day. Ultrashortacting human insulin analogue (lispro is registered in Croatia, while aspart insulin is also registered in other countries) is more fastly absorbed, and maximal serum concentration is faster achieved. Blood glucose profile in a patient on intensified insulin therapy with regular insulin and human insulin analogue lispro. In these individuals, postprandial hyperglycemia in terms of impaired glucose tolerance is frequently present. If these measures fail, in type II diabetes oral agents can be used, either non-betacytotropic (acarbose, metformin), or betacytotropic (sulphonylurea, repaglinide). One dose of long acting or several doses of intermediate acting insulin can be used to cover the basal secretion and are likely to improve endogenous secretion after prandial stimulation.
The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus.
The absence of a glycemic threshold for the development of long-term complications: the perspective of the Diabetes Control and Complications Trial. High blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men.
The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.
The effect of intensive diabetes therapy on measures of autonomic nervous system function in the Diabetes Control and Complications Trial (DCCT). Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin-dependent diabetes mellitus: a randomized prospective 6-year study. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study.
Oral glucose tolerance and its relationship to overweight and other cardiovascular risk factors in men aged 33-42. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose: the Funagata Diabetes Study. Hyperglycaemia is associated with all-cause and cardiovascular mortality in the Hoorn population: the Hoorn Study.
Isolated postchallenge hyperglycemia and the risk of fatal cardiovascular disease in older women and men: the Rancho Bernardo Study. Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11-year follow-up. Impaired postprandial tissue regulation of blood flow in insulin resistance: a determinant of cardiovascular risk?
Triglyceride-rich lipoproteins in non-insulin-dependent diabetes mellitus: post-prandial metabolism and relation to premature atherosclerosis. Relative contribution of insulin and its precursors to fibrinogen and PAI-1 in a large population with different states of glucose tolerance: the Insulin Resistance Atherosclerosis Study (IRAS). Activation of the tissue factor pathway of blood coagulation during prolonged hyperglycemia in young healthy men.
Demonstration that polyol accumulation is responsible for diabetic cataract by use of transgenic mice expressing the aldose reductase gene in the lens.
Normalizing mitochondrial superoxide production blocks three patways of hypeglycemic damage.
Effect of hyperglycaemia on arterial pressure, plasma renin activity and renal function in early diabetes. In vivo beta-cell function at the transition to early non-insulin-dependent diabetes mellitus.
Loss of the first phase insulin response to intravenous glucose in subjects with persistent impaired glucose tolerance.
Prolonged exposure of human beta cells to elevated glucose levels results in sustained cellular activation leading to a loss of glucose regulation.
Risk factors for fetal macrosomia: the importance of a positive oral glucose challenge test. Treatment of women with an abnormal glucose challenge test (but a normal oral glucose tolerance test) decreases the prevalence of macrosomia. Postprandial plasma glucose: a good index of glycemic control in type 2 diabetic patients having near-normal fasting glucose levels. Nonfasting plasma glucose is a better marker of diabetic control than fasting plasma glucose in type 2 diabetes. Minimal influence of the time interval between injection of regular insulin and food intake on blood glucose control of type 1 diabetic patients on a basal-bolus insulin scheme. The efficacy of acarbose in the treatment of patients with non-insulin-dependent diabetes mellitus. Reduction of glycosylated hemoglobin and postprandial hyperglycemia by acarbose in patients with NIDDM. A comparison of acarbose versus metformin as an adjuvant therapy in sulfonylurea-treated NIDDM patients.
The impact of metformin therapy on hepatic glucose production and skeletal muscle glycogen synthase activity in overweight type II diabetic patients.
Efficacy of metformin in type II diabetes: results of a double-blind, placebo-controlled, dose-response trial. Effect of metformin on postprandial lipemia in patients with fairly to poorly controlled NIDDM. The effect of chronic sulfonylurea therapy on hepatic glucose production in non-insulin-dependent diabetes. Efficacy, safety, and dose-response characteristics of glipizide gastrointestinal therapeutic system on glycemic control and insulin secretion in NIDDM. Secondary failures in modern therapy of diabetes mellitus with blood glucose lowering sulfonamides. United Kingdom Prospective Diabetes Study 24: a 6-year, randomized, controlled trial comparing sulfonylurea, insulin, and metformin therapy in patients with newly diagnosed type 2 diabetes that could not be controlled with diet therapy.
Stimulation of insulin release by repaglinide and glibenclamide involves both common and distinct processes.


