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DR VASIF MAYAN M C
M2 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 DINNER
Yes B 8 AM 1 30 PM 7 PM
No 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
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%
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
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 secretion
 reduce glycemic response after lunch and dinner
FFA
extension of the overnight fast [NoB day]
Reduced early insulin release
Higher glucose
Higher 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..
effect of skipping breakfast on glycemic response

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effect of skipping breakfast on glycemic response

  • 1. DR VASIF MAYAN M C M2 UNIT
  • 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.
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  • 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
  • 31. CIRCADIAN CLOCK circadian misalignment of meal timing Prolonged fasting [No B] Altered transcription of circadian clock genes Impaired glycemia
  • 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