CoChat
Sign Up
Cited by 141Diabetes Treatment and ManagementDiabetes Management and ResearchDiabetes, Cardiovascular Risks, and Lipoproteins

Prevalence and correlates of post-prandial hyperglycaemia in a large sample of patients with type 2 diabetes mellitus

Open access
Bonora, E., Corrao, G., Bagnardi, V., Ceriello, A., Comaschi, M., Montanari, P., Meigs, J. B.·2006·Diabetologia
DOI 10.1007/s00125-006-0203-x
Open this paper in CoChat — free accountOpen PDF

Abstract

Aims/hypothesis Post-prandial glucose may be a risk factor for cardiovascular disease and chronic diabetic complications. We tested the hypothesis that post-prandial hyperglycaemia is common in type 2 diabetes, even among patients in apparently good glycaemic control, and that simple clinical characteristics identify subsets of diabetic patients with frequent post-prandial hyperglycaemia.Subjects and methods Three self-assessed daily blood glucose profiles over a 1-week period, including 18 glucose readings before and 2 h after meals, were obtained from 3,284 unselected outpatients (men 51%; age 63+/-10 years) with non-insulin-treated type 2 diabetes mellitus attending 500 different diabetes clinics operating throughout Italy.Results A post-prandial blood glucose value >8.89 mmol/l (160 mg/dl) was recorded at least once in 84% of patients, and 81% of patients had at least one Delta glucose > or =2.22 mmol/l (40 mg/dl). Among patients with apparently good metabolic control, 38% had >40% of post-prandial blood glucose readings >8.89 mmol/l (> or =4 of 9 meals in total), and 36% had >40% Delta glucose > or =2.22 mmol/l. In multivariate analysis adjusted for pre-prandial glucose levels, older age, longer duration of diabetes, absence of obesity, hyperlipidaemia and hypertension, as well as treatment with sulfonylureas, were significantly associated with greater glucose excursions after meals.Conclusions/interpretation These results indicate that post-prandial hyperglycaemia is a very frequent phenomenon in patients with type 2 diabetes mellitus on active treatment; can occur even when metabolic control is apparently good; and can be predicted by simple clinical features.

Integrity signals

Registry

Crossref · 10.1007/s00125-006-0203-x

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 30 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    Pre-meal blood glucose levels were on average similar across the three main meals.

    “Pre-meal blood glucose levels were, on average, quite similar”
    Quote in the paperNot a substantial claim
  • Findingown data

    The absolute and relative glucose increases after lunch and dinner were virtually identical.

    “the Δglucose and Δ% glucose increases with lunch and dinner were virtually identical.”
    Quote in the paperNot a substantial claim
  • Findingown data

    In the poor pre-prandial group (n=684), satisfactory post-prandial excursions were twice as common as exaggerated ones (481 vs 203).

    “Among subjects with poor pre-prandial glucose levels (n=684), those with satisfactory post-prandial excursions were twofold more common than those with exaggerated post-prandial excursions (481 vs 203).”
    Quote in the paperNot a substantial claim
  • Findingown data

    The most frequent phenotype was fair pre-prandial glucose with satisfactory post-prandial excursion (n=1,120, 34%).

    “The most common phenotype was fair pre-prandial with satisfactory post-prandial excursion (n=1,120, 34%)”
    Quote in the paperNot a substantial claim
  • Findingown data

    The second most common phenotype was good pre-prandial glucose with satisfactory post-prandial excursion (n=718, 22%).

    “followed by good pre-prandial and satisfactory post-prandial excursion (n=718, 22%)”
    Quote in the paperNot a substantial claim
  • May combine two claims. 29
  • Classified as probably not a substantial claim. 9

  • May combine two claims.

    Findingown data

    Among subjects with complete profiles, those with HbA1c <7% and ≥7% had similar clinical features, except for time since diagnosis, smoking, fasting plasma glucose and treatment.

    “Among subjects providing complete glucose profiles, those with HbA 1c <7 and ≥7% had quite similar clinical features.Only time since diagnosis, smoking, fasting plasma glucose and treatment were different.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    BMI was inversely correlated with mean absolute glucose rise (r=-0.073, p<0.0001) and relative glucose rise (r=-0.098, p<0.0001).

