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Influences of breakfast on clock gene expression and postprandial glycemia in healthy individuals and individuals with diabetes : A randomized clinical trial

Jakubowicz, Daniela; Wainstein, Julio; Landau, Zohar; Raz, Itamar; Ahren, Bo LU ; Chapnik, Nava; Ganz, Tali; Menaged, Miriam; Barnea, Maayan and Bar-Dayan, Yosefa, et al. (2017) In Diabetes Care 40(11). p.1573-1579
Abstract

OBJECTIVE The circadian clock regulates glucose metabolism by mediating the activity of metabolic enzymes, hormones, and transport systems. Breakfast skipping and night eating have been associated with high HbA1c and postprandial hyperglycemia after lunch and dinner. Our aim was to explore the acute effect of breakfast consumption or omission on glucose homeostasis and clock gene expression in healthy individuals and individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS In a crossover design, 18 healthy volunteers and 18 volunteers with 14.5 ± 1.5 years diabetes, BMI 30.7 ± 1.1 kg/m2, andHbA1c 7.6 ± 0.1% (59.6 ± 0.8mmol/mol) were randomly assigned to a test day with breakfast and lunch (YesB) and a test day with only lunch... (More)

OBJECTIVE The circadian clock regulates glucose metabolism by mediating the activity of metabolic enzymes, hormones, and transport systems. Breakfast skipping and night eating have been associated with high HbA1c and postprandial hyperglycemia after lunch and dinner. Our aim was to explore the acute effect of breakfast consumption or omission on glucose homeostasis and clock gene expression in healthy individuals and individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS In a crossover design, 18 healthy volunteers and 18 volunteers with 14.5 ± 1.5 years diabetes, BMI 30.7 ± 1.1 kg/m2, andHbA1c 7.6 ± 0.1% (59.6 ± 0.8mmol/mol) were randomly assigned to a test day with breakfast and lunch (YesB) and a test day with only lunch (NoB). Postprandial clock and clock-controlled gene expression, plasma glucose, insulin, intact glucagon-like peptide 1 (iGLP-1), and dipeptidyl peptidase IV (DPP-IV) plasma activity were assessed after breakfast and lunch. RESULTS In healthy individuals, the expression level of Per1, Cry1, Rorα, and Sirt1 was lower (P < 0.05) but Clock was higher (P < 0.05) after breakfast. In contrast, in individuals with type 2 diabetes, Per1, Per2, and Sirt1 only slightly, but significantly, decreased and Rora increased (P < 0.05) after breakfast. In healthy individuals, the expression level ofBmal1, Rora, andSirt1was higher (P < 0.05) after lunch on YesB day,whereas the other clock genes remained unchanged. In individuals with type 2 diabetes, Bmal1, Per1, Per2, Rev-erba, and Ampk increased (P < 0.05) after lunch on the YesB day. Omission of breakfast altered clock and metabolic gene expression in both healthy and individuals with type 2 diabetes. CONCLUSIONS Breakfast consumption acutely affects clock and clock-controlled gene expression leading to normal oscillation. Breakfast skipping adversely affects clock and clockcontrolled gene expression and is correlated with increased postprandial glycemic response in both healthy individuals and individuals with diabetes.

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organization
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published
subject
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Diabetes Care
volume
40
issue
11
pages
7 pages
publisher
American Diabetes Association
external identifiers
  • scopus:85033215942
  • wos:000413557200028
ISSN
0149-5992
DOI
10.2337/dc16-2753
language
English
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yes
id
00abeecf-3b42-45e3-af89-8fff9039fb13
date added to LUP
2017-11-22 14:46:31
date last changed
2018-05-20 04:38:55
@article{00abeecf-3b42-45e3-af89-8fff9039fb13,
  abstract     = {<p>OBJECTIVE The circadian clock regulates glucose metabolism by mediating the activity of metabolic enzymes, hormones, and transport systems. Breakfast skipping and night eating have been associated with high HbA1c and postprandial hyperglycemia after lunch and dinner. Our aim was to explore the acute effect of breakfast consumption or omission on glucose homeostasis and clock gene expression in healthy individuals and individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS In a crossover design, 18 healthy volunteers and 18 volunteers with 14.5 ± 1.5 years diabetes, BMI 30.7 ± 1.1 kg/m2, andHbA1c 7.6 ± 0.1% (59.6 ± 0.8mmol/mol) were randomly assigned to a test day with breakfast and lunch (YesB) and a test day with only lunch (NoB). Postprandial clock and clock-controlled gene expression, plasma glucose, insulin, intact glucagon-like peptide 1 (iGLP-1), and dipeptidyl peptidase IV (DPP-IV) plasma activity were assessed after breakfast and lunch. RESULTS In healthy individuals, the expression level of Per1, Cry1, Rorα, and Sirt1 was lower (P &lt; 0.05) but Clock was higher (P &lt; 0.05) after breakfast. In contrast, in individuals with type 2 diabetes, Per1, Per2, and Sirt1 only slightly, but significantly, decreased and Rora increased (P &lt; 0.05) after breakfast. In healthy individuals, the expression level ofBmal1, Rora, andSirt1was higher (P &lt; 0.05) after lunch on YesB day,whereas the other clock genes remained unchanged. In individuals with type 2 diabetes, Bmal1, Per1, Per2, Rev-erba, and Ampk increased (P &lt; 0.05) after lunch on the YesB day. Omission of breakfast altered clock and metabolic gene expression in both healthy and individuals with type 2 diabetes. CONCLUSIONS Breakfast consumption acutely affects clock and clock-controlled gene expression leading to normal oscillation. Breakfast skipping adversely affects clock and clockcontrolled gene expression and is correlated with increased postprandial glycemic response in both healthy individuals and individuals with diabetes.</p>},
  author       = {Jakubowicz, Daniela and Wainstein, Julio and Landau, Zohar and Raz, Itamar and Ahren, Bo and Chapnik, Nava and Ganz, Tali and Menaged, Miriam and Barnea, Maayan and Bar-Dayan, Yosefa and Froy, Oren},
  issn         = {0149-5992},
  language     = {eng},
  month        = {11},
  number       = {11},
  pages        = {1573--1579},
  publisher    = {American Diabetes Association},
  series       = {Diabetes Care},
  title        = {Influences of breakfast on clock gene expression and postprandial glycemia in healthy individuals and individuals with diabetes : A randomized clinical trial},
  url          = {http://dx.doi.org/10.2337/dc16-2753},
  volume       = {40},
  year         = {2017},
}