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Cited by 298Nitric Oxide and Endothelin EffectsDiabetes, Cardiovascular Risks, and LipoproteinsLipoproteins and Cardiovascular Health

Effect of Atorvastatin and Irbesartan, Alone and in Combination, on Postprandial Endothelial Dysfunction, Oxidative Stress, and Inflammation in Type 2 Diabetic Patients

Ceriello, Antonio, Assaloni, Roberta, Da Ros, Roberto, Maier, Amabile, Piconi, Ludovica, Quagliaro, Lisa, Esposito, Katherine, Giugliano, Dario·2005·Circulation
DOI 10.1161/01.cir.0000165070.46111.9f
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Abstract

BACKGROUND: Postprandial hypertriglyceridemia and hyperglycemia are considered risk factors for cardiovascular disease. Evidence suggests that postprandial hypertriglyceridemia and hyperglycemia induce endothelial dysfunction and inflammation through oxidative stress. Statins and angiotensin type 1 receptor blockers have been shown to reduce oxidative stress and inflammation, improving endothelial function. METHODS AND RESULTS: Twenty type 2 diabetic patients ate 3 different test meals: a high-fat meal, 75 g glucose alone, and a high-fat meal plus glucose. Glycemia, triglyceridemia, endothelial function, nitrotyrosine, C-reactive protein, intercellular adhesion molecule-1, and interleukin-6 were assayed during the tests. Subsequently, diabetics took atorvastatin 40 mg/d, irbesartan 300 mg/d, both, or placebo for 1 week. The 3 tests were performed again between 5 and 7 days after the start of each treatment. High-fat load and glucose alone produced a decrease in endothelial function and increases in nitrotyrosine, C-reactive protein, intercellular adhesion molecule-1, and interleukin-6. These effects were more pronounced when high-fat load and glucose were combined. Short-term atorvastatin and irbesartan treatments significantly counterbalanced these phenomena, and their combination was more effective than either therapy alone. CONCLUSIONS: This study confirms an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial function and inflammation, suggesting oxidative stress as a common mediator of such an effect. Short-term treatment with atorvastatin and irbesartan may counterbalance this phenomenon; the combination of the 2 compounds is most effective.

Integrity signals

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Crossref · 10.1161/01.cir.0000165070.46111.9f

Cites

52 of 52 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 65 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    During the tests, nitrotyrosine, C-reactive protein, ICAM-1 and IL-6 moved in the opposite direction to flow-mediated dilation.

    “NT, C-reactive protein, ICAM-1, and IL-6 concentration changed during the studies; those variations were opposite those of FMD (PϽ0.05 versus baseline; Figure 1).”
    Quote in the paperSubstantial claim
  • Findingown data

    In diabetic patients, triglycerides did not change after 75 g glucose alone.

    “whereas triglycerides remained unchanged during the 75-g glucose challenge alone (Figure 1).”
    Quote in the paperNot a substantial claim
  • Findingown data

    One week of irbesartan, given alone or with atorvastatin, did not alter lipid parameters or blood pressure in diabetic patients.

    “Short-term irbesartan treatment, alone or in combination, had no effect on lipid parameters or blood pressure in diabetic patients (Table 2).”
    Quote in the paperNot a substantial claim
  • Findingown data

    In type 2 diabetic patients, a short course of atorvastatin or irbesartan offsets the harmful postprandial effects on endothelial function, oxidative stress, and inflammation.

    “They also show that short-term treatment with atorvastatin and irbesartan may counterbalance this phenomenon”
    • Also stated in: § Discussion · boosted
      “Our data provide evidence for the efficacy of both statins and AT-1 receptor blockers during short-term administration.”
    Quote in the paperSubstantial claim
  • Findingown data

    In diabetic patients, serum triglycerides rose from 1 to 4 hours after the high-fat meal and after the high-fat meal with glucose.

    “Compared with preprandial values, serum triglycerides were increased from 1 to 4 hours (PϽ0.05versus baseline; Figure 1) during the high-fat meal and the high-fat meal plus 75 g glucose.”
    Quote in the paperNot a substantial claim
  • May combine two claims. 23
  • Classified as probably not a substantial claim. 7

  • May combine two claims.

