title: Nesfatin-1 exerts long-term effect on food intake and body temperature.
abstract: OBJECTIVE
  To determine whether the anorexigenic peptide, nesfatin-1 affects energy expenditure, and to follow the time course of its effects.
  
  
  METHODS
  Food intake duration, core body temperature, locomotor activity and heart rate of rats were measured by telemetry for 48 h after a single intracerebroventricular injection of 25 or 100 pmol nesfatin-1 applied in the dark or the light phase of the day. Body weight, food and water intake changes were measured daily. Furthermore, cold-responsive nesfatin-1/NUCB2 neurons were mapped in the brain.
  
  
  RESULTS
  Nesfatin-1 reduced duration of nocturnal food intake for 2 days independently of circadian time injected, and raised body temperature immediately, or with little delay depending on the dose and circadian time applied. The body temperature remained higher during the next light phases of the 48 h observation period, and the circadian curve of temperature flattened. After light phase application, the heart rate was elevated transiently. Locomotion did not change. Daily food and water intake, as well as body weight measurements point to a potential decrease in all parameters on the first day and some degree of compensation on the second day. Cold-activated (Fos positive) nesfatin-1/NUCB2 neurones have been revealed in several brain nuclei involved in cold adaptation. Nesfatin-1 co-localised with prepro-thyrotropin-releasing hormone in cold responsive neurones of the hypothalamic paraventricular nucleus, and in neurones of the nucleus raphe pallidus and obscurus that are premotor neurones regulating brown adipose tissue thermogenesis and skin blood flow.
  
  
  CONCLUSIONS
  Nesfatin-1 has a remarkably prolonged effect on food intake and body temperature. Time course of nesfatin-1's effects may be varied depending on the time applied. Many of the nesfatin-1/NUCB2 neurones are cold sensitive, and are positioned in key centres of thermoregulation. Nesfatin-1 regulates energy expenditure a far more potent way than it was recognised before making it a preferable candidate anti-obesity drug.
authors.affiliation: Neuromorphological and Neuroendocrine Research Laboratory, Department of Anatomy, Histology and Embryology, Semmelweis University and the Hungarian Academy of Sciences, Budapest, Hungary. konkat6@gmail.com
authors.forename: K
authors.initials: K
authors.lastname: Könczöl
authors.forename: O
authors.initials: O
authors.lastname: Pintér
authors.forename: S
authors.initials: S
authors.lastname: Ferenczi
authors.forename: J
authors.initials: J
authors.lastname: Varga
authors.forename: K
authors.initials: K
authors.lastname: Kovács
authors.forename: M
authors.initials: M
authors.lastname: Palkovits
authors.forename: D
authors.initials: D
authors.lastname: Zelena
authors.forename: Z E
authors.initials: ZE
authors.lastname: Tóth
mesh_terms: D000818:Animals; D019440:Anti-Obesity Agents / Q000494:pharmacology; D001831:Body Temperature; D001931:Brain Mapping; D002135:Calcium-Binding Proteins / Q000378:metabolism* / Q000494:pharmacology; D004268:DNA-Binding Proteins / Q000378:metabolism* / Q000494:pharmacology; D004195:Disease Models, Animal; D004435:Eating / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D005247:Feeding Behavior / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism* / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism*; D000080866:Nucleobindins; D051381:Rats; D017208:Rats, Wistar; D012528:Satiety Response / Q000187:drug effects; D015398:Signal Transduction
chemical_list: D019440:Anti-Obesity Agents; D002135:Calcium-Binding Proteins; D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C000630652:Nucb1 protein, rat; D000080866:Nucleobindins