Objective: Despite the fact that the total energy intake of Japanese people
has decreased, the percentage of obese people has increased. This suggests that the timing
of meals is related to obesity. The purpose of the study was to investigate the
relationship between the timing of meals and obesity, based on analyses of physical
measurements, serum biochemical markers, nutrient intake, and lifestyle factors in the
context of Chrononutrition.Participants and Methods: We analyzed data derived from 766 residents of
Toon City (286 males and 480 females) aged 30 to 79 years who underwent detailed medical
examinations between 2011 and 2013. These medical examinations included. (1) physical
measurements (waist circumference, blood pressure, etc.); (2) serum biochemical markers
(total cholesterol, etc.); (3) a detailed questionnaire concerning lifestyle factors such
as family structure and daily habits (22 issues), exercise and eating habits (28 issues),
alcohol intake and smoking habits; (4) a food frequency questionnaire based on food groups
(FFQg); and (5) a questionnaire concerning the times at which meals and snacks are
consumed.Results: The values for body mass index (BMI) and waist circumference were
higher for participants who ate dinner less than three hours before bedtime (<3-h
group) than those who ate more than three hours before bedtime (>3-h group). The
Chi-square test showed that there was a significant difference in eating habits, e.g.,
eating snacks, eating snacks at night, having dinner after 8 p.m., and having dinner after
9 p.m., between the <3-h group and the >3-h group. Multiple linear regression
analysis showed that skipping breakfast significantly influenced both waist circumference
(β = 5.271) and BMI (β = 1.440) and that eating dinner <3-h before going to bed only
influenced BMI (β = 0.581).Conclusion: Skipping breakfast had a greater influence on both waist
circumference and BMI than eating dinner <3-h before going to bed.
Induction of brown-like adipocytes (beige/brite cells) in white adipose tissue (WAT) suggests a new approach for preventing and treating obesity via induction of thermogenesis associated with uncoupling protein 1 (UCP1). However, whether diet-derived factors can directly induce browning of white adipocytes has not been well established. In addition, the underlying mechanism of induction of brown-like adipocytes by diet-derived factors has been unclear. Here, we demonstrate that artepillin C (ArtC), which is a typical Brazilian propolis-derived component, significantly induces brown-like adipocytes in murine C3H10T1/2 cells and primary inguinal WAT (iWAT)-derived adipocytes. This significant induction is due to activation of peroxisome proliferator-activated receptor γ and stabilization of PRD1-BF-1-RIZ1 homologous domain-containing protein-16 (PRDM16). Furthermore, the oral administration of ArtC (10 mg/kg) for 4 weeks significantly induced brown-like adipocytes accompanied by significant expression of UCP1 and PRDM16 proteins in iWAT of mice, and was independent of the β3-adrenergic signaling pathway via the sympathetic nervous system. These findings may provide insight into browning of white adipocytes including the molecular mechanism mediated by dietary factors and demonstrate that ArtC has a novel biological function with regard to increasing energy expenditure by browning of white adipocytes.
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