    “BMI was negatively correlated with mean Δglucose (r=-0.073,p<0.0001) and Δ% glucose (r=-0.098,p<0.0001).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Patients with HbA1c ≥7% had higher post-meal blood glucose levels and higher Δglucose than those with HbA1c <7%.

    “Higher levels of blood glucose and higher Δglucose following the meals were observed in patients with HbA 1c ≥7% compared with those with HbA 1c <7%.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Age showed positive correlations with mean post-prandial glucose (r=0.089, p<0.0001), absolute glucose rise (r=0.064, p=0.0003) and relative glucose rise (r=0.048, p=0.005).

    “Age was positively correlated with mean post-prandial glucose (r=0.089,p<0.0001),Δglucose (r=0.064,p=0.0003) and Δ% glucose (r=0.048,p=0.005).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    After adjustment for sex, age, diabetes duration and preprandial glucose, patients on sulfonylureas alone or with biguanide had higher mean post-prandial glucose (p<0.0001), average absolute glucose rise (p=0.0005) and mean relative glucose rise (p=0.008) than those on diet only or metformin alone.

    “after adjusting for sex, age, duration of diabetes and preprandial glucose, subjects treated with sulfonylureas alone or in combination with biguanide had mean post-prandial glucose (p<0.0001),average Δglucose (p=0.0005) and mean Δ% glucose (p=0.008)higher than those observed in subjects treated with diet only or with metformin alone.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Subjects with poorer control had higher average pre-prandial, post-prandial and Δglucose than subjects with better control.

    “Subjects with poorer control had average pre-prandial, post-prandial and Δglucose higher than subjects with better control.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingnone given

    Older age, longer duration of diabetes, absence of obesity, hypertension and dyslipidaemia are clinical features associated with exaggerated postprandial glucose peaks.

    “Older age, longer duration of diabetes, absence of obesity, hypertension and dyslipidaemia are clinical features related to exaggerated post-prandial glucose peaks.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Across the whole sample, pre-prandial glucose and, less strongly, post-prandial glucose were significantly correlated with HbA1c.

    “In the whole sample, pre-prandial and, to a lesser extent, post-prandial glucose levels were significantly correlated to HbA 1c .”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Absolute glucose rise and, more strongly, relative glucose rise fell significantly across increasing pre-prandial glucose groups.

    “Δglucose and, to a greater extent, Δ% glucose significantly decreased across groups of pre-prandial glucose levels (Table 4).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    High glucose peaks and exaggerated glucose excursions with meals were very common in subjects with both better control (HbA1c <7%) and poorer control (HbA1c ≥7%).

    “both events were very common in subjects with both better control (HbA 1c <7%) and poorer control (HbA 1c ≥7%) (Table 3).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In mixed-effects ANOVA adjusted for pre-prandial glucose, older age, longer diabetes duration, normal body weight, no hypertension, no dyslipidaemia, and sulfonylurea treatment alone or combined were independently linked to higher post-prandial glucose.

    “In mixed-effects ANOVA models adjusted for pre-prandial glucose level, older age, longer duration of diabetes, normal body weight, absence of hypertension, absence of dyslipidaemia, and treatment with sulfonylureas alone or in combination were independently associated with higher post-prandial glucose (Table 5).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Among those with poor control (HbA1c ≥7.5%), pre-prandial glucose was significantly associated with HbA1c (p<0.0001), but post-prandial glucose was not (p=0.5).

    “pre-prandial (p<0.0001)but not post-prandial (p=0.5)glucose was significantly associated with HbA 1c in subjects with poor control (HbA 1c ≥7.5%).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Diabetes duration was positively correlated with average post-prandial glucose (r=0.190, p<0.0001), absolute glucose rise (r=0.108, p<0.0001) and relative glucose rise (r=0.064, p=0.0003).

