Agrp
- Known as:
- Agrp
- Catalog number:
- 065354A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Agrp
Related genes to: Agrp
- Gene:
- AGRP NIH gene
- Name:
- agouti related neuropeptide
- Previous symbol:
- -
- Synonyms:
- Agrt, ART, ASIP2
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-22
- Date modifiied:
- 2016-10-05
Related products to: Agrp
Related articles to: Agrp
- Glucocorticoids (GCs) are key regulators of energy homeostasis. Clinically, patients with Cushing's syndrome exhibit obesity, whereas adrenal insufficiency is associated with weight loss. However, circulating biomarkers reflecting GC action have not been established. Agouti-related protein (AgRP), an orexigenic neuropeptide, is upregulated by GC in the rodent hypothalamus. Here, we investigated whether AgRP is a surrogate marker of GC action through in vitro and in vivo experiments as well as a clinical study. - Source: PubMed
Publication date: 2026/07/15
Aoyama NatsukiNishiyama MitsuruIwasaki YasumasaNakayama ShuichiOkazaki MizuhoTaguchi TakafumiTsuda MasayukiHashimoto KoshiMakino ShinyaFujimoto Shimpei - - Source: PubMed
Zhang Yan - - Source: PubMed
Detomas MarioDischinger Ulrich - An appropriate stress response is essential for properly responding to, coping with, and subsequently recovering from disturbing environmental stimuli. However, how the brain dynamically encodes the scalability of stress responses remains poorly understood. Here, we found that, GABAergic neurons in the arcuate nucleus (Arc, denoted as Arc neurons) send direct inputs to corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus (PVH, denoted as PVH neurons), the primary regulators of the hypothalamic-pituitary-adrenal (HPA) axis. Although PVH neurons exhibited time-locked activation in response to various environmental stressors, both GABA release onto PVH neurons and the activity of PVH -projecting Arc neurons were selectively reduced during exposure to prolonged, high-intensity stressors, but not following exposure to transient, low-intensity stressors. Notably, GABA release onto PVH neurons was positively correlated with PVH -projecting Arc neuron activity, yet anticorrelated with PVH neuronal activity in response to the same prolonged, high-intensity stressors. Selective silencing of PVH projecting Arc neurons was sufficient to elevate HPA axis activity and stress levels, phenocopying the effect of direct of PVH neuron activation. Conversely, selective activation of PVH projecting Arc neurons reduced both HPA axis activity and stress levels, this effect was completely abolished by concurrent excitation of PVH neurons. Molecular identity screening further revealed that these PVH -projecting Arc neurons are not subsets expressing agouti-related peptide (AgRP) and tyrosine hydroxylase (TH) markers. Collectively, these findings indicate that the non-AgRP/TH Arc PVH neurocircuit serves as a critical neural substrate that directly encodes the scalability of stress responses to environmental stressors by modulating inhibitory GABA release in a stimulus intensity-dependent manner. - Source: PubMed
Publication date: 2026/07/02
Cao YuhanSeese Megumi HJiang ZhiyingSu CunjinYang MaojieMonte Fabricio H DoTong QingchunXu Yuanzhong - Fasting, as a non-pharmacological intervention, elicits antidepressant-like effects. However, its neural and molecular mechanisms remain unclear. This study investigated whether intermittent fasting (IF) alleviates corticosterone (CORT)-induced depressive-like behaviors in mice and explored the underlying mechanisms. This study demonstrated that IF reversed the CORT-induced reduction in hypothalamic glucocorticoid and mineralocorticoid receptor (GR/MR) expression in mice. In addition, IF reversed a CORT-induced decrease in arcuate nucleus (ARC) AgRP/NPY neuronal activity and NPY output from these neurons while concurrently suppressing the activity of neighboring POMC neurons. This rebalanced ARC output attenuated paraventricular nucleus (PVN) hyperactivity, as evidenced by reduced c-fos and increased NPY immunoreactivity. Remarkably, co-administration of GR and MR antagonists (RU486 and spironolactone) abolished both the behavioral benefits and hypothalamic neuropeptidergic and activity changes induced by IF. Together, these findings identify a mechanism involving GR/MR signaling through which IF alleviates depressive-like states by rescuing the functional output of AgRP/NPY neurons from a state of activity-output dissociation, thereby restoring HPA axis homeostasis. - Source: PubMed
Tang MiaomiaoSun QihanSong JinfangPiao XinmiaoGeng ZihuiHan XuLi RunxinLi YueHan MengyiCui RanjiLi Bingjin