Diet and Meal Pattern Determinants of Glucose Levels and Variability in Adults with and without Prediabetes or Early-Onset Type 2 Diabetes: A Pilot Study

Author:

Santos-Báez Leinys S.1ORCID,Díaz-Rizzolo Diana A.12ORCID,Popp Collin J.3,Shaw Delaney1,Fine Keenan S.1,Altomare Annemarie1,St-Onge Marie-Pierre4ORCID,Manoogian Emily N. C.5ORCID,Panda Satchidananda5,Cheng Bin6,Laferrère Blandine1ORCID

Affiliation:

1. Division of Endocrinology, Nutrition Obesity Research Center, Columbia University Irving Medical Center, New York, NY 10032, USA

2. Health Science Faculty, Universitat Oberta de Catalunya (UOC), 08018 Barcelona, Spain

3. Institute for Excellence in Health Equity, Department of Population Health, New York Langone Health Grossman School of Medicine, New York, NY 10016, USA

4. Center of Excellence for Sleep & Circadian Research, Division of General Medicine, Department of Medicine, Columbia University Irving Medical Center, New York, NY 10032, USA

5. Regulatory Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA

6. Department of Biostatistics, Columbia University Irving Medical Center, New York, NY 10032, USA

Abstract

This observational pilot study examined the association between diet, meal pattern and glucose over a 2-week period under free-living conditions in 26 adults with dysglycemia (D-GLYC) and 14 with normoglycemia (N-GLYC). We hypothesized that a prolonged eating window and late eating occasions (EOs), along with a higher dietary carbohydrate intake, would result in higher glucose levels and glucose variability (GV). General linear models were run with meal timing with time-stamped photographs in real time, and diet composition by dietary recalls, and their variability (SD), as predictors and glucose variables (mean glucose, mean amplitude of glucose excursions [MAGE], largest amplitude of glucose excursions [LAGE] and GV) as dependent variables. After adjusting for calories and nutrients, a later eating midpoint predicted a lower GV (β = −2.3, SE = 1.0, p = 0.03) in D-GLYC, while a later last EO predicted a higher GV (β = 1.5, SE = 0.6, p = 0.04) in N-GLYC. A higher carbohydrate intake predicted a higher MAGE (β = 0.9, SE = 0.4, p = 0.02) and GV (β = 0.4, SE = 0.2, p = 0.04) in N-GLYC, but not D-GLYC. In summary, our data suggest that meal patterns interact with dietary composition and should be evaluated as potential modifiable determinants of glucose in adults with and without dysglycemia. Future research should evaluate causality with controlled diets.

Publisher

MDPI AG

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