    “Duration of diabetes was positively correlated with average post-prandial glucose (r=0.190,p<0.0001),Δglucose (r=0.108,p<0.0001) and Δ% glucose (r=0.064,p=0.0003).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Post-prandial hyperglycaemia and peaks were common even among patients with apparently good control (HbA1c <7%) and those with average pre-prandial glucose within recommended goals (≤6.66 mmol/l; ≤120 mg/dl).

    “Importantly, post-prandial hyperglycaemia and postprandial peaks were common even in subjects with an apparently good metabolic control (HbA 1c <7%) and in subjects with average pre-prandial glucose levels within recommended goals (≤6.66 mmol/l; ≤120 mg/dl).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    At low HbA1c, post-prandial glucose contributed most to HbA1c; at high HbA1c, pre-prandial glucose contributed most.

    “When HbA 1c was low, the main contribution came from post-prandial glucose, whereas when HbA 1c was high, the main contribution came from pre-prandial glucose.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Among those with very good control (HbA1c <6.5%), post-prandial glucose was linked to HbA1c (p=0.006), while pre-prandial glucose was not (p=0.06).

    “In subjects with very good control (HbA 1c <6.5%), post-prandial (p=0.006)but not pre-prandial glucose (p=0.06) was associated with HbA 1c”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Absolute and relative glucose rises did not differ significantly by sex.

    “Mean post-prandial glucose but not Δglucose or Δ% glucose was significantly higher in women than in men”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    In this large, representative sample of non-insulin-treated type 2 diabetes patients, post-prandial hyperglycaemia and post-prandial glucose peaks were very common.

    “We examined the epidemiology of post-prandial hyperglycaemia in a very large, representative sample of non-insulin-treated type 2 diabetic patients and found that post-prandial hyperglycaemia and post-prandial glucose peaks were very common.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Premisecitation

    The adverse effect of post-prandial or post-challenge hyperglycaemia appears stronger than that of fasting hyperglycaemia.

    “The adverse impact of post-prandial or post-challenge (OGTT) hyperglycaemia seems to be even stronger than that of fasting hyperglycaemia [5][6][7][8][9].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [5] Hanefeld M, Fischer S, Julius U et al (1996) Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11-year follow-up. Diabetologia 39:1577–1583 source

      Not checked in the free run.

    • cites [6] Bonora E (2002) Postprandial peaks as a risk factor for cardiovascular disease: epidemiological perspectives. Int J Clin Pract Suppl 129:5–11

      Not checked in the free run.

    • cites [7] Cavalot F, Petrelli A, Traversa M et al (2005) Postprandial blood glucose is a stronger predictor of cardiovascular events than fasting blood glucose in type 2 diabetes mellitus, particularly in women. J Clin Endocrinol Metab [Epub ahead of print] source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Only two small series of type 2 diabetes subjects have collected data on circadian glucose levels, and their results were partially conflicting.

    “only in two small series of subjects with type 2 diabetes have data on circadian glucose levels been collected, and the results were partially conflicting [13][14][15][16].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [13] Bonora E, Calcaterra F, Lombardi S et al (2001) Plasma glucose levels throughout the day and HbA1c interrelationships in type 2 diabetes. Implications for treatment and monitoring of metabolic control. Diabetes Care 24:2023–2029 source

      Not checked in the free run.

    • cites [14] Avignon A, Radauceanu A, Monnier L (1997) Non-fasting plasma glucose is a better marker of diabetic control than fasting plasma glucose in type 2 diabetes. Diabetes Care 20:1822–1826 source

      Not checked in the free run.

    • cites [15] Monnier L, Colette C, Rabasa-Lhoret R et al (2002) Morning hyperglycaemic excursions. A constant failure in the metabolic control of non-insulin-using patients with type 2 diabetes. Diabetes Care 25:737–741 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Poorly controlled post-prandial glucose contributes to high HbA1c concentrations and to chronic diabetic complications, especially cardiovascular disease.

    “poorly controlled post-prandial glucose significantly contributes to high HbA 1c concentrations and to the development of chronic diabetic complications, particularly cardiovascular disease (CVD) [1][2][3][4].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [1] Gerich JE (2003) Clinical significance, pathogenesis, and management of postprandial hyperglycaemia. Arch Intern Med 163:1306–1316 source

      Not checked in the free run.