Effect of repaglinide addition to metformin monotherapy on glycemic control in patients with type 2 diabetes. Use of the short-acting insulin analogue lispro in intensive treatment of type 1 diabetes mellitus: importance of appropriate replacement of basal insulin and time-interval injection-meal. Insulin lispro (Humalog), the first marketed insulin analogue: indications, contraindications and need for further study. Improved postprandial metabolic control after subcutaneous injection of a short-acting insulin analog in IDDM of short duration with residual pancreatic beta-cell function. The cause of hyperglycemia in type I diabetes is absolute insulinopenia, whereas in type II the postprandial rise in glycemia is influenced by glucose influx from the gut, nonsuppressed hepatic glucose production and secretion, decreased muscular glucose uptake, and diminished insulin secretion (2,3) (Figs.
Results of a meta-analysis show that the cardiovascular mortality risk increases with end-point glucose value of 120-minute oral glucose tolerance test in individuals without diabetes (5), which points to the significance of postprandial hyperglycemia as a risk factor.
One of the first defects in insulin secretion seen in the course of diabetes (and already in impaired glucose tolerance) is the loss of the first phase of insulin secretion (2,32,33). With strict glycemic control, it is possible to significantly reduce the incidence of chronic complications (6). Insulin resistance accompanied by hyperlipoproteinemia, hypertension and visceral obesity constitute the so-called metabolic syndrome (36). Devices for self-monitoring of blood glucose have enabled the patient to perform multiple daily controls and provided him with a better overview of the treatment effects.
The only drawback is that the renal threshold for glucose must be estimated by parallel measurements of blood and urine glucose levels. This fact probably conceals the reason for decreasing the frequency of chronic complications, and not banishing them completely. On the other hand, unwanted weight loss in individuals with diabetes is a sign of particularly poor glycemic regulation. A shorter interval between insulin application and meal is better reflected in postprandial glycemic levels than in glycosylated hemoglobin values (43).
Regular exercise decreases insulin requirement and consequently indirectly acts on glycemic regulation.
With decreased insulin resistance, the beta cell function improves, and with decreased insulin demand the capability of the first phase secretion returns. Insulin is secreted into portal circulation, where it enters the liver and reduces hepatic glucose production, and later upon entering the systemic circulation reduces postprandial hyperglycemia (62,63). Likewise sulphonylureas, it induces beta cell depolarization and exocytosis of secretory granula, but it binds to a different region of the receptor.
Finally, the results of DCCT have undoubtedly proved the importance of good glycemic regulation in individuals with type I diabetes.
If a patient with preserved endogenous insulin secretion (yet not sufficient to maintain satisfactory glycemic regulation) receives his basal secretion as a substitute, it is possible that his own endogenous secretion will be sufficient to cover the postprandial insulin demands (Fig. Duration of action is also shorter than with regular human insulin, so the overall plasma profile is better matching that of endogenous insulin (74). Insulin secretion is stimulated by the increase of glycemia within the physiologic boundaries, but with high glycemia the stimulation fails (glucotoxicity). Repaglinide is better in stimulating the first phase insulin response and has short duration of action, therefore it is indicated in patients who have postprandial hypoglycemia on sulphonylureas.
Ultrashortacting human insulin analogues (lispro) can be used if regular insulin fails to produce a satisfactory glycemic regulation. The use of regular insulin or ultrashortacting analogue is aimed to eliminate postprandial hyperglycemia, and to improve endogenous secretion to cover the basal needs between the meals. 20-year follow-up in the Whitehall Study, the Paris Prospective Study, and the Helsinki Policemen Study.
A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential. Results of large clinical trials show that strict glycemic control can significantly decrease the risk of developing chronic complications of diabetes (6-10).
As exactly the fast insulin secretion reduces postprandial hyperglycemia, the first apparent defect is postprandial hyperglycemia, which is the principle of oral glucose tolerance test. Glycemic regulation in the Diabetes Control and Complications Trial (DCCT) was estimated by the values of glycosylated hemoglobin, which reflect the mean glycemic levels during the preceding 3 months.
In everyday situations, it is important not to lie down but to do some exercise for 15 to 30 minutes after the meal (45).
Intensified insulin therapy should be suggested to all individuals with type I diabetes who understand the goals and are able to handle the procedures involved.
However, the problem of the right timing of the administration remains, as does the problem of overdosage and hypoglycemia. Furthermore, it can be added to metformin in obese patients who have postprandial hyperglycemia. There is yet no evidence that any of these strategies has advantage over the other, therefore it should be chosen for each patient individually, changes being permitted. Human ultralente insulin: a comparison with porcine lente insulin as a twice-daily insulin in insulin-dependent diabetic patients with fasting hyperglycaemia. Deficiency in the second phase response becomes evident later in the developed phase of type II diabetes (34). Episodes of hypoglycemia were the limiting factor in achieving as good a glycemic regulation as in healthy individuals. Development of new possibilities of storing the results (memorizing by the device) can greatly facilitate the results tracking.
Therefore, the measurement of urine glucose and ketone bodies should be regarded as a valuable auxiliary method for the estimate of glycemic regulation. Technical resources (injecting devices and devices for self-control) are available to patients as well as a specific health care as a necessary component. The use of ultrashortacting analogues of human insulin additionally improves intensified insulin therapy, as it shortens the interval between its administration and the meal, decreases the frequency of hypoglycemia, and is able to improve glycemic regulation (75,76) (Fig.
Stimulation of insulin secretion is of shorter duration than with sulphonylureas, which is favorable for the regulation of body weight. It is important to note that patients randomized in the conventional treatment group in DCCT with the same levels of glycosylated hemoglobin had faster progression of retinopathy than the intensified group. Some of the devices have the necessary software to transfer the results into a PC and then to analyze them, which can also facilitate the estimate of glycemic control. Metformin is primarily indicated in obese patients with marked insulin resistance, where it is the drug of choice. Hypoglycemia episodes are also less frequent, because of the short duration of action and mainly renal excretion. This suggests the importance of postprandial control of hyperglycemia, which is better targeted with basal-bolus treatment.
The newer techniques of bloodless glucose measurement are slowly entering the routine use, for the time being with some limitations (41). During the evolution of type II diabetes, the first apparent defect is the loss of the first phase insulin secretion (35), which results in postprandial hyperglycemia with preserved glycemia in fasting and between the meals. Insulin secretion from beta cells after stimulation with glucose becomes sluggish and insufficient, while basal and maximal insulin secretion remain within the normal limits but with blood glucose rise (34).



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Control of blood glucose levels


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