    Findingown data

    In people with type 2 diabetes, high blood glucose and triglycerides after meals impair endothelial function and cause oxidative stress and inflammation.

    “In conclusion, our data confirm that in diabetic patients postprandial hyperglycemia and hypertriglyceridemia have a damaging effect on endothelial function, producing oxidative stress and inflammation.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    At baseline, type 2 diabetic patients had higher fasting glucose, HbA1c, triglycerides, nitrotyrosine, C-reactive protein, ICAM-1 and IL-6, and lower flow-mediated dilation, than healthy controls.

    “Baseline glycemia, HbA1c, triglycerides, NT, C-reactive protein, ICAM-1, and IL-6 were increased in diabetic patients, whereas FMD was reduced (Table 1).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Combining the high-fat meal with glucose lowered flow-mediated dilation and raised nitrotyrosine, C-reactive protein, ICAM-1 and IL-6 more than either nutrient alone.

    “The combination of high-fat and glucose load, ie, test 3, produced a decrease in FMD and increases in NT, C-reactive protein, ICAM-1, and IL-6 (PϽ0.05 versus baseline; Figure 1), even more pronounced than with either nutrient alone (PϽ0.05; Figure 1).”
    • Also stated in: § Abstract · plain
      “These effects were more pronounced when high-fat load and glucose were combined.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In diabetic patients, blood glucose rose at 1, 2 and 3 hours after 75 g glucose alone and after the high-fat meal with glucose.

    “Glycemia increased at 1, 2, and 3 hours in diabetics during the 75-g glucose challenge and the high-fat meal plus 75 g glucose (PϽ0.05versus baseline; Figure 1)”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Atorvastatin lessened the changes in endothelial function, nitrotyrosine, C-reactive protein, ICAM-1 and IL-6 seen during every test, while postprandial hypertriglyceridemia was unaffected.

    “Such treatment was able to reduce the effect on endothelial function, NT, C-reactive protein, ICAM-1, and IL-6 observed during every test, even though postprandial hypertriglyceridemia was not affected (PϽ0.05versus placebo; Figures 2 through 4).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Combined atorvastatin and irbesartan improved all measured parameters more than either drug alone, both at rest and during each test.

    “Short-term combination therapy produced a more marked improvement in all the studied parameters both in basal conditions and during each test compared with the single treatments (Figures 2 through 4).”
    • Also stated in: § Abstract · plain
      “Short-term atorvastatin and irbesartan treatments significantly counterbalanced these phenomena, and their combination was more effective than either therapy alone.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In diabetic patients, the high-fat meal alone lowered flow-mediated dilation and raised nitrotyrosine, C-reactive protein, ICAM-1 and IL-6 from 1 to 4 hours.

    “High-fat load alone produced a decrease in FMD and increases in NT, C-reactive protein, ICAM-1, and IL-6 from 1 to 4 hours (PϽ0.05versus baseline; Figure 1).”
    • Also stated in: § Abstract · plain
      “High-fat load and glucose alone produced a decrease in endothelial function and increases in nitrotyrosine, C-reactive protein, intercellular adhesion molecule-1, and interleukin-6.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Irbesartan treatment improved resting flow-mediated dilation and lowered resting nitrotyrosine, C-reactive protein, ICAM-1 and IL-6.

    “However, as with atorvastatin treatment, significant improvements in basal FMD, NT, C-reactive protein, ICAM-1, and IL-6 were observed (Table 2).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In type 2 diabetic patients, combining atorvastatin with irbesartan reduces postprandial endothelial dysfunction, oxidative stress, and inflammation more than either agent alone.

    “with the combination of the 2 compounds being more effective.”
    • Also stated in: § Discussion · hedged
      “Because they work through different ways, it seems true that by combining the 2 compounds the effect on oxidative stress can be amplified, as demonstrated by our data.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Atorvastatin treatment improved resting flow-mediated dilation and lowered resting nitrotyrosine, C-reactive protein, ICAM-1 and IL-6.

    “However, significant improvements in basal FMD, NT, C-reactive protein, ICAM-1, and IL-6 were observed (Table 2).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    In healthy people, a sudden rise in blood glucose raises nitrotyrosine and impairs endothelial function at the same time.

