The Second-Meal Phenomenon in Type 2 Diabetes

Jovanović, Ana; Gerrard, J; Taylor, Roy

doi:10.2337/dc08-2196

Cited by 86 publications

(117 citation statements)

References 13 publications

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“…The prolonged elevation of plasma FFA levels triggered by the extension of the overnight fast on the NoB day correlated with reduced early insulin release, higher glucose, and less suppressed glucagon and FFA levels after lunch and dinner. A similar positive correlation was observed between FFA and glucose levels after lunch in people with and without diabetes when breakfast was omitted (17)(18)(19). Acute elevation of FFA by intravenous infusion or omission of breakfast has been reported to cause inhibition of insulin-stimulated muscular glucose transport.…”

Section: Discussionsupporting

confidence: 60%

“…Although omission of breakfast has been demonstrated to be associated with a higher glycemic response after a liquid preload (16) or lunch in healthy individuals (17) and in individuals with type 2 diabetes (10,18,19), postprandial glycemia after other meals ingested later during the day has never been assessed. A recent study showed that breakfast skipping resulted in a higher postprandial glycemic response after lunch and dinner in healthy individuals (20).…”

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confidence: 99%

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Fasting Until Noon Triggers Increased Postprandial Hyperglycemia and Impaired Insulin Response After Lunch and Dinner in Individuals With Type 2 Diabetes: A Randomized Clinical Trial

et al. 2015

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OBJECTIVESkipping breakfast has been consistently associated with high HbA 1c and postprandial hyperglycemia (PPHG) in patients with type 2 diabetes. Our aim was to explore the effect of skipping breakfast on glycemia after a subsequent isocaloric (700 kcal) lunch and dinner. RESEARCH DESIGN AND METHODSIn a crossover design, 22 patients with diabetes with a mean diabetes duration of 8.4 6 0.7 years, age 56.9 6 1.0 years, BMI 28.2 6 0.6 kg/m 2 , and HbA 1c 7.7 6 0.1% (61 6 0.8 mmol/mol) were randomly assigned to two test days: one day with breakfast, lunch, and dinner (YesB) and another with lunch and dinner but no breakfast (NoB). Postprandial plasma glucose, insulin, C-peptide, free fatty acids (FFA), glucagon, and intact glucagon-like peptide-1 (iGLP-1) were assessed. RESULTSCompared with YesB, lunch area under the curves for 0-180 min (AUC 0-180 ) for plasma glucose, FFA, and glucagon were 36.8, 41.1, and 14.8% higher, respectively, whereas the AUC 0-180 for insulin and iGLP-1 were 17% and 19% lower, respectively, on the NoB day (P < 0.0001). Similarly, dinner AUC 0-180 for glucose, FFA, and glucagon were 26.6, 29.6, and 11.5% higher, respectively, and AUC 0-180 for insulin and iGLP-1 were 7.9% and 16.5% lower on the NoB day compared with the YesB day (P < 0.0001). Furthermore, insulin peak was delayed 30 min after lunch and dinner on the NoB day compared with the YesB day. CONCLUSIONSSkipping breakfast increases PPHG after lunch and dinner in association with lower iGLP-1 and impaired insulin response. This study shows a long-term influence of breakfast on glucose regulation that persists throughout the day. Breakfast consumption could be a successful strategy for reduction of PPHG in type 2 diabetes.

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Section: Discussionsupporting

confidence: 60%

mentioning

confidence: 99%

Fasting Until Noon Triggers Increased Postprandial Hyperglycemia and Impaired Insulin Response After Lunch and Dinner in Individuals With Type 2 Diabetes: A Randomized Clinical Trial

et al. 2015

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“…Degree of fasting serum FFA reduction from the baseline level at 24 weeks in the attained group of the present study was similar to that in the above report. Interestingly, Taylor et al observed a positive correlation between the preprandial serum FFA level and postprandial plasma glucose for 4 hours (AUC-PG 0-4h ) in diabetic patients [16]. Therefore, suppression of fasting FFA by Gla may contribute to improvement of postprandial plasma glucose excursion.…”

Section: Appendixmentioning

confidence: 99%

Effect of insulin glargine on endogenous insulin secretion and beta-cell function in Japanese type 2 diabetic patients using oral antidiabetic drugs

