effect of skipping breakfast on glycemic response
TRANSCRIPT
DR VASIF MAYAN M CM2 UNIT
OBJECTIVE Explore the effects of skipping breakfast on glycemia after a
subsequent isocaloric (700kcal) lunch and dinner
HYPOTHESIS : skipping breakfast has been consistently associated with high HbA1c and PPHG ( Post prandial Hyperglycemia)
STUDY DESIGN and METHODS Open label Randomised controlled trial – crossover design
22 individuals with type 2 Diabetes <10yr duration HbA1c 7-9% Age 30 – 70 yrs BMI 22-35 kg/m2
Postprandial hyperglycemia has tremendous effect on HbA1c and associated with future development of vascular complications even when glycemic control is restored
Beta cell secretory function, insulin sensitivity, muscular glucose uptake, muscle glycogen storage, hepatic glucose output are controlled by circardian clock
MEAL TIMINGS are a potent synchronizer of circadian clock
Skipping breakfast increasingly common nowadays skipping breakfast associated with weight gain and other
adverse health outcomes, including insulin resistance and an increased risk for developing type 2 diabetes
In T2DM , skipping breakfast associated with a significant increase in HbA1c and all-day PPHG even without overeating in the evening
consumption of a highenergy breakfast and a low-energy dinner results in a significant reduction of all-day postprandial glycemia
3 months of a high-energy breakfast led to a 5% reduction in HbA1c levels in participants with type 2 diabetes
in this study, the skipped breakfast was compensated for by extra calories at lunch and dinner, making it difficult to determine whether the high glycemic response was a consequence of breakfast omission or the extra calories
Inclusion criteria 22 individuals with type 2 Diabetes <10yr duration HbA1c 7-9% Age 30 – 70 yrs BMI 22-35 kg/m2
Exclusion criteria Patients on OHA other than metformin Severe Complications of diabetes Thyroid/renal/hepatic/pulmonary dysfunction
methodology 2 separate all day meal tests with 2-4 week interval in
between
Advised to take for 2 days prior to test and on day of testing as well.
EACH 700kcal meal with 20% FAT, 54% CHO, 26% PROTEIN, 7% FIBER
BREAKFAST LUNCH DINNERYes B 8 AM 1 30 PM 7 PMNo B - 1 30 PM 7 PM
Catheter in antecubital vein Samples taken at 8am ( O mins) 0, 15,30,60,90,120,150 and 180 mt after eating commenced
Primary outcome Assessment of post prandial glycemia after lunch and dinner
Secondary outcomes Plasma insulin, C-petide, intact GLP-1 (iGLP-1), FFA, Glucagon
levels after lunch and dinner
RESULTSBREAKFAST LUNCH DINNER
YES B NO B YES B NO B YES B NO BGLUCOSEMg/dl
218 124-43%
192 269+40%
235 294+25%
INSULIN microIU/ml
40.5 11.3-72%
48.5 36.5-25%
38.6 34.4-11%
C Peptideng/ml
6.4 2.4-63%
7.6 6.6-14%
7.2 6.2-15%
iGLP -1pmol/L
16.2 6.4-60%
18 14-21%
16 14-15%
FFAmmol/L
231 630+172%
280 38136%
350 42120%
Glucagonpg/ml
130 103-20%
125 13710%
132 1449%
Results Skipping breakfast lead to higher glycemic index response,
High levels of FFA and Glucagon to a reduced level of insulin
Breakfast consumption solved the problem!
CONCLUSION Omission of breakfast in patients with type 2 diabetes is
associated with a significantly higher glycemic response after subsequent lunch and dinner
plasma FFA and glucagon levels were significantly higher
omission of breakfast also resulted in impaired insulin secretion after lunch and dinner
breakfast is of major importance for glucose homeostasis including islet function and incretin hormones throughout the day
Second meal phenomenon Enhanced β-cell responsiveness at the second meal as
induced by the first meal
the first and the second phase of insulin release are both influenced by β-cell memory, and the magnitude of insulin release is enhanced significantly by previous glucose exposure
As per this study, this effect is also is extended to dinner
How do we explain ?
No Breakfast day
Absence of glucose elevation because of fasting until noon
Diminish β -cell responsiveness and memory
Reduced and delayed insulin response after lunch and dinner
lower insulin release by β -cells in response to nutrient depletion or starvation induces lysosomal degradation of nascent secretory insulin granules
This is controlled by protein kinase D, a key player in secretory granule biogenesis
GLP - 1 impaired insulin secretion at lunch and dinner maybe due to
perturbed incretin regulation, because GLP-1 enhance β -cell memory and sensitivity to glucose.
higher levels of GLP-1 on the YesB day enhance insulin secretionreduce glycemic response after lunch and dinner
FFAextension of the overnight fast [NoB day]
Reduced early insulin release
Higher glucoseHigher Glucagon
Higher FFA levels after lunch and dinner
FFA Inhibit insulin mediated muscle glucose transport Induce hepatic insulin resistance Increase hepatic glucose production Inhibit glycogen synthase after 4-6hr thereby decreasing
muscle glycogen content
Glucagon
-cells producing glucagon become insensitive to the inhibitory effects of glucose and/or insulin
lead to postprandial hyperglucagonemia and hepatic glucose overproduction
high glucagon levels were observed throughout the NoB day
CIRCADIAN CLOCK
circadian misalignment of meal timing
Prolonged fasting [No B]
Altered transcription of circadian clock genes
Impaired glycemia
Postprandial glucose – insulin relationship is characteristic of β cell failure This is lost in nocturnal lifestyle group CIRCADIAN RHYTHM has role in controlling glycemia
SUMMARY Extended fasting via breakfast skipping leads to
plasma FFA levels Glucagon Insulin GLP-1 levels
deleterious effects on all-day glucose metabolism were reversed by breakfast consumption
Old is gold..
Thank you