NPY۱ and MC۳/MC۴ receptors mediate BDNF-induced hypophagia in ۵-day-old chickens

Distinguishing the variables that control craving and examining the interaction between them can improve the efficiency of livestock breeding, genetic modification, and drug treatments of obesity-related complications. Hence, in the current study, we investigated the interaction between neuropeptide Y and melanocortinergic systems with brain-derived neurotrophic factor (BDNF) in regulating broilers' feed intake. The present study was conducted on ۲۶۴ broiler chickens in ۶ experiments. In experiment ۱, chickens received intracerebroventricular (ICV) infusion of BDNF (۷.۵, ۱۵, and ۳۰ μg) after ۳ h of food deprivation. BIBP-۳۲۲۶ (NPY۱ receptor antagonist, ۱.۲۵ nmol), BDNF (۳۰ μg), and BDNF + BIBP-۳۲۲۶ were administrated in the second treatment. Experiments ۳-۶ were similar to treatment ۲, except birds were infused with BIIE ۰۲۴۶ (NPY۲ receptor antagonist, ۱.۲۵ nmol), CGP۷۱۶۸۳A (NPY۵ receptor antagonist, ۱.۲۵ nmol), SHU۹۱۱۹ (MC۳/MC۴ receptor antagonist, ۰.۵ nmol) and MCL۰۰۲۰ (MC۴ receptor antagonist, ۰.۵ nmol) instead of BIBP-۳۲۲۶. Then, cumulative meal intake was recorded for ۲ hours. Based on observations, BDNF injection (۱۵ and ۳۰ μg) caused significant hypophagia at all test times (p<۰.۰۵). The co-infusion of NPY۲ and NPY۵ receptor antagonists with BDNF did not affect BDNF-induced hypophagia (p>۰.۰۵), while the infusion of NPY۱ receptor antagonist + BDNF caused a significant strengthening of this effect (p<۰.۰۵). Also, despite the lack of significant effect of MC۴ receptor antagonist + BDNF administration on the appetite-reducing effect of BDNF (p>۰.۰۵), simultaneous infusion of MC۳/MC۴ receptor antagonist and BDNF suppressed hypophagia (p<۰.۰۵). Finally, it appears that MC۳/MC۴ and NPY۱ receptors mediate BDNF-induced hypophagia in ۵-day-old broiler chickens.Distinguishing the variables that control craving and examining the interaction between them can improve the efficiency of livestock breeding, genetic modification, and drug treatments of obesity-related complications. Hence, in the current study, we investigated the interaction between neuropeptide Y and melanocortinergic systems with brain-derived neurotrophic factor (BDNF) in regulating broilers' feed intake. The present study was conducted on ۲۶۴ broiler chickens in ۶ experiments. In experiment ۱, chickens received intracerebroventricular (ICV) infusion of BDNF (۷.۵, ۱۵, and ۳۰ μg) after ۳ h of food deprivation. BIBP-۳۲۲۶ (NPY۱ receptor antagonist, ۱.۲۵ nmol), BDNF (۳۰ μg), and BDNF + BIBP-۳۲۲۶ were administrated in the second treatment. Experiments ۳-۶ were similar to treatment ۲, except birds were infused with BIIE ۰۲۴۶ (NPY۲ receptor antagonist, ۱.۲۵ nmol), CGP۷۱۶۸۳A (NPY۵ receptor antagonist, ۱.۲۵ nmol), SHU۹۱۱۹ (MC۳/MC۴ receptor antagonist, ۰.۵ nmol) and MCL۰۰۲۰ (MC۴ receptor antagonist, ۰.۵ nmol) instead of BIBP-۳۲۲۶. Then, cumulative meal intake was recorded for ۲ hours. Based on observations, BDNF injection (۱۵ and ۳۰ μg) caused significant hypophagia at all test times (p<۰.۰۵). The co-infusion of NPY۲ and NPY۵ receptor antagonists with BDNF did not affect BDNF-induced hypophagia (p>۰.۰۵), while the infusion of NPY۱ receptor antagonist + BDNF caused a significant strengthening of this effect (p<۰.۰۵). Also, despite the lack of significant effect of MC۴ receptor antagonist + BDNF administration on the appetite-reducing effect of BDNF (p>۰.۰۵), simultaneous infusion of MC۳/MC۴ receptor antagonist and BDNF suppressed hypophagia (p<۰.۰۵). Finally, it appears that MC۳/MC۴ and NPY۱ receptors mediate BDNF-induced hypophagia in ۵-day-old broiler chickens.

کلیدواژه ها:

Appetite ، Brain-derived neurotrophic factor ، Melanocortin ، Neuropeptide Y ، Chickens