    • cites [2] Haffner SM (1998) The importance of hyperglycaemia in the nonfasting state to the development of cardiovascular disease. Endocr Rev 19:583–592 source

      Not checked in the free run.

    • cites [3] Ceriello A (2003) The possible role of post-prandial hyperglycaemia in the pathogenesis of diabetic complications. Diabetologia 46 (Suppl 1):M9–M16 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The Diabetes European Policy Group under the IDF recommends monitoring and controlling post-prandial hyperglycaemia with a goal of <8.89 mmol/l.

    “the guidelines of the Diabetes European Policy Group, under the auspices of the International Diabetes Federation (IDF), have recommended monitoring and controlling post-prandial hyperglycaemia, with a goal of <8.89 mmo/l (160 mg/dl) [12].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [12] European Diabetes Policy Group (1999) A desktop guide to type 2 diabetes mellitus. Diabetic Med 16:716–730 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    The ADA consensus is that post-prandial glucose need not be systematically monitored and post-prandial peaks need not be targeted and corrected, though if monitored the goal is <10.0 mmol/l.

    “the current consensus of the American Diabetes Association (ADA) is that post-prandial glucose should not necessarily be systematically monitored, and that post-prandial glucose peaks should not necessarily be targeted and corrected [10], although, if monitored, the recommended goal for post-prandial glucose is <10.0 mmol/l (180 mg/dl) [11].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [10] American Diabetes Association (2001) Post-prandial blood glucose. Diabetes Care 24:775–778 source

      Not checked in the free run.

    • cites [11] American Diabetes Association (2005) Standard of medical care for patients with diabetes mellitus. Diabetes Care 28 (Suppl 1):S4–S40 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S2 (checkable). May combine two claims.

    Interpretationreasoning

    To achieve optimal glucose control and prevent diabetic complications, metabolic assessment should not rely only on periodic HbA1c, and self-monitoring should not be restricted to pre-prandial readings.

    “The logical conclusion is that for optimal glucose control to prevent diabetic complications, assessment of metabolic control cannot rely solely on periodical HbA 1c measurements and that blood glucose self-monitoring cannot be limited to pre-prandial glucose readings.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Adding post-meal blood glucose self-assessment to routine self-monitoring policies aligns with IDF guidelines and current ADA recommendations.

    “This approach meets guidelines of the IDF [12] and is consistent with current recommendations of the ADA [11].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [12] European Diabetes Policy Group (1999) A desktop guide to type 2 diabetes mellitus. Diabetic Med 16:716–730 source

      Not checked in the free run.

    • cites [11] American Diabetes Association (2005) Standard of medical care for patients with diabetes mellitus. Diabetes Care 28 (Suppl 1):S4–S40 source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    On average, non-insulin-treated type 2 patients return to pre-meal glucose concentrations before the next meal, without a substantially progressive increase in blood glucose throughout the day despite additional meals.

    “This means that, on average, non-insulin-treated type 2 patients are able to return to pre-meal glucose concentrations before the next meal, without a substantially progressive increase in blood glucose throughout the day despite additional meals.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The sample of type 2 diabetes patients receiving routine care in diabetes clinics is representative of the broader population of such patients.

  • May combine two claims.

    Interpretationown data

    Neither HbA1c nor pre-prandial glucose measurement can reliably identify patients whose post-prandial glucose levels or excursions are acceptable.

    “neither HbA 1c nor pre-prandial glucose measurement can reliably be expected to identify patients with acceptable post-prandial glucose levels or excursions.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Controlling postprandial hyperglycaemia with repaglinide compared with glyburide produced similar HbA1c improvement but was associated with regression of carotid artery atherosclerosis.

    “specifically controlling post-prandial hyperglycaemia using a rapid-acting secretagogue (repaglinide) compared with glyburide resulted in a similar improvement of HbA 1c but was associated with a regression of carotid artery atherosclerosis [28]”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [28] Esposito K, Giugliano D, Nappo F, Martella and the Campanian Postprandial Hyperglycaemia Study Group (2004) Regression of carotid atherosclerosis by control of postprandial hyperglycaemia in type 2 diabetes mellitus. Circulation 110:214–219 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    This result agrees with data from Monnier et al.

