AgRP Protein
- Known as:
- AgRP Protein
- Catalog number:
- 10070-H02H
- Product Quantity:
- 20
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- AgRP Protein
Related genes to: AgRP Protein
- 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 Protein
Related articles to: AgRP Protein
- Loss of appetite is a hallmark of acute and chronic inflammation, and sustained anorexia causes malnutrition and worsens disease outcomes. Interleukin-1β (IL-1β) is one of the most potently anorexigenic inflammatory cytokines, yet how it engages neural circuits that suppress feeding remains incompletely understood. Specifically, the role of peripheral sensory neurons in mediating IL-1β-induced anorexia is unresolved. Here, using DREADD-mediated inhibition of discrete peripheral sensory neuron populations and fiber photometry, we show that IL-1β-induced anorexia occurs in at least two temporally and mechanistically distinct phases. Shortly after IL-1β administration, prostaglandin signaling through non-vagal sensory afferents rapidly inhibits hypothalamic AgRP neurons to suppress food intake. At later time points, anorexia becomes partially prostaglandin-independent and vagal afferent neuron-dependent. Our findings demonstrate that multiple molecular signals mediate IL-1β-induced anorexia, and that diverse peripheral sensory pathways, including a previously unappreciated contribution from non-vagal afferents, are critical links between systemic inflammation and neural control of appetite. - Source: PubMed
Publication date: 2026/02/24
Hayes Nikolas WXia Jessica LFrydman Joshua ADuran Marcos JGebis Kamil KLorch Carolyn MProvince Haley STang EstherBeutler Lisa R - The accumulation of microplastics in aquatic ecosystems poses a significant threat to fish physiology and welfare. This study investigated the impact of exposure to virgin polystyrene microplastics (15 µm) on energy balance and welfare in goldfish (). Fish were exposed for 14 days, and the effects were assessed through an integrated analysis of behavioral, metabolic, neuroendocrine, and physiological parameters. Microplastic exposure significantly reduces feed intake and feed anticipatory activity, indicating a potent anorexigenic effect. This effect was driven by neuroendocrine disruption, characterized by the downregulation of orexigenic neuropeptides (, , ) and the upregulation of anorexigenic signaling (, , ). Simultaneously, exposed fish exhibited increased oxygen consumption, suggesting elevated metabolic demands. These factors converged to impaired growth and reduced hepatosomatic index, suggesting altered energy allocation. Furthermore, microplastic exposure induced anxiety-like responses and increased plasma cortisol levels, confirming the activation of the physiological stress response. Overall, these findings demonstrate that microplastics disrupt energy homeostasis and trigger behavioral shifts that ultimately compromise fish welfare and the biological resilience of aquatic species. - Source: PubMed
Publication date: 2026/04/30
Herrera-Castillo LisbethNavajas-Jiménez NereaBarany AndréIsorna EstherGómez-Boronat Miguelde Pedro Nuria - Niemann-Pick disease, type C1 (NPC1), is a rare, fatal, neurodegenerative lysosomal disorder caused by pathological variants in NPC1. Defects in lysosomal cholesterol transport result in the accumulation of unesterified cholesterol within the endo-lysosomal compartments. Delayed diagnosis, limited treatment options, and phenotypic heterogeneity characterized by a broad range of signs/symptoms underscore the urgent need for effective biomarkers to facilitate diagnosis, monitor disease progression and assess therapeutic response. The goal of this study was to identify serum protein biomarkers for NPC1. - Source: PubMed
Publication date: 2026/05/09
Singhal KhushbooMenold Matthew TCawley Niamh XCampbell KierstenFarhat Nicole YAlexander DerekDale Ryan KPorter Forbes D - Energy homeostasis relies on interconnected brain circuits that integrate hormonal signals with behavioral outputs. Building upon the established roles of canonical transcriptional regulators like STAT3 and FOXO1 in metabolic neurons, we synthesize emerging evidence positioning basonuclin-2 (BNC2), a deeply conserved zinc-finger transcription factor, as a putative coordinator of energy balance. Spatial transcriptomic mapping highlights selective BNC2 expression within the hypothalamic arcuate nucleus and ventral pallidum. Recent functional studies demonstrate that hypothalamic BNC2 neurons suppress appetite via leptin-driven GABAergic inhibition of AgRP/NPY neurons, whereas ventral pallidum BNC2 neurons modulate reward-driven food intake. Together, these findings suggest BNC2 functions as a critical bridge between homeostatic and hedonic feeding circuits. Future investigations addressing isoform specificity, direct hormonal sensing, and human genetic relevance will be essential to evaluate BNC2 as a therapeutic target for obesity and related metabolic disorders. - Source: PubMed
Publication date: 2026/04/17
Zhang ZixuHu ShengruHua KaiyiLi PengDuan YikeShao WangqiSun ShihaoZhang HongboMu Mingdao - Sulfur amino acid restriction (SAAR) paradoxically increases food intake while inducing weight loss, but the mechanisms underlying these outcomes remain unclear. To investigate the role of leptin in this response, we assessed food intake, body weight, and metabolic markers in diet-induced obese (DIO), leptin-deficient (ob/ob), and leptin receptor-deficient (db/db) mice. In DIO-SAAR mice, increased food intake was associated with hypothalamic upregulation of orexigenic (Agrp, Npy, and Mchr1) and downregulation of anorexigenic (Pomc, Cartpt, and Bdnf) mRNA levels. This orexigenic profile is accompanied by reduced adiposity and lower circulating leptin levels, suggesting that decreased leptin may induce compensatory increased food intake. Despite increased food intake, SAAR also induces weight loss, which is associated with enhanced β3-adrenergic signaling in brown and inguinal white AT (BAT and iWAT), as reflected by elevated Adrb3 and Ucp1 mRNA levels but downregulated protein expression, suggesting post-transcriptional regulation. These phenotypes induced by SAAR may possibly involve thyroid hormone metabolism, as indicated by increased circulating T3 and T4 concentrations and upregulation of BAT deiodinase 2 (D2) mRNA. Importantly, these metabolic effects of SAAR are attenuated in ob/ob and abolished in db/db mice, despite reductions in circulating SAA levels. Furthermore, leptin treatment during SAAR reduced food intake, induced weight loss, demonstrating preserved leptin sensitivity in low fat diet-fed and ob/ob mice. These findings reveal that leptin is required for both increased food intake and weight loss during SAAR. - Source: PubMed
Publication date: 2026/05/05
Cooke DianaOuattara AmadouAbles Gene P