Physicians' Academy for Cardiovascular Education

Skipping breakfast yields a higher glycaemic response in T2DM

Jakubowicz et al., Diabetes Care 2015

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

Jakubowicz D, Wainstein J, Ahren B et al.
Diabetes Care published ahead of print July 28, 2015, doi:10.2337/dc15-0761

Postprandial hyperglycaemia (PPHG) greatly affects HbA1c values in diabetes type 2 (T2DM). Even when glycaemic control is restored, it is strongly associated with future development of vascular complications [1-3]. Lessening glycaemic peaks could therefore serve as an important target in the initial stages of disease.
Since most of the metabolic pathways involved in postprandial glycaemia are controlled by the circadian clock [4], PPHG displays a circadian rhythm. Since meal time potently synchronises the circadian clock, it affects the daily variations of postprandial glycaemia in healthy individuals and in persons with T2DM [4-7]. Meal time could be a means to mitigate glycaemic peaks.
Breakfast has been shown to be important for the 24-hour regulation of glucose [8]. While the benefits of breakfast consumption on overall PPHG and HbA1c levels are quite clear, the relationship between breakfast skipping and all-day glycaemic excursions in T2DM is less clear. This randomised, open-label, cross-over-within-subject clinical trial investigated the postprandial glycaemic response to identical lunch and dinner meal tests, with (YesB) or without (noB) breakfast, in patients with T2DM. Patients were tested on two days, one that started with breakfast, and one that did not.

Main results

  • Area under the curve  of the whole meal response (AUC(0-180 min) were 35.7%, 68.6%, 62.1% and 52.9% higher for glucose, insulin, C-peptide and iGLP-1, respectively after breakfast vs. breakfast skipping.
  • Plasma levels were 16.5%, 45%, 50% and 33% higher for glucose, insulin, C-peptide and iGLP-1 before lunch in the YesB vs. NoB group.
  • The AUC(0-30: early response interval) value for glucagon was higher after breakfast, while the late response (AUC(60-180min)) value was lower, on the YesB vs. the NoB day.
  • Overall, skipping breakfast leads to prolonged high levels of glucagon and FFA, and lower levels of glucose, insulin, C-peptide and iGLP-1, and breakfast consumption induced the opposite metabolic state.
  • Peaks of plasma glucose after lunch and dinner were 39.8% and 24.9% higher on the NoB day than the YesB day. The AUC(0-180min) values for glucose were 36.8% and 26.6% higher after lunch and dinner on NoB vs. YesB, and lower for insulin (17% and 7.9%). C-peptide levels mirrored those of insulin after lunch and dinner.
  • iGLP-1 showed a peak 60 min later on the NoB vs. YesB day, and was 21.5% lower.
  • Glucagon levels increased after lunch and dinner, yielding higher AUC(0-180 min) values on the NoB day.
  • Overall, skipping breakfast lead to higher glycaemic index response and high levels of glucagon and FFA, as well as lower levels of insulin, C-peptide, and iGLP-1 after lunch and dinner, while eating breakfast had the opposite effect.


Omission of breakfast in patients with T2DM is associated with a significantly higher glycaemic response after subsequent lunch and dinner, as compared to after identical meals but having eaten breakfast. Insulin secretion was also impaired after skipping breakfast, since the peak was delayed and plasma concentrations of insulin and C-peptide were reduced. Thus, breakfast is important for glucose homeostasis and preventing PPHG throughout the day.
Find this article online at Diabetes Care


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