    “Evidence that an acute increase in glycemia simultaneously induces an increase in nitrotyrosine (NT) and endothelial dysfunction in healthy subjects 14”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [14] 14. Marfella R, Quagliaro L, Nappo F, Ceriello A, Giugliano D. Acute hyperglycemia induces an oxidative stress in healthy subjects. J Clin Invest. 2001;108:635-636. Letter. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Prior studies show that postprandial hyperglycemia and hypertriglyceridemia act independently and cumulatively on endothelial function, with oxidative stress as the shared mediator.

    “Indeed, recent studies demonstrate both an independent and a cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial function, with oxidative stress the common mediator.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [13] 13. Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K, Giugliano D. Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes. 2004; 53:701-710. source

      Not checked in the free run.

    • cites [15] 15. Ceriello A, Taboga C, Tonutti L, Quagliaro L, Piconi L, Bais B, Da Ros R, Motz E. Evidence for an independent and cumulative effect of post- prandial hypertriglyceridemia and hyperglycemia on endothelial dys- function and oxidative stress generation: effects of short-and long-term simvastatin treatment. Circulation. 2002;106:1211-1218. source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Premisecitation

    Earlier work reported that short-term statin therapy can prevent the endothelial dysfunction and oxidative stress caused by hyperglycemia and hypertriglyceridemia.

    “In previous studies, the possibility of preventing hyperglycemia-and hypertriglyceridemia-induced endothelial dysfunction and oxidative stress with short-term treatment with statin has been reported.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [13] 13. Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K, Giugliano D. Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes. 2004; 53:701-710. source

      Not checked in the free run.

    • cites [15] 15. Ceriello A, Taboga C, Tonutti L, Quagliaro L, Piconi L, Bais B, Da Ros R, Motz E. Evidence for an independent and cumulative effect of post- prandial hypertriglyceridemia and hyperglycemia on endothelial dys- function and oxidative stress generation: effects of short-and long-term simvastatin treatment. Circulation. 2002;106:1211-1218. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Statins and AT-1 receptor blockers are commonly prescribed to prevent cardiovascular disease and diabetic complications, and their ancillary effects have been attributed to strong intracellular antioxidant activity.

    “Statins and angiotensin type 1 (AT-1) receptor blockers are widely used in preventing CVD and diabetic complications, and it has been suggested that many of their ancillary effects are due to strong intracellular antioxidant activity.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [18] 18. Mason RP, Walter MF, Jacob RF. Effects of HMG-CoA reductase inhib- itors on endothelial function: role of microdomains and oxidative stress. Circulation. 2004;109(suppl II):II-34 -II-41. source

      Not checked in the free run.

    • cites [19] 19. Ceriello A, Motz E. Angiotensin-receptor blockers, type 2 diabetes, and renoprotection. N Engl J Med. 2002;346:705-707. Letter. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Statins and angiotensin type 1 receptor blockers lower oxidative stress and inflammation and thereby improve endothelial function.

    “Statins and angiotensin type 1 receptor blockers have been shown to reduce oxidative stress and inflammation, improving endothelial function.”
    Quote in the paperSubstantial claim0 of 5 sources checked
    • cites [13] 13. Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K, Giugliano D. Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes. 2004; 53:701-710. source

      Not checked in the free run.

    • cites [15] 15. Ceriello A, Taboga C, Tonutti L, Quagliaro L, Piconi L, Bais B, Da Ros R, Motz E. Evidence for an independent and cumulative effect of post- prandial hypertriglyceridemia and hyperglycemia on endothelial dys- function and oxidative stress generation: effects of short-and long-term simvastatin treatment. Circulation. 2002;106:1211-1218. source

      Not checked in the free run.

    • cites [17] 17. Ceriello A, Assaloni R, Da Ros R, Maier A, Quagliaro L, Piconi L, Esposito K, Giugliano D. Effect of irbesartan on nitrotyrosine generation in non-hypertensive diabetic patients. Diabetologia. 2004;47:1535-1540. source

      Not checked in the free run.

    • cites [18] 18. Mason RP, Walter MF, Jacob RF. Effects of HMG-CoA reductase inhib- itors on endothelial function: role of microdomains and oxidative stress. Circulation. 2004;109(suppl II):II-34 -II-41. source

      Not checked in the free run.

