Contributions of Fasting and Postprandial Plasma Glucose Increments to the Overall Diurnal Hyperglycemia of Type 2 Diabetic Patients

Monnier, L.; Lapinski, H; Colette, C

doi:10.2337/diacare.26.3.881

Cited by 1,345 publications

(1,031 citation statements)

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“…When seeking to contextualise our findings within the body of existing research, the findings differ from a meta‐analysis which indicated a stronger association between PPG and HbA1c compared with FPG and HbA1c 2. Regarding the reasons for this discrepancy, it can be argued that, depending on the method used for assessment of PPG (ie, after breakfast, lunch or dinner; at 1 or 2 h after the start of the meal), the impact of PPG can appear as slightly lower or greater than that of FPG.…”

Section: Tablecontrasting

confidence: 67%

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Association of postprandial and fasting plasma glucose with HbA1c across the spectrum of glycaemic impairment in type 2 diabetes

et al. 2017

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Section: Tablecontrasting

confidence: 67%

“…A higher contribution of PPG relative to FPG in patients with HbA1c levels of ≤7% (53 mmol/mol) has been observed in a seminal article published in 20032 and further observed in several studies 3. Collectively, such data seem to make a convincing case for targeting postprandial glucose excursions in patients with mild hyperglycaemia.…”

Section: Tablementioning

confidence: 65%

Association of postprandial and fasting plasma glucose with HbA1c across the spectrum of glycaemic impairment in type 2 diabetes

et al. 2017

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“…Loss of postprandial glycaemic control occurs early in patients with T2D subsequent to sequential loss of glycaemic control during the nocturnal fasting period 2. The absolute contribution that PPG makes to hyperglycaemia in T2D is generally constant at different HbA1c levels, but becomes proportionately greater than the contribution of FPG as HbA1c decreases 2, 3, 4. Hence, targeting PPG control rather than relying on managing FPG alone may increase the opportunity for patients to meet their recommended HbA1c targets 1, 3, 4, 5.…”

Section: Introductionmentioning

confidence: 99%

“…The absolute contribution that PPG makes to hyperglycaemia in T2D is generally constant at different HbA1c levels, but becomes proportionately greater than the contribution of FPG as HbA1c decreases 2, 3, 4. Hence, targeting PPG control rather than relying on managing FPG alone may increase the opportunity for patients to meet their recommended HbA1c targets 1, 3, 4, 5. Because targeting PPG control may mitigate the risk of diabetes‐related complications,1 the American Association of Clinical Endocrinologists/American College of Endocrinology and the International Diabetes Federation recommend a target level for 2‐hour PPG of ≤140 mg/dL (≤7.8 mmol/L),1, 6 and the American Diabetes Association recommend a higher target level for 2‐hour PPG of ≤180 mg/dL (≤10.0 mmol/L) 7…”

Section: Introductionmentioning

confidence: 99%

Reduction of postprandial glucose by lixisenatide vs sitagliptin treatment in Japanese patients with type 2 diabetes on background insulin glargine: A randomized phase IV study (NEXTAGE Study)

