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Circadian Rhythms, Metabolism, and Chrononutrition in Rodents and Humans.
Johnston, JD, Ordovás, JM, Scheer, FA, Turek, FW
Advances in nutrition (Bethesda, Md.). 2016;7(2):399-406
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Plain language summary
Chrononutrition is an emerging field that links the body’s metabolism to its endogenous circadian rhythm. It is now recognised that numerous circadian clocks are found within all major tissues and most cells of the body. This complex network of clocks influences a wide range of biological processes including neuronal, endocrine, metabolic and behavioural function. When there is a disruption in a single circadian clock, whole-organism homeostasis can be impacted, potentially resulting in the development of disease. This review explains the potential mechanisms by which circadian clocks influence biological processes through transgenic animal studies, and how they are being translated to human genetics and metabolomics. The principles of chrononutrition are clinically significant factors that should be considered when managing and treating metabolic disease, as well as maintaining health in the general population.
Abstract
Chrononutrition is an emerging discipline that builds on the intimate relation between endogenous circadian (24-h) rhythms and metabolism. Circadian regulation of metabolic function can be observed from the level of intracellular biochemistry to whole-organism physiology and even postprandial responses. Recent work has elucidated the metabolic roles of circadian clocks in key metabolic tissues, including liver, pancreas, white adipose, and skeletal muscle. For example, tissue-specific clock disruption in a single peripheral organ can cause obesity or disruption of whole-organism glucose homeostasis. This review explains mechanistic insights gained from transgenic animal studies and how these data are being translated into the study of human genetics and physiology. The principles of chrononutrition have already been demonstrated to improve human weight loss and are likely to benefit the health of individuals with metabolic disease, as well as of the general population.
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Nighttime snacking reduces whole body fat oxidation and increases LDL cholesterol in healthy young women.
Hibi, M, Masumoto, A, Naito, Y, Kiuchi, K, Yoshimoto, Y, Matsumoto, M, Katashima, M, Oka, J, Ikemoto, S
American journal of physiology. Regulatory, integrative and comparative physiology. 2013;304(2):R94-R101
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Night eating syndrome (NES) is defined by night time eating (25% or more of the total energy of the day is consumed after the evening meal or by waking up in the middle of the night to eat at least three times per week). Research suggests that it is associated with obesity and a higher BMI. Those with NES may have higher glucose and insulin levels, and lower levels of ghrelin during the night compared to those without NES. This randomised crossover study aimed to explore the impact of nighttime eating on energy, glucose and lipid metabolism in normal weight young women. Participants were asked to either complete a 2 week nighttime snacking intervention or a daytime snacking intervention. The snack represented 10% of the average energy requirement (1950 k/cal per day) with a protein:fat:carbohydrate ratio of 5:50:45. The study found no impact of nighttime snacking on body weight, energy expenditure or glucose metabolism compared to daytime snacking. However, it did find a decrease in fat oxidation and increases in total and LDL cholesterol. Hunger levels before lunch were also higher during the nighttime snacking intervention.
Abstract
The increase in obesity and lipid disorders in industrialized countries may be due to irregular eating patterns. Few studies have investigated the effects of nighttime snacking on energy metabolism. We examined the effects of nighttime snacking for 13 days on energy metabolism. Eleven healthy women (means ± SD; age: 23 ± 1 yr; body mass index: 20.6 ± 2.6 kg/m(2)) participated in this randomized crossover trial for a 13-day intervention period. Subjects consumed a specified snack (192.4 ± 18.3 kcal) either during the daytime (10:00) or the night time (23:00) for 13 days. On day 14, energy metabolism was measured in a respiratory chamber without snack consumption. An oral glucose tolerance test was performed on day 15. Relative to daytime snacking, nighttime snacking significantly decreased fat oxidation (daytime snacking: 52.0 ± 13.6 g/day; nighttime snacking: 45.8 ± 14.0 g/day; P = 0.02) and tended to increase the respiratory quotient (daytime snacking: 0.878 ± 0.022; nighttime snacking: 0.888 ± 0.021; P = 0.09). The frequency of snack intake and energy intake, body weight, and energy expenditure were not affected. Total and low-density lipoprotein (LDL) cholesterol significantly increased after nighttime snacking (152 ± 26 mg/dl and 161 ± 29 mg/dl; P = 0.03 and 76 ± 20 mg/dl and 83 ± 24 mg/dl; P = 0.01, respectively), but glucose and insulin levels after the glucose load were not affected. Nighttime snacking increased total and LDL cholesterol and reduced fat oxidation, suggesting that eating at night changes fat metabolism and increases the risk of obesity.