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Circadian disruption of feeding-fasting rhythm and its consequences for metabolic, immune, cancer, and cognitive processes.

Biomed J

January 2025

ٰLaboratorio de Cronobiología, Departamento de Ciencia y Tecnología, Universidad Nacional de Quilmes/CONICET. Buenos Aires, Argentina. Electronic address:

The circadian system is composed by a central hypothalamic clock at the suprachiasmatic nuclei (SCN) that communicates with peripheral circadian oscillators for daily coordination of behavior and physiology. The SCN entrain to the environmental 24-h light-dark (LD) cycle and drive daily rhythms of internal synchronizers such as core body temperature, hypothalamic-hypophysary hormones, sympathetic/parasympathetic activity, as well as behavioral and feeding-fasting rhythms, which supply signals setting core molecular clocks at central and peripheral tissues. Steady phase relationships between the SCN and peripheral oscillators keep homeostatic processes such as microbiota/microbiome composition/activity, metabolic supply/demand, energy balance, immunoinflammatory process, sleep amount and quality, psychophysiological stress, etc.

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Background: Human adamantinomatous craniopharyngioma (ACP) is a brain tumor that originates at the base of the skull and shows aggressive local behavior, invading sensitive structures such as the optic pathways and hypothalamus. The conventional treatment of the tumor has been surgery and radiotherapy with the consequent development of serious sequelae. It is well known that Substance P (SP) peptide and Neurokinin-1 receptor (NK-1R) are involved in inflammation and cancer progression and its blockage with NK-1R antagonists has been shown to effectively counteract tumor development in preclinical trials.

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The neural mechanisms of the affective-motivational symptoms of chronic pain are poorly understood. In chronic pain, our innate coping mechanisms fail to provide relief. Hence, these behaviors are manifested at higher frequencies.

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Hormonal mechanisms in the paraventricular nuclei associated with hyperalgesia in Parkinson's disease model rats.

Biochem Biophys Res Commun

January 2025

Department of Dental Anesthesiology, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka, 565-0871, Japan. Electronic address:

Pain is a major non-motor symptom of Parkinson's disease (PD). The relationship between hyperalgesia and neuropeptides originating from paraventricular nucleus (PVN) in 6-hydroxydopamine (6-OHDA) rats has already been investigated for oxytocin (OXT), but not yet for arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH). The present study aimed to investigate the alterations in these neuropeptides following nociceptive stimulation in PD model rats and to examine the mechanisms of hyperalgesia.

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Introduction: Congenital and acquired damage to hypothalamic nuclei or neuronal circuits controlling satiety and energy expenditure results in hypothalamic obesity (HO). To date, successful weight loss and satiety has only been achieved in a limited number of affected patients across multiple drug trials. Glucagon-like peptide-1 (GLP-1) acts via central pathways that are independent from the hypothalamus to induce satiety.

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