Circadian and Metabolic Effects of Light: Implications in Weight Homeostasis and Health

Abstract

Daily interactions between the hypothalamic circadian clock at the suprachiasmatic nucleus (SCN) and peripheral circadian oscillators regulate physiology and metabolism to set temporal variations in homeostatic regulation. Phase coherence of these circadian oscillators is achieved by the entrainment of the SCN to the environmental 24-h light:dark (LD) cycle, coupled through downstream neural, neuroendocrine, and autonomic outputs. The SCN coordinate activity and feeding rhythms, thus setting the timing of food intake, energy expenditure, thermogenesis, and active and basal metabolism. In this work, we will discuss evidences exploring the impact of different photic entrainment conditions on energy metabolism. The steady-state interaction between the LD cycle and the SCN is essential for health and wellbeing, as its chronic misalignment disrupts the circadian organization at different levels. For instance, in nocturnal rodents, non-24 h protocols (i.e., LD cycles of different durations, or chronic jet-lag simulations) might generate forced desynchronization of oscillators from the behavioral to the metabolic level. Even seemingly subtle photic manipulations, as the exposure to a “dim light” scotophase, might lead to similar alterations. The daily amount of light integrated by the clock (i.e., the photophase duration) strongly regulates energy metabolism in photoperiodic species. Removing LD cycles under either constant light or darkness, which are routine protocols in chronobiology, can also affect metabolism, and the same happens with disrupted LD cycles (like shiftwork of jetlag) and artificial light at night in humans. A profound knowledge of the photic and metabolic inputs to the clock, as well as its endocrine and autonomic outputs to peripheral oscillators driving energy metabolism, will help us to understand and alleviate circadian health alterations including cardiometabolic diseases, diabetes, and obesity.

Potential circadian and circannual rhythm contributions to the obesity epidemic in elementary school age children

“…In addition, shortened sleep duration is associated with a shift in melatonin rhythms, resulting in high melatonin levels in the morning upon awakening and eating the morning meal during the biological night [108], which reflects misalignment of the central and peripheral clocks. Long-term dysregulation of glucose levels may lead to alterations in caloric intake and storage which have also been attributed to shortened sleep duration [108], suggesting that the mis-timing of eating and sleep/wake patterns with endogenous rhythms may increase risk for type 2 diabetes and possibly obesity [109].…”

Duración subóptima del sueño y fenotipo circadiano en mujeres adultas residentes de Valencia, Venezuela atendidas en jornadas de salud. Perfil cardiometabólico asociado

“…La exposición de ratones a avance crónico de fase induce ganancia de peso e incremento de la grasa corporal, trigliceridemia y tamaño de los adipocitos, sin incremento de la ingesta dietaria (54) . Plano et al (55) han propuesto que la desalineación circadiana debida a desincronización por comportamiento o exposición a la luz altera vías endocrinas y autónomas que regulan el balance de nutrientes y el uso/almacenamiento de combustibles, lo que reduce la tolerancia a la glucosa postpandrial y el uso de la glucosa, con el consecuente aumento de la glicemia basal, ácidos grasos libres y tejido adiposo. Cuando se establece crónicamente, la desalineación puede conducir a SM y obesidad.…”

The Role of Prenatal Melatonin in the Regulation of Childhood Obesity

“…As a consequence, melatonin shows a negative correlation with circulating insulin levels, with the suppression of pineal melatonin, as in night-shift work, leading to hyperinsulinemia, insulin resistance, and hyperleptinemia as well as a significant decrease in glucose transporter (GLUT)4 levels, which are characteristic of type 2 diabetes [40,41]. The prolonged exposure to artificial light that is characteristic of most cultures also drives down melatonin levels in correlation with an increase in abdominal obesity, arterial hypertension, and lipid and carbohydrate metabolism disorder [42,43].…”