Determinants of progression from impaired fasting glucose and impaired glucose tolerance to diabetes in a high-risk screened population: 3 year follow-up in the ADDITION study, Denmark

Rasmussen, Søren; Glümer, Charlotte; Sandbæk, Annelli; Lauritzen, Torsten; Borch‐Johnsen, Knut

doi:10.1007/s00125-007-0893-8

Cited by 86 publications

(73 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These conclusions need to be seen in context. Several previous studies have reported on the predictive role of fasting or post-load glucose levels for incident type 2 diabetes, but the two have rarely been assessed together and after controlling for other strong predictors (age, BMI and familial diabetes) [4,5]. The present analysis shows that an equivalent (i.e.…”

Section: Discussionmentioning

confidence: 47%

“…Criteria for lesser degrees of dysglycaemia are less well established. Impaired glucose tolerance (IGT), defined by the 2 h glucose concentration, carries heightened risk of diabetes [3][4][5] and, possibly, cardiovascular disease [6][7]. The pathophysiology of IGT is a combination of insulin resistance, hepatic as well as peripheral, and beta cell dysfunction [8] that is similar to that of diabetes, only of a milder degree.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Plasma glucose levels as predictors of diabetes: the Mexico City diabetes study

Ferrannini

Massari²,

Nannipieri

et al. 2009

Diabetologia

View full text Add to dashboard Cite

Aims/hypothesis The value of diagnostic categories of glucose intolerance for predicting type 2 diabetes is much debated. We therefore sought to estimate relative and population-attributable risk of different definitions based on fasting (impaired fasting glucose [IFG]) or 2 h plasma glucose concentrations (impaired glucose tolerance [IGT]) and to describe the associated clinical phenotypes. Methods We prospectively observed a population-based cohort of 1,963 non-diabetic participants (mean age 47 years), in whom an OGTT was performed at baseline and 7 years later. Results IGT was fivefold more prevalent (13.5%) than IFG. In both categories, participants were older, heavier, hyperinsulinaemic, hyperproinsulinaemic and dyslipidaemic compared with participants with normal glucose tolerance. Relative risk of incident diabetes was similar for IFG and IGT categories (3.73 [95% CI: 2.18-6.39] and 4.01 [95% CI: 3.12-5.14], respectively), but the population-attributable risk was fivefold higher for IGT (29% [95% CI: 26-32]) than for IFG (6% [95% CI: 5-7]). Isolated IFG carried no increase in risk. Lowering the threshold to 5.6 mmol/l raised the population-attributable risk of IFG to 23% (95% CI: 20-25); its contribution to diabetes progression, however, was largely due to co-existent IGT. In multivariate analysis adjusting for sex, age, familial diabetes and BMI, fasting and 2 h glucose were independent predictors. Conclusions/interpretation Fasting and 2 h glucose values are independent predictors of incident diabetes. Isolated IFG is not a high-risk condition; lowering the diagnostic threshold increases the population-attributable risk of IFG fourfold, but performing an OGTT captures additional diabetes progressors compared with the number identified by IFG.

show abstract

Section: Discussionmentioning

confidence: 47%

mentioning

confidence: 99%

Plasma glucose levels as predictors of diabetes: the Mexico City diabetes study

Ferrannini

Massari²,

Nannipieri

et al. 2009

Diabetologia

View full text Add to dashboard Cite

show abstract

“…Setting and population The study population was drawn from the Danish arm (DK) of the Anglo-Danish-Dutch Study of Intensive Treatment in People with ScreenDetected Diabetes in Primary Care (ADDITION), which evaluated a systematic screening for people at high risk of type 2 diabetes conducted among all listed patients aged 40 to 69 years in the 175 participating Danish practices [9]. Blood samples collected at baseline screening (2001 to 2006) were used.…”

Section: Methodsmentioning

confidence: 99%

“…Blood samples collected at baseline screening (2001 to 2006) were used. Details on the original ADDITION recruitment strategy can be found elsewhere [9]. Of the people who completed the risk score questionnaire (n=134,016, response rate 82%), those who had a high risk score (n= 28,041) underwent a step-wise clinical assessment comprising the following: determination of random blood glucose and HbA 1c , and measurement of fasting blood glucose and an OGTT.…”