    • cites [19] 19. Ceriello A, Motz E. Angiotensin-receptor blockers, type 2 diabetes, and renoprotection. N Engl J Med. 2002;346:705-707. Letter. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In these conditions oxidative stress may arise from excess superoxide anion production in mitochondria, which inactivates nitric oxide and yields peroxynitrite.

    “The production of oxidative stress in such conditions may involve the overgeneration of superoxide anion (O 2 Ϫ ) at the mitochondrial level, which in turn inactivates nitric oxide (NO), producing peroxynitrite, a potent long-lived oxidant.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [16] 16. Ceriello A, Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited. Arterioscler Thromb Vasc Biol. 2004; 24:816 -823. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Endothelial dysfunction, nitrotyrosine, C-reactive protein, IL-6, and ICAM-1 each independently predict cardiovascular disease.

    “It is noteworthy that all the studied parameters-endothelial dysfunction, 49 NT, 50 C-reactive protein, 51 IL-6, 51 and ICAM-1 51 -have been shown to be independent predictors of CVD.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [49] 49. Landmesser U, Hornig B, Drexler H. Endothelial function: a critical determinant in atherosclerosis? Circulation. 2004;109(suppl II): II-27-II-33. source

      Not checked in the free run.

    • cites [50] 50. Shishehbor MH, Aviles RJ, Brennan ML, Fu X, Goormastic M, Pearce GL, Gokce N, Keaney JF Jr, Penn MS, Sprecher DL, Vita JA, Hazen SL. Association of nitrotyrosine levels with cardiovascular disease and mod- ulation by statin therapy. JAMA. 2003;289:1675-1680. source

      Not checked in the free run.

    • cites [51] 51. Rackley CE. New clinical markers predictive of cardiovascular disease: the role of inflammatory mediators. Cardiol Rev. 2004;12:151-157. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    In diabetic patients, postprandial hyperglycemia and hypertriglyceridemia each contribute independently and additively to endothelial dysfunction accompanied by oxidative stress and inflammation.

    “This study confirms that in diabetic patients both postprandial hyperglycemia and hypertriglyceridemia have an independent and cumulative effect in favoring endothelial dysfunction accompanied by generation of oxidative stress and inflammation.”
    • Also stated in: § Abstract · hedged
      “study confirms an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial function and inflammation, suggesting oxidative stress as a common mediator of such an effect.”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [10] 10. Nappo F, Esposito K, Cioffi M, Giugliano G, Molinari AM, Paolisso G, Marfella R, Giugliano D. Postprandial endothelial activation in healthy subjects and in type 2 diabetic patients: role of fat and carbohydrate meals. J Am Coll Cardiol. 2002;39:1145-1150. source

      Not checked in the free run.

    • cites [12] 12. Anderson RA, Evans ML, Ellis GR, Graham J, Morris K, Jackson SK, Lewis MJ, Rees A, Frenneaux MP. The relationship between post- prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes. Atherosclerosis. 2001;154: 475-483. source

      Not checked in the free run.

    • cites [13] 13. Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K, Giugliano D. Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes. 2004; 53:701-710. source

      Not checked in the free run.

    • Rests on an assumption: The high-fat meal and the 75 g glucose challenge reproduce the postprandial metabolic state relevant to diabetic patients' daily lives.

  • May combine two claims.

    Interpretationown data

    Irbesartan's effects are not attributable to blood pressure lowering and occur after short-term treatment.

    “Even for irbesartan, the results are not linked to the blood pressure-lowering effect and are obtained after a short-term treatment.”
    Quote in the paperSubstantial claim

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

    Premisecitation

    Irbesartan lowers proteinuria independently of its blood pressure-lowering action.

    “Interestingly, the ability of irbesartan to reduce the proteinuria independently from its blood pressure-lowering action has also been confirmed in a study with an ad hoc design, 27”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [27] 27. Sasso FC, Carbonara O, Persico M, Iafusco D, Salvatore T, D'Ambrosio R, Torella R, Cozzolino D. Irbesartan reduces the albumin excretion rate in microalbuminuric type 2 diabetic patients independently of hyper- tension. Diabetes Care. 2002;25:1909 -1913. source

      Not checked in the free run.

  • Classified as probably not a substantial claim.

    Study design and conductown data

    Diabetic patients were randomly allocated to placebo, atorvastatin, irbesartan, or both.

