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
- Obesity-induced ectopic lipid accumulation inside skeletal muscle (SKM) (myosteatosis) and the liver (hepatosteatosis) contributes to local metabolic dysfunction and serves as a launchpad for the progression of diabetes. While stearoyl-CoA desaturase 1 (SCD1), an ER-bound enzyme that catalyzes the rate-limiting step in monounsaturated fatty acid (MUFA) synthesis, is widely recognized as a lynchpin facilitator of steatosis, much controversy exists on its efficacy as a therapeutic target. In particular, a total lack of SKM-specific SCD1 KO models has greatly limited our understanding of SCD1-mediated myosteatosis' relative contribution to metabolic syndrome. - Source: PubMed
Publication date: 2026/08/03
Guilfoyle-Speese AndrewBridgewater CodyPadgett CalebSellars HunterMintz JamesFulton DavidStepp David - Macroautophagy/autophagy is a critical cellular degradation pathway essential for neuronal proteostasis and synaptic function. Its decline with aging is associated with synaptic dysfunction and reduced circuit resilience. NPY (neuropeptide Y), a highly abundant brain neuropeptide, has emerged as an important regulator of autophagy and aging-related processes. In , the NPY-family peptide sNPF modulates age-related changes in presynaptic architecture via non-cell autonomous mechanisms. Here, we examined whether autophagy and NPY interact within hypothalamic NPY AGRP neurons to regulate presynaptic organization in distant brain regions. We show that autophagy in these neurons non-cell autonomously controls hippocampal presynaptic active zone architecture and proteostasis, while maintaining NPY peptide levels. Importantly, dietary supplementation of the natural polyamine spermidine restored NPY expression in the aged hippocampus, highlighting its potential to rejuvenate neuropeptide signaling. Together, these findings reveal a pathway by which hypothalamic autophagy and NPY signaling regulate hippocampal synaptic architecture, linking metabolic state to synaptic resilience. - Source: PubMed
Publication date: 2026/08/17
Cazzolla GiovannaToppe DavidKrause GinaKochlamazashvili GagaLützkendorf JanineSchedina Ina MStephanowitz HeikeReisenbichler Anna MariaChen XingxiangKerkhoff YannicReifenstein EricErnst Helen Mvon Kleist MaxZimmermann AndreasEisenberg TobiasMadeo FrankLiu FanHerzog HerbertAlbrecht AnneSchmitz DietmarHaucke VolkerSigrist Stephan JMaglione Marta - Glucagon-like peptide-1 receptor agonists (GLP-1RAs), including semaglutide, produce robust and sustained weight loss, yet the central mechanisms supporting their long-term efficacy remain incompletely understood. Agouti-related peptide (AgRP) neurons of the arcuate nucleus are classically activated by negative energy balance and promote feeding and energy conservation. Based on this framework, GLP-1RAs have generally been expected to suppress or bypass AgRP neuron activity. Here, we report that AgRP neuron activation is required for the full weight-lowering effects of GLP-1RAs in female mice. Across complementary AgRP loss-of-function models, disruption of AgRP circuit integrity reduced the full weight-lowering effects of GLP-1RAs. This requirement varies with sex, diet, and mode of AgRP disruption. We found that GLP-1RA treatment is associated with increased markers of neuronal activation, mitochondrial engagement, and synaptic remodeling in AgRP neurons. We further identify a glucocorticoid-to-AgRP signaling axis as an important pathway mediating this functional recruitment of AgRP neurons. Together, these findings reveal that contrary to prevailing assumptions, GLP-1RA engages AgRP neurons to sustain weight loss, highlighting an unexpected role for these neurons in coordinating adaptive metabolic responses to pharmacologically induced negative energy balance. - Source: PubMed
Publication date: 2026/08/04
d'Ávila MateusCavalcanti-de-Albuquerque JoãoCollado-Pérez RobertoLiu Zhong-WuHunter JennaWhite AnneSchlessinger JosephD'Agostino GiuseppeHorvath Tamas L - The timing of diagnosis is a critical factor that significantly impacts medical treatment and patient outcomes in individuals with intracerebral hemorrhage (ICH). The study primarily aimed to evaluate the diagnostic potential of four brain-specific biomarkers, glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), tau, and ubiquitin C-terminal hydrolase-L1 (UCH-L1) to differentiate CT-confirmed ICH patients from healthy controls. Secondary aims included comparing results between younger (18-59 years) and older (≥60 years) ICH patients and exploring neuroendocrine hormone levels (adrenocorticotropic hormone [ACTH], agouti-related peptide [AgRP], ciliary neurotrophic factor [CNTF], and growth hormone [GH]) as potential diagnostic tools. - Source: PubMed
Publication date: 2026/07/31
Apiliogullari SezaElbayoumi EmanCollier NinaCai GuangzhengOcloo Otis KofiGolpich MojtabaKobeissy FirasZhu JiepeiYadikar HamadNg StephaniaPoon Wai SWang Kevin K - Feeding behavior, which is crucial for all mammals, is regulated by a delicate equilibrium between the orexigenic and anorexigenic activities of hypothalamic neurons. This exquisite control of the neuropeptides that govern the feeding behavior could be a focal point in the pathogenesis of obesity. We reported that inactivation of C-terminal binding protein 2 (CtBP2), a transcriptional corepressor with metabolite-sensing capabilities, contributes to the pathogenesis of obesity in liver tissues and pancreatic β-cells. Here, we describe a transcriptional system regulated by CtBP2 in the hypothalamus. Our global mapping of CtBP2 binding sites using ChIP-seq combined with functional analyses revealed that CtBP2 functions as a corepressor for orexigenic neuropeptide promoters. In response to the metabolic abnormalities associated with obesity, CtBP2 undergoes allosteric inactivation and dissociates from these promoters, thereby resulting in the derepression of orexigenic neuropeptide expression. Consistently, the loss of CtBP2 in hypothalamic neurons in mice increases the expression of orexigenic neuropeptides, thus leading to increased feeding behavior. These findings highlight how obesity disrupts homeostatic mechanisms that normally maintain body weight within a healthy range. - Source: PubMed
Chen WanpeiKainoh KentaSaito KenjiMatsuda TakaakiYamazaki DaichiKobari YutoNakata AyumiAono-Soma NaoMiyamoto TakafumiMurayama YukiSugano YokoOsaki YoshinoriIwasaki HitoshiMatsuzaka TakashiShimano HitoshiSekiya Motohiro