Section: Methodsmentioning

confidence: 99%

The pro-inflammatory biomarker soluble urokinase plasminogen activator receptor (suPAR) is associated with incident type 2 diabetes among overweight but not obese individuals with impaired glucose regulation: effect modification by smoking and body weight status

et al. 2013

Self Cite

View full text Add to dashboard Cite

Aims/hypothesis Recent evidence links the soluble urokinase plasminogen activator receptor (suPAR), a stable biomarker of systemic immune activation, to several chronic diseases, including type 2 diabetes. suPAR is also associated with adiposity and smoking. We hypothesised that this biomarker would be linked to incident type 2 diabetes in individuals with impaired glucose regulation and that this association would be modified by smoking and body weight status. Methods The study included 1,933 participants with impaired glucose regulation, who were drawn from the Danish arm of the Anglo-Danish-Dutch Study of Intensive Treatment in People with Screen-Detected Diabetes in Primary Care (ADDITION) and for whom data on suPAR, BMI and smoking were available. Logistic regression analysis was used to estimate the odds for incident type 2 diabetes per twofold increase in suPAR levels. Interactions between both smoking and body weight status and suPAR were tested. Results During a 3-year follow-up (599 incident diabetes cases), there was a 48% overall increase in the odds of developing type 2 diabetes per twofold increase in suPAR (p = 0.006). This association was modified by body weight status in overweight, but not in obese individuals (OR 2.36, 95% CI 1.48, 3.76 in overweight group), and by smoking status (OR 2.05, 95% CI 1.20, 3.51 in non-smokers). After adjustment for other diabetes risk factors, the association between suPAR and type 2 diabetes was attenuated in the whole sample and among non-smokers, but remained robust among overweight participants. Conclusions/interpretation suPAR may be a good novel biomarker for systemic sub-clinical inflammation and immune activation linked to incident type 2 diabetes risk in overweight individuals and non-smokers. The observed

show abstract

“…Certainly, weight loss can slow or halt the pathogenesis of type 2 diabetes. When a group of individuals with impaired glucose tolerance was followed over time, weight loss of only 1 kg decreased the incidence of diabetes by 20% [43].…”

Section: Assembling the Time-course To Type 2 Diabetesmentioning

confidence: 99%

Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause

2008

View full text Add to dashboard Cite

The metabolic abnormalities of type 2 diabetes can be reversed reproducibly by bariatric surgery. By quantifying the major pathophysiological abnormalities in insulin secretion and insulin action after surgery, the sequence of events leading to restoration of normal metabolism can be defined. Liver fat levels fall within days and normal hepatic insulin sensitivity is restored. Simultaneously, plasma glucose levels return towards normal. Insulin sensitivity of muscle remains abnormal, at least over the weeks and months after bariatric surgery. The effect of the surgery is explicable solely in terms of energy restriction. By combining this information with prospective observation of the changes immediately preceding the onset of type 2 diabetes, a clear picture emerges. Insulin resistance in muscle, caused by inherited and environmental factors, facilitates the development of fatty liver during positive energy balance. Once established, the increased insulin secretion required to maintain plasma glucose levels will further increase liver fat deposition. Fatty liver causes resistance to insulin suppression of hepatic glucose output as well as raised plasma triacylglycerol. Exposure of beta cells to increased levels of fatty acids, derived from circulating and locally deposited triacylglycerol, suppresses glucose-mediated insulin secretion. This is reversible initially, but eventually becomes permanent. The essential time sequence of the pathogenesis of type 2 diabetes is now evident. Muscle insulin resistance determines the rate at which fatty liver progresses, and ectopic fat deposition in liver and islet underlies the related dynamic defects of hepatic insulin resistance and beta cell dysfunction. These defects are capable of dramatic reversal under hypoenergetic feeding conditions, completely in early diabetes and to a worthwhile extent in more established disease.

show abstract

Determinants of progression from impaired fasting glucose and impaired glucose tolerance to diabetes in a high-risk screened population: 3 year follow-up in the ADDITION study, Denmark

Cited by 86 publications

References 36 publications

Plasma glucose levels as predictors of diabetes: the Mexico City diabetes study

Plasma glucose levels as predictors of diabetes: the Mexico City diabetes study

The pro-inflammatory biomarker soluble urokinase plasminogen activator receptor (suPAR) is associated with incident type 2 diabetes among overweight but not obese individuals with impaired glucose regulation: effect modification by smoking and body weight status

Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause

Contact Info

Product

Resources

About