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Obesity afflicts approximately 42% of the adult population in the United States and contributes to the development of chronic diseases, including diabetes, cancer, and other conditions.
While the popular healthy diet mantra advises avoiding late-night snacking, no study comprehensively investigated the simultaneous effects of late eating on the three major players in weight regulation, namely obesity risk. Almost never. adipose tissue.
A new study by researchers at the Harvard Medical School at Brigham and Women’s Hospital found that diet has a profound effect on energy expenditure, appetite, and molecular pathways in adipose tissue. The result is cell metabolism.
“We wanted to test the mechanisms that explain why slow eating increases the risk of obesity,” the senior author explained. Frank ShearProfessor of Medicine at HMS and Director of the Medical Chronobiology Program in the Division of Sleep and Circadian Disorders at Brigham and Women’s University.
“Previous research by us and others has shown that slow eating is associated with increased risk of obesity, increased body fat, and hindered successful weight loss. I wanted to understand,” he said.
“In this study, we asked whether meal times mattered when everything else was held constant,” said first author Nina Bjovic, a researcher in the Medical Chronobiology Program. I’m here.
Vujović, Scheer, and their team studied 16 patients with body mass index in the overweight or obese range. Each participant completed two protocols. One was a rigidly scheduled early meal schedule and the other was the same meal, each scheduled about 4 hours later in the day.
During the last 2–3 weeks before starting each protocol in the laboratory, participants maintained a constant sleep-wake schedule and followed the same diet and diet at home for the last 3 days before entering the laboratory. strictly followed the schedule of
In the laboratory, participants recorded hunger and appetite regularly, provided small blood samples frequently throughout the day, and measured body temperature and energy expenditure.
To determine how meal time affects the molecular pathways involved in adipogenesis, or how the body stores fat, the researchers studied early We collected adipose tissue biopsies from a subset of participants during laboratory trials on both dietary protocols and late/levels between these two dietary conditions.
They found that eating later had a significant effect on hunger and the appetite-regulating hormones leptin and ghrelin. Specifically, levels of leptin, a hormone that signals satiety, decreased over 24 hours in him in the slow-eating condition compared to the fast-eating condition.
When participants ate later, they burned calories at a slower rate, indicating adipose tissue gene expression toward increased adipogenesis and decreased lipolysis, promoting fat growth.
In particular, these findings inform converging physiological and molecular mechanisms underlying the correlation between slow eating and increased risk of obesity.
Vujović said these findings are not only in line with numerous studies suggesting that eating later may make you more likely to become obese, but also provide new insight into how this occurs. I explained that I would shine a light.
By using randomized crossover studies and tightly controlling behavioral and environmental factors such as physical activity, posture, sleep, and light exposure, researchers can explore the different control systems involved in energy balance. I was able to detect the change. We use the food we consume.
In future studies, Scheer’s team aims to recruit more women so that the findings can be generalized to a wider population. Although this study cohort included only five female participants, the study was set up to control for menstrual periods, which reduced confounding but made recruitment of women more difficult. .
In the future, Scheer and Vujović are also interested in better understanding the impact of the relationship between mealtime and bedtime on energy balance.
“This study shows the effects of late versus early eating. Here, we separated these effects by controlling for confounding variables such as calorie intake, physical activity, sleep and light exposure.” , in fact, many of these factors can be affected by meal timing.
“A large-scale study, where tight control over all these factors is not possible, would at least consider how other behavioral and environmental variables alter these biological pathways that underlie obesity risk.” need to do it.
This research was funded by R01DK099512, UL1TR001102, and UL1TR002541. FAJLS was supported by NIH grants R01DK099512, R01HL118601, R01DK102696, R01DK105072 and R01HL140574. MJP and MJB are supported in DK020595. MG was supported by the Spanish Government Research, Development and Innovation (SAF2017-84135-R), including co-funding from FEDER. The Seneca Foundation (20795/PI/18), and the Autonomous Community of the Region of Murcia through NIDDK R01DK099512. SLC was supported by the Alexander von Humboldt Foundation. JQ was supported by the American Diabetes Association (award 1-17-PDF-103) and the NIH (grant K99HL148500 and R01DK10269).6).
Disclosure: During the execution of this project, Scheer received speaking fees from Bayer Healthcare, Centara Healthcare, Philips, Vanda Pharmaceuticals and Pfizer Pharmaceuticals. Received consulting fees from the University of Alabama, Birmingham. He also served on the board of directors of the Sleep Research Society. Scheer’s interests were reviewed and managed by Brigham and Women’s Hospital and Partners HealthCare in accordance with their conflict of interest policies. None of these are related to my current work. Vujović is compensated for consulting services rendered to the Novartis Institutes of BioMedical Research, also unrelated to his current work.
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