et al. 2014

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INSULIN DEFICIENCY and insulin resistance are major causes of type 2 diabetes (T2DM) [1]. In particular, delayed and inadequate postprandial insulin secretion is a significant problem for Japanese T2DM patients [2]. We previously analyzed 2,021 Japanese subjects who underwent a 75g oral glucose tolerance test (75g OGTT). We found that the area under the plasma insulin curve (AUC-Ins) of 483 subjects with newly diagnosed diabetes increased along with the increment of fasting plasma glucose (FPG) until it reached the maximum at an FPG of 110 mg/dL, after which AUC-Ins declined as FPG increased further [3]. This result sug- Abstract. The aim of the present study was to evaluate the effect of insulin glargine (Gla) (as part of basal-supported oral therapy) on endogenous insulin secretion and beta-cell function in type 2 diabetic patients. In 33 insulin-naive patients showing poor glycemic control on treatment with sulfonylurea (SU)-based OADs without DPP4 inhibitors, once-daily injection of Gla was added without changing OADs, and the dose of Gla was titrated to attain a fasting plasma glucose (FPG) <110 mg/dL over 24 weeks. Morning meal tests were done at baseline, 12 weeks and 24 weeks. FPG and 2-hour plasma glucose (2HPG) and serum C-peptide (FCPR and 2HCPR) were measured 3 times, while serum intact proinsulin (FPI and 2HPI) was measured at baseline and 24 weeks. Levels of FPG, FCPR, 2HPG, and HbA1c were significantly reduced from baseline at 24 weeks (176±52 to 117±27 mg/dL, p<0.01; 2.0±0.9 to 1.6±1.0 ng/mL, p<0.01; 257±53 to 202±27 mg/dL, p<0.01; and 8.4±0.9 to 7.3±0.6%, p<0.01, Mean±SD), but 2HCPR was unchanged. The patients were divided into two groups depending on whether FPG at 24 weeks was <110 mg/dL or not: attained group (n=15) and not attained group (n=18). The dose of Gla did not differ between the two groups, but the 2HPI/2HCPR ratio at 24 weeks showed a significant decrease from baseline in the attained group. Supplementation with Gla improved glycemic control and maintained intrinsic basal insulin secretion, without changing 2-hour postprandial secretion. Achieving good glycemic control with an FPG<110 mg/dL by adding Gla decreased the 2HPI/2HCPR ratio at 24 weeks.Key words: Type 2 diabetes, Insulin glargine, Proinsulin/C-peptide ratio, Free fatty acids gested that the compensatory increase of postprandial insulin secretion may reach a limit around an FPG of 110 mg/dL in Japanese persons. Thus, it would be interesting to investigate whether the impaired postprandial insulin secretion of patients with poor glycemic control and an FPG>110 mg/dL could recover if FPG was reduced below 110 mg/dL by basal insulin supplementation. Basal insulin combined with oral antidiabetic drugs (OADs) is called basal-supported oral therapy (BOT), and the FPG-lowering effect of BOT in T2DM patients with insufficient control by OADs has been reported previously [4]. Insulin glargine (Gla) is a longacting insulin analog with a sustained profile of action over 24 hours that causes hypoglycemia much less frequently than NPH...

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“…These findings contradict those of Axelsen et al [40] who found that carbohydrates in the form of uncooked starch (slow digesting starch) consumed as an evening meal improved glycemic response in individuals with type 2 diabetes to a breakfast meal compared to white bread. Jovanovic et al [41] also found that in individuals with type 2 diabetes, eating breakfast can lower PPGR to a lunch meal compared to not eating breakfast. They also reported that while eating breakfast did not influence insulin levels in individuals with type 2 diabetes, it did suppress FFA levels, which correlated with glucose AUC values.…”

Section: Second Meal Effect and Type 2 Diabetesmentioning

confidence: 98%

The Second Meal Effect and Its Influence on Glycemia

Fletcher¹

2012

J Nutrition Disorder Ther

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The study of factors that influence blood glucose homeostasis is becoming increasingly important as prevalence rates for insulin resistance and type 2 diabetes have increased. Diets with a low glycemic index (lowGI) have been shown to reduce the risk for diseases by limiting the increase of glucose in the blood. LowGI intake in one meal also has been shown to limit the postprandial glycemic response (PPGR) to a subsequent meal; a concept termed the "second meal effect". Although there have been many theories for the mechanisms responsible for the second meal effect, the exact cause has yet to be elucidated. It is important for both research investigators as well as patients to consider food consumption prior to testing PPGR, as there is evidence that the GI of one meal not only affects the PPGR of that meal, but will also influence the PPGR of the following meal(s). Here we will review recent evidence regarding factors believed to contribute to the second meal effect and the magnitude of their impact.

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The Second-Meal Phenomenon in Type 2 Diabetes

Cited by 86 publications

References 13 publications

Fasting Until Noon Triggers Increased Postprandial Hyperglycemia and Impaired Insulin Response After Lunch and Dinner in Individuals With Type 2 Diabetes: A Randomized Clinical Trial

Fasting Until Noon Triggers Increased Postprandial Hyperglycemia and Impaired Insulin Response After Lunch and Dinner in Individuals With Type 2 Diabetes: A Randomized Clinical Trial

Effect of insulin glargine on endogenous insulin secretion and beta-cell function in Japanese type 2 diabetic patients using oral antidiabetic drugs

The Second Meal Effect and Its Influence on Glycemia

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