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• W2041797130 abstract "Type 2 diabetes is associated with increased mortality, especially from macrovascular complications. The United Kingdom Prospective Diabetes Study (UKPDS) outlined the importance of intensive glycaemic control to reduce the risk of diabetic complications.1 However, our current therapeutic approaches to controlling hyperglycaemia are inadequate, with as many as 50% of patients not meeting glycaemic control targets. In the past, these targets have been defined by HbA1c. Evidence suggests that control of postprandial hyperglycaemia (glucose peaks) may be just as important as reducing fasting glycaemic levels. The role of postprandial hyperglycaemia is gaining importance as the primary association between this perturbation and the risk of developing diabetic complications becomes apparent. This review discusses the clinical implications of postprandial hyperglycaemia in the pathogenesis of diabetic complications, as well as the impact of hyperglycaemia on the risk of cardiovascular complications and mortality in patients with type 2 diabetes. Type 2 diabetes is characterised by insufficient production of insulin by pancreatic β-cells and reduced target-tissue sensitivity to the effects of insulin (insulin resistance). An important defect in insulin secretion is the impairment of early-phase insulin release, which is always present in type 2 diabetic patients and occurs early in the development of this disease.2 In normal individuals, the early phase is a burst of insulin release beginning within minutes of glycaemic stimulus. Early-phase insulin primes tissues that are sensitive to it, in particular the liver, 3 resulting in reduction of hepatic glucose output. In patients with impaired glucose tolerance, the early-phase insulin response to glucose is reduced, and in type 2 diabetic patients it is both delayed and blunted.4 The loss of early-phase insulin release during and after the prandial phase has several deleterious effects on normal glucose homeostasis including hepatic glycogenolysis and gluconeogenesis, and insufficient muscle glucose uptake. This leads to the postprandial hyperglycaemia observed in glucose intolerant and type 2 diabetic patients.5 While attention is usually focused on the pathogenic effects of chronic hyperglycaemia indicated by high fasting glucose, acute and transient increases in blood glucose, particularly in the postprandial state, should not be overlooked. The mechanisms by which postprandial hyperglycaemia causes tissue damage are complex. Damage occurs through mechanisms shared with, and in addition to, those related to basal hyperglycaemia (Figure 1). The pathogenic role of chronic and acute hyperglycaemia in the development of diabetic complications. Postprandial hyperglycaemia is implicated in increased production of free radicals through the glycation of amino acids, leading to oxidative stress – a known pathogenic factor in diabetic complications.6 Evidence shows that damage to the endothelium of blood vessels resulting from postprandial hyperglycaemia may be caused through a number of mechanisms implicated in the atherogenic process.7 In addition to postprandial hyperglycaemia, type 2 diabetes is also associated with postprandial increase in lipids, particularly VLDL, and activation of a prothrombotic state. It is probable that in the correction of such abnormalities, prevention of postprandial hyperglycaemia plays a central role. Traditionally, investigators studying the association between hyperglycaemia and the development of diabetic complications have focused on fasting plasma glucose levels. However, type 2 diabetes is characterised by both fasting and postprandial hyper glycaemia (Figure 2). Evidence suggests that control of the latter may be of greater importance than previously thought. The Honolulu Heart Program was designed to study development of cardiovascular disease in over 8000 men aged 45–70 years. A 12-year follow-up investigated the relationship between one-hour fasting glucose and coronary heart disease, and concluded that an increasing risk gradient exists between them.8 Relative contribution of fasting plasma glucose and mealtime glucose peaks to 24-hour glycaemic control. Adapted from Riddle MC. Evening insulin strategy. Diabetes Care 1990; 13: 676–686. One-hour postchallenge glucose level after oral glucose tolerance test is not included among the measures of glycaemia in current diagnostic recommendations. Therefore, it is important to look at results found in studies using the currently recommended two-hour postchallenge glucose testing. In the Funagata diabetes study, analysis of survival rates concluded that impaired glucose tolerance, but not impaired fasting glucose, was a risk factor for cardiovascular disease.9 In the Hoorn study of older patients without previous history of diabetes, an association was found between two-hour postchallenge glucose levels and the risk of mortality.10 In addition, Balkau et al. conducted a 20-year follow-up using data from the Whitehall, Paris Prospective and Helsinki Policemen studies. The resulting analysis showed that men in the upper 20% of the postchallenge glucose distribution had a significantly higher risk of early death.11 Studies have also been carried out in asymptomatic subjects with type 2 diabetes defined by a diabetic postchallenge plasma glucose level (≥11.1 mmol/L), but a normal fasting plasma glucose level (<7.0 mmol/L). Shaw and colleagues found that this abnormality (isolated post-challenge hyperglycaemia) is common and doubles the mortality risk.12 The Rancho Bernado Study confirmed that, in older women, isolated postchallenge hyperglycaemia more than doubles the risk of fatal cardiovascular and heart disease.13 It is important to note that fasting glucose levels in the population do not change much with age whereas postchallenge glucose levels do increase with advancing age. In addition to postchallenge glucose, studies have investigated postprandial hyperglycaemia. The 11-year follow-up of the Diabetes Intervention Study identified postprandial hyperglycaemia to be an independent risk factor for myocardial