Yamada

Senda

Naito

et al. 2017

Diabetes Obesity Metabolism

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AimTo evaluate the pharmacodynamics of lixisenatide once daily vs sitagliptin once daily in Japanese patients with type 2 diabetes receiving insulin glargine U100.Materials and methodsThis multicentre, open‐label, phase IV study (NEXTAGE Study; ClinicalTrials.gov number, NCT02200991) randomly assigned 136 patients to either lixisenatide once daily via subcutaneous injection (10 µg initially increased weekly by 5 up to 20 µg) or once‐daily oral sitagliptin 50 mg. The primary endpoint was the change in postprandial glucose (PPG) exposure 4 hours after a standardized breakfast (PPG area under the plasma glucose concentration–time curve [AUC0 :00‐4:00h]) from baseline to day 29.ResultsLixisenatide reduced PPG exposure to a statistically significantly greater extent than sitagliptin: least squares (LS) mean change from baseline in PPG AUC0 :00‐4:00h was −347.3 h·mg/dL (−19.3 h·mmol/L) in the lixisenatide group and −113.3 h·mg/dL (−6.3 h·mmol/L) in the sitagliptin group (LS mean between‐group difference −234.0 h·mg/dL [−13.0 h·mmol/L], 95% confidence interval −285.02 to −183.00 h·mg/dL [−15.8 to −10.2 h·mmol/L]; P < .0001). Lixisenatide led to significantly greater LS mean reductions in maximum PPG excursion than sitagliptin (−122.4 vs −46.6 mg/dL [−6.8 vs −2.6 h·mmol/L]; P < .0001). Change‐from‐baseline reductions in exposure to C‐peptide, fasting glycoalbumin levels, and the gastric emptying rate were greater in the lixisenatide than in the sitagliptin group. The incidence of treatment‐emergent adverse events was higher with lixisenatide (60.9%) than with sitagliptin (16.4%), with no serious events or severe hypoglycaemia reported.ConclusionLixisenatide reduced PPG significantly more than sitagliptin, when these agents were added to basal insulin glargine U100, and was well tolerated.

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“…The major reason for this failure is that postprandial glycemia cannot be corrected as strictly under the therapy as fasting glycemia 7,8 . The next step to target postprandial hyperglycemia is subsequently required after overcoming fasting hyperglycemia 9 . Although it has been shown that additional prandial insulin can provide better glycemic control 10 , substantial numbers of patients in clinical practice hesitate to receive this intensive insulin therapy because of the inconvenience of daily multiple injections, which would burden their lifestyle.…”

Section: Introductionmentioning

confidence: 99%

Efficacy of liraglutide therapy in Japanese type 2 diabetic patients insufficiently controlled with basal‐supported oral therapy

Takahara

Shiraiwa²,

Ohtoshi³

et al. 2012

J of Diabetes Invest

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(J Diabetes Invest, doi: 10.1111/j.2040‐1124.2012.00223.x, 2012) Aims/Introduction: We assessed the efficacy of liraglutide therapy in Japanese type 2 diabetic patients insufficiently controlled with basal‐supported oral therapy (BOT).Materials and Methods: We retrospectively analyzed the data of 37 patients who had postprandial hyperglycemia (≥10.0 mmol/L) with BOT (long‐acting insulin plus glimepiride) with their insulin titrated enough to keep preprandial glycemia <7.2 mmol/L, and who had their treatment changed to liraglutide monotherapy, with the subsequent addition of glimepiride, when required. Those who achieved the glycemic target at all points (preprandial glycemia <7.2 mmol/L and postprandial glycemia <10.0 mmol/L) were regarded as responders and the efficacy of liraglutide therapy was assessed. We also explored the predictive clinical characteristics associated with its efficacy.Results: Daily doses of insulin and glimepiride with BOT were 14 ± 9 units and 1.5 ± 0.9 mg, respectively. After the change to liraglutide therapy, 37% of the patients appeared to be responders to the therapy, whereas 12% had their glycemic control rather deteriorated. Efficacy of liraglutide therapy was significantly associated with baseline insulin dosage and post‐breakfast glycemia with BOT. The C‐statistic of the model was calculated to be 0.90.Conclusions: There were responders and non‐responders to liraglutide therapy in Japanese BOT failures. It is likely that baseline insulin dosage and post‐breakfast glycemia with BOT are clinically useful indicators for the efficacy of liraglutide therapy.

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Contributions of Fasting and Postprandial Plasma Glucose Increments to the Overall Diurnal Hyperglycemia of Type 2 Diabetic Patients

Cited by 1,345 publications

References 20 publications

Association of postprandial and fasting plasma glucose with HbA1c across the spectrum of glycaemic impairment in type 2 diabetes

Association of postprandial and fasting plasma glucose with HbA1c across the spectrum of glycaemic impairment in type 2 diabetes

Reduction of postprandial glucose by lixisenatide vs sitagliptin treatment in Japanese patients with type 2 diabetes on background insulin glargine: A randomized phase IV study (NEXTAGE Study)

Efficacy of liraglutide therapy in Japanese type 2 diabetic patients insufficiently controlled with basal‐supported oral therapy

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