    “All diabetic patients were randomly assigned to take placebo or atorvastatin 40 mg/d, irbesartan 300 mg/d, or atorvastatin 40 mg/d plus irbesartan 300 mg/d for 7 days.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationnone given

    Mitochondrial superoxide production is likely the initial and possibly the most important source of free radicals during hyperglycemia and lipid overload.

    “However, superoxide generation at the mitochondrial level is probably only the first, perhaps the most important, source of free radicals in the conditions described above.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Statins and AT-1 receptor blockers protect endothelial function and reduce inflammation in diabetic and nondiabetic subjects, an effect convincingly attributed to their intracellular antioxidant activity.

    “Statins and AT-1 receptor blockers protect endothelial function and reduce inflammation in diabetic and nondiabetic subjects, and these effects are convincingly mediated through their intracellular antioxidant activity.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [18] 18. Mason RP, Walter MF, Jacob RF. Effects of HMG-CoA reductase inhib- itors on endothelial function: role of microdomains and oxidative stress. Circulation. 2004;109(suppl II):II-34 -II-41. source

      Not checked in the free run.

    • cites [19] 19. Ceriello A, Motz E. Angiotensin-receptor blockers, type 2 diabetes, and renoprotection. N Engl J Med. 2002;346:705-707. Letter. source

      Not checked in the free run.

    • cites [20] 20. Ceriello A. New insights on oxidative stress and diabetic complications may lead to a "causal" antioxidant therapy. Diabetes Care. 2003;26: 1589 -1596. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    Atorvastatin's counterbalancing effect is probably due to its ancillary, non-lipid properties, since it appeared after short-term dosing that left fasting and postprandial lipids unchanged.

    “The action of atorvastatin is reasonably due to its ancillary properties, being evident after short-term administration, which does not influence the lipid profile, either fasting or postprandial.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Study design and conductcitation

    Endothelial function was measured as flow-mediated dilation of the brachial artery, a method validated in earlier studies.

    “Endothelial function was evaluated by measuring the flow-mediated vasodilation (FMD) of the brachial artery.”
    • Also stated in: § Endothelial Function · boosted
      “The validity of this method has been confirmed in previous studies.24,25”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [24] 24. Corretti MC, Plotnick GD, Vogel RA. Technical aspects of evaluating brachial artery endothelium-dependent vasodilation using high frequency ultrasound. Am J Physiol. 1995;268:H1397-H1404.

      Not checked in the free run.

    • cites [25] 25. Ramsey MW, Goodfellow J, Jones CJ, Luddington LA, Lewis MJ, Hen- derson AH. Endothelial control of arterial distensibility is impaired in chronic heart failure. Circulation. 1995;92:3212-3219.

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductown data

    The treatment phase was double-blind, crossover and placebo-controlled.

    “Subsequently, a double-blind, crossover, placebo-controlled study was started.”
    Quote in the paperSubstantial claim

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

    Study design and conductown data

    The three test meals were eaten in randomized order.

    “Diabetic patients ate, in randomized order, 3 different menus on 3 different days”
    Quote in the paperNot a substantial claim

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

    Study design and conductown data

    Interobserver and intraobserver variability for repeated resting arterial diameter measurements were 0.04±0.02 mm and 0.02±0.02 mm.

    “In our study, the interobserver variability for the repeated measurements of resting arterial diameter was 0.04Ϯ0.02mm.The intraobserver variability for the repeated measurements of resting arterial diameter was 0.02Ϯ0.02mm.”
    Quote in the paperNot a substantial claim
28 of 28

  • The paper relies on this without support.

    The high-fat meal and the 75 g glucose challenge reproduce the postprandial metabolic state relevant to diabetic patients' daily lives.

    “Diabetic patients ate, in randomized order, 3 different menus on 3 different days: test 1, a high-fat meal; test 2, 75 g glucose alone; and test 3, a high-fat meal plus 75 g glucose.”

  • The paper relies on this without support.

    The subjects kept to their usual diets throughout the study.

    “All subjects were recommended to consume their habitual diets during the entire study period.”
2 of 2

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?

  • Excessive ingestion of calorie-dense, easily digestible foods causes abnormal surges in blood glucose and triglyceride levels.

