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
2. 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)
3. 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
4. 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
5. 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
6.
7.
8. 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
9. 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
10. Inclusion criteria
22 individuals with type 2 Diabetes <10yr duration
HbA1c 7-9%
Age 30 – 70 yrs
BMI 22-35 kg/m2
11. Exclusion criteria
Patients on OHA other than metformin
Severe Complications of diabetes
Thyroid/renal/hepatic/pulmonary dysfunction
12. 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 DINNER
Yes B 8 AM 1 30 PM 7 PM
No B - 1 30 PM 7 PM
13. Catheter in antecubital vein
Samples taken at 8am ( O mins)
0, 15,30,60,90,120,150 and 180 mt after eating commenced
14. 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
15. RESULTS
BREAKFAST LUNCH DINNER
YES B NO B YES B NO B YES B NO B
GLUCOSE
Mg/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 Peptide
ng/ml
6.4 2.4
-63%
7.6 6.6
-14%
7.2 6.2
-15%
iGLP -1
pmol/L
16.2 6.4
-60%
18 14
-21%
16 14
-15%
FFA
mmol/L
231 630
+172%
280 381
36%
350 421
20%
Glucagon
pg/ml
130 103
-20%
125 137
10%
132 144
9%
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22. 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!
23. 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
24. 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
25. 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
26. 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
27. 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 secretion
reduce glycemic response after lunch and dinner
28. FFA
extension of the overnight fast [NoB day]
Reduced early insulin release
Higher glucose
Higher Glucagon
Higher FFA levels after lunch and dinner
29. 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
30. 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
32. Postprandial glucose – insulin relationship is characteristic of β cell failure
This is lost in nocturnal lifestyle group
CIRCADIAN RHYTHM has role in controlling glycemia
33. 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