    “This is consistent with data from Monnier et al. [16].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [16] Monnier L, Lapinski H, Colette C (2003) Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycaemia of type 2 diabetic patients: variations with increasing levels of HbA1c. Diabetes Care 26:881–885 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductown data

    Although laboratory testing was not centralised, every laboratory took part in quality control for HbA1c and lipid assays.

    “Laboratory assessment was not centralised.However, all laboratories participated in quality control procedures for HbA 1c and lipid assays.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Trials that specifically target postprandial glucose appear more effective and support the idea that postprandial hyperglycaemia is a key contributor to diabetes complications.

    “trials specifically targeting postprandial glucose appear to have been more effective and add further support to the hypothesis that post-prandial hyperglycaemia is a key contributor to diabetes complications [25,26]”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [25] Malmberg K for the DIGAMI Study Group (1997) Prospective randomised study of intensive insulin treatment on long term survival after acute myocardial infraction in patients with diabetes mellitus. BMJ 314:1512–1515 source

      Not checked in the free run.

    • cites [26] Shichiri M, Kishikawa H, Ohkubo Y, Wake N (2000) Long term results of the Kumamoto Study on optimal diabetes control in type 2 diabetic patients. Diabetes Care 23 (Suppl 2):B21–B29

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S2 (checkable).

    Interpretationreasoning

    Assessment of postprandial glucose levels and evaluation of post-meal glucose excursions is likely to contribute to improved glycaemic control for prevention of chronic complications of type 2 diabetes.

    “and is likely to contribute to improved glycaemic control for prevention of the devastating chronic complications of type 2 diabetes.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: The sample of type 2 diabetes patients receiving routine care in diabetes clinics is representative of the broader population of such patients.

  • Probably not a substantial claim: may not pass S2 (checkable). May combine two claims.

    Interpretationreasoning

    Assessment of postprandial glucose levels and evaluation of post-meal glucose excursions can establish the glycaemic phenotype and help tailor the most appropriate treatment for individual patients.

    “The assessment of postprandial glucose levels and the evaluation of post-meal glucose excursions can establish the glycaemic phenotype and help to tailor the most appropriate treatment for individual patients”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: The sample of type 2 diabetes patients receiving routine care in diabetes clinics is representative of the broader population of such patients.
33 of 33

  • The paper relies on this without support.

    Adherence to diet and physical activity did not differ across the participating centres.

    “There was no reason to think that adherence to diet and physical activity was different across centres.”

  • The paper relies on this without support.

    The large number of subjects minimises possible variations in diet and physical activity across centres.

    “the very large number of subjects is expected to minimise possible variations.”

  • The paper relies on this without support.

    The structure of diet in terms of composition, number of meals and energy supply was very similar across Italian regions.

    “the structure of diet in terms of composition, number of meals and energy supply was very similar.”

  • The paper relies on this without support.

    The sample of type 2 diabetes patients receiving routine care in diabetes clinics is representative of the broader population of such patients.

    “data from this large, representative sample of type 2 diabetes patients receiving routine care in diabetes clinics”
4 of 4

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • A transient post-meal rise in free radicals acutely triggers atherogenic changes, including inflammation, endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity.

    “The transient increase in free radicals acutely triggers atherogenic changes including inflammation, endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity.”

    From Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardiovascular Health (2008) · cites this paper as [4]

    The Discussion (page unavailable) says acute glucose elevations may harm functions related to atherogenesis. The References list studies of endothelial dysfunction and thrombin formation, including one proposing a possible role for oxidative stress. Our copy does not establish that a transient rise in free radicals triggers these changes, or support the full list of effects, particularly sympathetic hyperactivity. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Postprandial dysmetabolism causes immediate oxidative stress.

    “This state, called postprandial dysmetabolism, induces immediate oxidant stress, which increases in direct proportion to the increases in glucose and triglycerides after a meal.”

