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