Time-restricted feeding does not improve daily rhythms in locomotion and drinking disrupted by artificial light at night.

Exposure to artificial light at night (ALAN) disrupts natural darkness and desynchronizes daily rhythms in physiological processes and behavior. Previously, in rats, we have shown that dim ALAN disturbed the central circadian control and the temporal organization of behavior, and hormonal and metabolic pathways. The measurements of undisturbed daily behavioral (locomotor activity, feeding and drinking) patterns revealed reduced amplitudes and a transitory activity peak in the middle of the light (i.

Synergy between time-restricted feeding and time-restricted running is necessary to shift the muscle clock in male wistar rats.

Circadian disruption is an important factor driving the current-day high prevalence of obesity and type-2 diabetes. While the impact of incorrect timing of caloric intake on circadian disruption is widely acknowlegded, the contribution of incorrect timing of physical activity remains relatively understudied. Here, we modeled the incorrect timing of physical activity in nightshift workers in male Wistar rats, by restricting running wheel access to the innate inactive (light) phase (LR).

A neuronal circuit driven by GLP-1 in the olfactory bulb regulates insulin secretion.

Glucagon-like peptide 1 (GLP-1) stimulates insulin secretion and holds significant pharmacological potential. Nevertheless, the regulation of energy homeostasis by centrally-produced GLP-1 remains partially understood. Preproglucagon cells, known to release GLP-1, are found in the olfactory bulb (OB).

Dopamine in the nucleus accumbens shell controls systemic glucose metabolism via the lateral hypothalamus and hepatic vagal innervation in rodents.

Background: Growing evidence demonstrates the role of the striatal dopamine system in the regulation of glucose metabolism. Treatment with dopamine antagonists is associated with insulin resistance and hyperglycemia, while dopamine agonists are used in treatment of type 2 diabetes. The mechanism underlying striatal dopamine effects in glucose metabolism, however is not fully understood.

The Addiction-Susceptibility TaqIA/Ankk1 Controls Reward and Metabolism Through D Receptor-Expressing Neurons.

Background: A large body of evidence highlights the importance of genetic variants in the development of psychiatric and metabolic conditions. Among these, the TaqIA polymorphism is one of the most commonly studied in psychiatry. TaqIA is located in the gene that codes for the ankyrin repeat and kinase domain containing 1 kinase (Ankk1) near the dopamine D receptor (D2R) gene.