    From Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardiovascular Health (2008) · cites this paper as [4]

    The Discussion describes post-meal glucose peaks as common in patients with type 2 diabetes and suggests they may contribute to chronic complications. It does not say that postprandial dysmetabolism causes immediate oxidative stress or that stress rises in proportion to post-meal glucose and triglycerides. Searches for oxidative stress, dysmetabolism, and triglycerides found no passage establishing that mechanism. (LLM, conf=0.74)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Normal body weight is called an independent predictor despite a nonsignificant result

    Major

    The results identify normal body weight as independently associated with higher post-prandial glucose, but Table 5 reports p=0.1 for BMI and the same adjusted post-prandial value for normal-weight and obese patients.

  • Overall relative glucose change is below both subgroup means

    Major

    The two HbA1c groups account for all 3,284 patients, so their overall mean relative change cannot be 24.9% when the subgroup means are 27.3% and 26.6%. The reported lunch and dinner overall means are likewise below both corresponding subgroup means.

  • Overall triglyceride mean conflicts with subgroup means

    Minor

    Weighting the triglyceride means of 1.62 and 1.85 mmol/l by the respective HbA1c subgroup sizes of 1,283 and 2,001 gives about 1.76 mmol/l. Table 1 instead reports 1.69 mmol/l for those same 3,284 patients.

  • Zero absolute-excursion percentage does not match subgroup counts

    Minor

    The subgroup percentages of 22.3% among 1,283 patients and 14.2% among 2,001 patients imply about 17.4% overall, not the reported 18.6%. The gap exceeds what rounding to one decimal place can explain.

  • Overall zero-excursion percentage exceeds both subgroup percentages

    Minor

    For patients with no meals showing a relative glucose increase of at least 25%, the overall figure is 11.6%, although the two exhaustive HbA1c subgroups are 11.5% and 11.3%. An overall percentage cannot exceed both subgroup percentages.

  • Two counts are given for the lowest pre-prandial glucose category

    Minor

    The results give 1,057 patients with mean pre-prandial glucose at or below 6.66 mmol/l, but later give 1,062 for the good pre-prandial category, which is defined by the same cutoff.

6 of 6

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Meigs JB, Nathan DM, D’Agostino RB Sr, Wilson PW; Framingham Offspring Study (2002) Fasting and postchallenge glycaemia and cardiovascular disease risk: the Framingham Offspring Study. Diabetes Care 25:1845–1850 · DOI · Paper page

Cited by

Sorted by citations

Related

Authors
Bonora, E., Corrao, G., Bagnardi, V., Ceriello, A., Comaschi, M., Montanari, P., & Meigs, J. B.
Affiliations
  • University of Verona (IT)
  • University of Milano-Bicocca (IT)
  • University of Warwick (GB)
  • Novartis (Italy) (IT)
  • Harvard University (US)
Corresponding author
Bonora, E.
ORCID
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
2006-03-11
Volume
49
Issue
5
Pages
846-854
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/s00125-006-0203-x
OpenAlex
W2032998015
Cited by
141
References
54
Citations by year
2025: 2 · 2024: 2 · 2023: 7 · 2022: 2 · 2021: 4 · 2020: 5 · 2019: 7 · 2018: 10 · 2017: 4 · 2016: 8 · 2015: 6 · 2014: 9 · 2013: 5 · 2012: 9
FWCI
9.32
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
  • Institutional Research Information System (University of Udine) (submittedVersion)
  • BOA (University of Milano-Bicocca) (submittedVersion)
Funders
  • American Diabetes Association
  • Bristol-Myers Squibb
  • Eli Lilly and Company
  • Pfizer
  • AstraZeneca
  • GlaxoSmithKline
  • Sanofi
  • Novo Nordisk
  • Servier
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
type 2 diabetes, glycemic excursions, glycemic control, cardiovascular risk, sulfonylureas, risk factors, self-monitoring of blood glucose, diabetes duration, obesity
MeSH terms
Aged, Diabetes Mellitus, Type 2, Diet, Female, United Kingdom, Humans, Hyperglycemia, Italy, Male, Middle Aged, Outpatients, Body Mass Index, Prevalence, Postprandial Period

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read under definition version 3 (extract-v3) on 2026-09-27.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-09-27.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review