    “Excessive ingestion of calorie-dense, easily digestible foods causes abnormal surges in blood glucose and triglyceride levels (11)(12)(13).”

    From Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardiovascular Health (2008) · cites this paper as [13]

    The Results (page unavailable) report that triglycerides rose after a high-fat meal and glucose rose after a glucose challenge; both rose when the two were combined in patients with type 2 diabetes. The High-Fat Load section describes a calorie-dense test meal, but the paper does not establish that excessive ingestion of easily digestible foods generally causes abnormal surges in both measures. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Postprandial hyperlipemia causes oxidative stress and inflammation and independently potentiates the adverse effects of postprandial hyperglycemia.

    “Post-prandial hyperlipemia, manifest as elevated levels of triglycerides, chylomicrons, and remnant lipoproteins, causes oxidative stress and inflammation, and independently potentiates the adverse effects of post-prandial hyperglycemia (13).”

    From Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardiovascular Health (2008) · cites this paper as [13]

    The Results and Abstract (page not provided) report that a high-fat meal increased triglycerides and markers of oxidative stress and inflammation, with more pronounced effects when glucose was added. The Biochemical Measurements section (page not provided) lists triglycerides but not chylomicrons or remnant lipoproteins; the paper therefore does not support those specific components of the citing sentence. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Ageing is characterised by a profound reduction in anti-inflammatory lipoxin A4 levels.

    “In line with this, it has recently been shown that ageing (two groups with a mean age of 77•9 and 102•5 years, respectively v. a group with a mean age of 43•5 years) is characterised by a profound reduction in anti-inflammatory lipoxin A 4 levels (183) .”

    From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [183]

Cites

Flagged first, then by citations

Research works printed but not linked: 6

  1. Warnick GR, Nguyen T, Albers AA. Comparison of improved precipitation methods for quantification of HDL cholesterol. Clin Chem. 1995; 31: 217–222.
  2. Corretti MC, Plotnick GD, Vogel RA. Technical aspects of evaluating brachial artery endothelium-dependent vasodilation using high frequency ultrasound. Am J Physiol. 1995; 268: H1397–H1404.
  3. 10.1161/circ.92.11.3212 · DOI
  4. 10.1161/atvb.22.2.300 · DOI
  5. 10.1161/circ.104.4.376 · DOI
  6. 10.1161/circ.101.20.2349 · DOI

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Authors
Ceriello, A., Assaloni, R., Da Ros, R., Maier, A., Piconi, L., Quagliaro, L., Esposito, K., & Giugliano, D.
Affiliations
  • University of Udine (IT)
  • From the Department of Pathology and Medicine, Experimental and Clinical, Chair of Internal Medicine, University of Udine, Udine (A.C., R.A., R.D.R., A.M.); Morpurgo-Hofman Research Laboratory on Aging, Udine (L.P., L.Q.); and Department of Geriatric and Metabolic Diseases, Second University of Naples, Naples (K.E., D.G.), Italy.
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2005-05-17
Volume
111
Issue
19
Pages
2518-2524
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.0000165070.46111.9f
OpenAlex
W2122166221
Cited by
298
References
52
Citations by year
2026: 1 · 2024: 3 · 2023: 6 · 2022: 9 · 2021: 7 · 2020: 11 · 2019: 6 · 2018: 15 · 2017: 8 · 2016: 11 · 2015: 15 · 2014: 16 · 2013: 21 · 2012: 23
FWCI
15.98
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
  • Institutional Research Information System (University of Udine) (submittedVersion)
  • Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Keywords
atorvastatin, irbesartan, combination therapy, endothelial dysfunction, oxidative stress, inflammation, type 2 diabetes, postprandial hypertriglyceridemia, postprandial hyperglycemia, high-fat meal, nitrotyrosine, C-reactive protein, interleukin-6, ICAM-1, statins, angiotensin receptor blockers
MeSH terms
Atorvastatin, Irbesartan, Anticholesteremic Agents, Biphenyl Compounds, Diabetes Mellitus, Type 2, Drug Therapy, Combination, Endothelium, Vascular, Female, Heptanoic Acids, Humans, Hyperglycemia, Inflammation, Male, Middle Aged, Pyrroles, Tetrazoles, Hypertriglyceridemia, Case-Control Studies, Treatment Outcome, Oxidative Stress, 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 ›

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