In mammals, rhythms in feeding and activity represent outputs of the so called “central” clock located in the hypothalamic area of the brain in the suprachiasmatic nuclei. The SCN are specialized to perceive information about external LD cycle due to their direct connection with the retina. The SCN clock adjusts its rhythmicity according to lighting information and passes the signal to so-called “peripheral” clocks, which are located in various bodily cells and drive rhythmically the tissue- and organ-specific programs. As a result, the processes driven by the central and peripheral clocks are synchronized. At the cellular level, the molecular mechanism responsible for generating circadian oscillations is composed of interconnected transcriptional/translational feedback loops among the clock genes and their Tulathromycin B protein products. The core clockwork consists of the transcriptional activators CLOCK and BMAL1, which bind as a heterodimer to E-box elements in the promoters of the clock genes Per1, Per2, Cry1, Cry2, Rev-erb��/�� and Ror��/��/�� and drive their transcription. The PER1,2 and CRY1,2 proteins accumulate in the cytoplasm, form complexes and translocate into the nucleus, where they inhibit the transcriptional activity of CLOCK-BMAL1. This feedback mechanism results in the rhythmic expression of the clock genes. Furthermore, REVERB�� and ROR�� create accessory feedback loops by binding to the promoter in Bmal1 to repress or activate its transcription, respectively. Bmal2 is a paralog of Bmal1, and its expression from a constitutively expressed promoter can restore the clock and metabolic phenotypes of Bmal1-knockout mice. The ROR��-mediated activation of Bmal1 transcription is enhanced by the PPAR�� coactivator 1��. Members of the PAR bZIP transcription factor family, including the activator DBP and the repressor E4BP4, act via Dbox elements in their target genes to form additional accessory feedback loops. Posttranslational modifications, such as phosphorylation, ubiquitination, sumoylation, and acetylation/ deacetylation, enhance the robustness and stability of the clock mechanism. The rhythmic regulation of Ebox elements by the BMAL1/CLOCK complex, D-box elements by PAR bZIP factors, or RORE sequences by ROR��/REVERB��, drive the rhythmic expression of so-called clockcontrolled genes, coding transcriptional factors or functional proteins involved in the regulation of various physiological pathways. In nature, food is rarely present ad libitum, and feeding regimes are affected by many factors. Under laboratory conditions, limiting food Folinic acid calcium salt pentahydrate access to a certain time of day, socalled restricted feeding, leads to the development of food-anticipatory behavior in advance of food availability, including increases in locomotor activity, body temperature, corticosterone levels, and plasma levels of ketone body and free fatty acids. Food-anticipatory activity is driven independently of the central clock because it occurs in SCN-lesioned animals as well as in animals with a genetically ablated clock. This phenomenon is thought to be driven by another oscillator, the so called food-entrainable clock, as it persists in conditions without periodic food availability. The food-entrainable oscillator likely communicates with the circadian clock, as FAA is absent when the period of the feeding cycle is too distant from 24 h. Moreover, this SCN-independent oscillator may depend partially on the canonical circadian clock components, as deficiencies in individual clock genes lead to variations in the circadian range of FAA entrainment. Therefore, clock genes are 
likely involved in the regulation of FAA in a circadian oscillatory manner. However, in spite of significant efforts to determine its localization in the body, the oscillator has not yet been identified. The SCN pathways entraining the peripheral clocks are of multiple origin.