By Jeff Unger, MD, FACE
Director, Unger Primary Care Concierge Medical Group, Rancho Cucamonga, CA
Dr. Unger reports that he participates on the speaker’s bureau for Janssen Pharmaceuticals, Novo Nordisk, and Valeritas; is an advisory board member for Janssen, Sanofi-Aventis, Novo Nordisk, Halozyme, and Abbott; is a consultant for Novo Nordisk, Sanofi-Aventis, Valeritas, and Dance Pharmaceuticals; and receives research/grant support from Boehringer Ingelheim, Novo Nordisk, GSK, Eli Lilly, Johnson and Johnson, Pfizer, Sanofi-Aventis, Takeda, and Merck.
SYNOPSIS: Skipping breakfast increases lunch and dinner postprandial glucose levels due to impaired GLP-1 secretion. The resultant escalation of insulin resistance can have an impact on long-term diabetes management. Breakfast consumption could be a successful strategy for reducing postprandial hyperglycemia in patients with type 2 diabetes.
SOURCE: Jakubowicz D, et al. Postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 diabetes: A randomized clinical trial. Diabetes Care 2015;38:1820-1826.
Twenty-six patients with type 2 diabetes, duration < 10 years, and an A1c 7-9 % were recruited for this randomized, open-label, crossover-within-subject clinical trial in Venezuela. Patients served as their own controls. None of the patients worked graveyard shifts, and all woke up between 6 a.m. and 7 a.m. and went to sleep between 10 p.m. and 11 p.m. nightly. Patients were insulin- and GLP-1 receptor agonist-naive and taking only metformin. Participants underwent two separate all-day meal tests with a washout of 2-4 weeks between testing days. On the day participants ate breakfast, three identical standard meals were provided in the clinic at planned times. On days when breakfast was not consumed, lunch and dinner were provided on the same schedule. Blood samples were obtained from all participants at 15, 30, 60, 90, 120, 150, and 180 minutes after eating commenced for each meal. The primary outcome was the assessment of postprandial glycemia following lunch and dinner in patients who ate or skipped breakfast. Secondary outcomes were the assessment levels of plasma insulin, C-peptide, intact GLP-1 (iGLP-1), free fatty acid, and glucagon.
When skipping breakfast, the peaks of plasma glucose after lunch and dinner were 39.8% and 24.9% higher, respectively. Skipping breakfast resulted in a 1-hour delay of iGLP-1 secretion and a 21.5% lowered peak response at lunch, compared with levels obtained when breakfast was consumed. Skipping breakfast induced insulin resistance by increasing levels of glucagon, free fatty acids, reducing endogenous insulin secretion, and iGLP-1 following lunch and dinner. Eating breakfast reversed this adverse metabolic state.
COMMENTARY
In type 2 diabetes, postprandial hyperglycemia has a significant effect on A1c and long-term outcomes. Reducing peaks in post-meal glucose levels may slow the progression of beta-cell function and improve microvascular and macrovascular disease. From a clinical perspective, many of our patients believe that skipping breakfast will result in a reduction in caloric consumption during the day. However, upon careful examination of their glucose logs, these patients actually have a rise in glucose levels beginning mid-day, which continues until bedtime. Breakfast has been demonstrated to be of major importance for the 24-hour regulation of glucose. Skipping breakfast has been associated with weight gain, increased insulin resistance, and an increased risk of developing type 2 diabetes. The omission of breakfast in patients with type 2 diabetes is associated with a significant rise in A1c and all-day postprandial hyperglycemia. Most of the metabolic pathways involved in postprandial glycemia, including beta-cell secretory function, insulin sensitivity, muscle glucose uptake, muscle glycogen storage, and hepatic glucose production, are controlled by the circadian clock. Skipping breakfast, therefore, has a tremendous metabolic impact on insulin resistance.
Based on the findings of this well-controlled study, patients with type 2 diabetes should be instructed that the consumption of breakfast will likely result in a reduction in postprandial hyperglycemia, improvement in GLP-1 secretion, and a decrease in overall insulin resistance.
REFERENCES
-
Froy O. Metabolism and circadian rhythms — implications for obesity. Endocr Rev 2010;31:1-24.
-
Saad A, et al. Diurnal pattern to insulin secretion and insulin action in healthy individuals. Diabetes 2012;61:2691-2700.
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Monnier L, et al. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetes patients: Variations with increasing levels of HbA1C. Diabetes Care 2003;26:881-885.
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Bi H, et al. Breakfast skipping and the risk of type 2 diabetes: A meta-analysis of observational studies. Public Health Nutr 17 Feb 2015:1-7.
