Writing in the British Journal of Nutrition, the researchers from the University of Southampton also noted a reverse effect in that a disrupted sleeping cycle could lead to, “attenuated circadian feeding rhythms”, along with, “hyperphagia, GI pathologies, metabolic disease and reduced life expectancy”.
“As food components and feeding time have the ability to reset biological rhythms, it is of paramount importance to understand the relationship between food, feeding and the circadian clock system,” they wrote.
“In so doing, we may be able to use food or feeding times as a therapeutic intervention to reset or re-entrain the circadian clock system for better functionality of physiological systems, preventing obesity, promoting well-being and extending lifespan.”
The researchers suggested oscillations in the gene and protein components in the ‘endogenous molecular clock network’ modulate circadian rhythms in physiological and metabolic outputs.
The oscillations are generated by positive and negative feedback loops involving a number of ‘clock genes’ and their protein components with the main clock located in the suprachiasmatic nucleus (SCN) of the anterior hypothalamus of the brain.
Other clock systems are found in the heart, liver, gastrointestinal (GI) tract and pancreas.
The systems interact with each other, and when the cycle is disturbed due to nutritional input or other factors, “…altered autonomic outflow from the SCN can result in an imbalanced rhythm between different fat compartments, and this may bring about increased fat accumulation and obesity.”
Those other factors include body temperature, mealtimes, restricted feeding and scheduled physical exercise.
“For peripheral tissues involved in nutritional and metabolic processes, such as the stomach, intestine, liver and pancreas, feeding schedules and restricted feeding become powerful zeitgebers [factors that can alter sleep cycles].”
“Feeding rhythms, including food anticipatory activities, are also regulated by the master SCN clock.”
“Nutritional zeitgebers such as malnutrition (over or undernutrition) and restricted mealtimes can also entrain the clock systems and rhythmic processes in peripheral tissues, as well as feeding rhythms via a food entrainable oscillator in non-SCN regions of the brain.”
The researchers noted studies that showed high levels of the appetite-suppressing hormone, leptin, in the overweight - a seemingly contrary finding.
“In humans, night-time plasma leptin levels are high when appetite decreases, favouring fasting and nocturnal rest, and low during the day, when hunger increases. In obese individuals, however, daytime and night-time leptin levels are much higher compared with lean healthy subjects, indicating a state of leptin resistance.”
Noting studies that showed mice bodily systems altered to compensate when feeding times were shifted to normal sleeping hours, they said, “nutrient availability at a cellular level has the greatest influence on molecular changes in the peripheral clock system.”
They referenced another study where, “exposure to high-fat nutrition resulted in long-term abnormal clock and clock-controlled gene expression” in mice.
“Since many of the clock-controlled genes have direct metabolic outputs, diet-induced perturbations in core clock genes can directly lead to altered metabolism, leading to an increased risk of metabolic disease.”
“Therefore, the circadian clock system is now an emerging research target and a putative candidate mechanism linking dietary influences to metabolic disease susceptibility.”
British Journal of Nutrition
‘The role of the circadian clock system in nutrition and metabolism’
Authors: Felino R. Cagampang and Kimberley D. Bruce