infarction and all-cause mortality.14 The detrimental effects of postprandial hyperglycaemia have been linked to the risk of developing atherosclerotic complications in non-diabetic subjects. Hanefeld and colleagues investigated the relationship between postprandial hyperglycaemia and thickening of the intima-media in the common carotid artery. Postprandial hyperglycaemia was associated with a significant increase in intima-media thickness, and the study concluded that mild to moderate postprandial hyperglycaemia is an independent risk factor for this marker of early atherosclerosis.15 Diabetes is diagnosed by assessment of the level of hyperglycaemia using fasting plasma glucose or an oral glucose tolerance test. In 1997, the American Diabetes Association (ADA) recommended that diabetes should be primarily defined by a fasting plasma glucose level of ≥7.0 mmol/L. This criterion was based on the prevalence of retinopathy, which increases at this fasting glucose concentration. The ADA did not, however, recommend use of the oral glucose tolerance test for defining diabetes. This means that diabetic patients with isolated postchallenge hyperglycaemia and those with impaired glucose tolerance will not be diagnosed and treated. In addition, diabetic patients and their physicians will have no knowledge of postprandial glucose levels. The recent WHO 1999 criteria for diabetes also recommend using a fasting plasma glucose level of ≥7.0 mmol/L to identify diabetic patients, but this is in addition to the primary diagnostic measure, a two-hour postchallenge plasma glucose level of ≥11.1 mmol/L. The unexpected decision by the ADA not to recommend the oral glucose tolerance test has raised interest in evaluating available prospective data to assess whether two-hour postchallenge glucose can predict mortality and morbidity, and to compare its predictive value with fasting glucose. The Diabetes Epidemiology: Collaborative Analysis of Diagnostic Criteria in Europe (DECODE) study is the largest effort to throw light onto these essential questions. The DECODE group analysed the effect of the recommended criteria on prognosis of diabetes and milder forms of hyperglycaemia in more than 25 000 subjects. The study used Cox proportional hazards regression analyses to calculate the risk of mortality (all-cause, cardiovascular disease and non-cardiovascular disease) in different groups of hyperglycaemia compared with people with both normal fasting and two-hour plasma glucose (Figure 3). When the hazard ratios for mortality related to fasting glucose were adjusted for two-hour glucose, they were drastically reduced and became mostly non-significant. However, adjusting for fasting glucose did not significantly change the hazard ratios related to two-hour glucose. The DECODE group concluded that postprandial hyperglycaemia after an oral glucose tolerance test is associated with an increased all-cause mortality risk, and that postchallenge glucose is a better and more sensitive predictor of mortality than fasting plasma glucose.16 Relative risk for all-cause mortality in subjects not known as diabetic (DECODE). Adapted from reference.16 Jackson and colleagues also found an association between postchallenge glucose and risk of developing diabetic complications. They studied the association between complications and fasting plasma glucose, postchallenge glucose and glycated haemoglobin (HbA1c). They concluded that the two-hour blood glucose level was a better predictor of coronary heart disease than HbA1c.17 Tight control of postprandial hyperglycaemia should be an integral element of the treatment strategy for patients with type 2 diabetes and for subjects with impaired glucose tolerance. Therapeutic targeting of postprandial hyperglycaemia improves overall glycaemic control. This was shown in the Avignon study, when type 2 diabetic patients were treated with either diet alone, diet plus an oral diabetic agent or diet with a combination of oral therapies. Various measurements of plasma glucose were made daily, and (HbA1c) levels were measured to assess overall control. The study concluded that postprandial plasma glucose correlated better with overall glycaemic control (HbA1c ≤7.0%) compared with fasting plasma glucose.18 Future pharmacotherapeutic strategies should consider restoration of early-phase insulin release. Studies evaluating compounds that restore the early phase of insulin release using exogenous insulin demonstrated efficacy at improving the glycaemic profile.19, 20 However, injecting insulin at mealtimes does not restore physiological secretion of insulin by beta cells. Recently developed oral therapies that restore early-phase insulin secretion and target postprandial hyperglycaemia are likely to reduce excessive glycaemic exposure, and may thereby reduce the risk of diabetic complications in patients with type 2 diabetes. Do you think patients should now be advised to have one meal a day as opposed to three? It really doesn't matter how many meals you have. There is a variation in your glucose whether you eat or not. One of the problems for today's diabetic patients and not only for diabetes but for many other diseases including Alzheimer's and cardiovascular disease – is that portion sizes are too large at meals. You were suggesting that HbA1c was really not a terribly useful measurement and two-hour values were better. Should we be measuring HbA1c, or should we be suggesting to patients that they measure their glucose after their midday meal? HbA1c is a good indicator of long-term glycaemia but if we are trying to predict mortality it is not good enough. When used alone it predicts a mortality and available data suggest that people with high HbA1c values also have elevated post-lunch glucose levels. We could say that two-hour glucose after an oral glucose tolerance test gives the same indication and even more. It's not a contradiction but HbA1c alone may not be sufficient for cardiovascular risk assessment." @default.
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• W2041797130 title "Glucose peaks - the hidden danger in type 2 diabetes" @default.
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