AgRP, Recombinant, mouse, 100 ug.
- Known as:
- AgRP, Recombinant, mouse, 100 ug.
- Catalog number:
- MO15090-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- AgRP Recombinant mouse 100 .
Related genes to: AgRP, Recombinant, mouse, 100 ug.
- 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, Recombinant, mouse, 100 ug.
Related articles to: AgRP, Recombinant, mouse, 100 ug.
- Hypothalamic kisspeptin, encoded by the Kiss1 gene, serves as an important regulator of the reproductive axis and sexual maturation. Since reproductive physiology is tightly coupled to metabolic cues, metabolic status exerts significant influence on puberty and fertility. Emerging evidence identifies kisspeptin signaling as a key determinant of central energy homeostasis. This review focuses on distinct Kiss1 neuronal populations in the arcuate nucleus of hypothalamus (Arc) and anteroventral periventricular/periventricular nucleus (AVPV/PeN) in regulating energy balance. Arc Kiss1 neurons suppress appetite via activation of POMC neurons and inhibition of AgRP/NPY neurons, while enhance energy expenditure through excitatory projections to the PVN and DMH. In contrast, AVPV/PeN Kiss1 neurons primarily exert inhibitory GABAergic regulation on PVN and DMH neurons. This indicates their suppressive modulatory function, which generally opposes the excitatory metabolic effects mediated by Arc Kiss1 neurons. Peripheral metabolic hormones, including leptin, adiponectin, insulin, and ghrelin, dynamically modulate Kiss1 neuronal activity through direct receptor or indirect POMC/AgRP pathways. By integrating these peripheral signals, Kiss1 neurons act as important modulators of metabolic homeostasis. Taken together, these findings indicate that Kiss1 neuronal pathway may be worth additional investigation in the field of metabolic disorders. - Source: PubMed
Publication date: 2026/06/10
Sun LingyuGao RuidongChen Jing - Fructose is a simple sugar and a major component of our diet, yet its effects on gut-brain feeding circuits remain poorly understood. Here, we investigated how fructose influences activity in hypothalamic agouti-related protein (AgRP) neurons-key regulators of hunger. Fructose was markedly less effective than equicaloric glucose at suppressing AgRP neuron activity in mice, challenging the prevailing model of AgRP neurons as indiscriminate calorie detectors. This blunted neural response to fructose did not alter short-term food consumption but was instructive for food preference, demonstrating that graded AgRP neuron activity changes are sufficient to guide food choice. Mechanistically, we discovered that fructose activates a distinct gut-brain pathway involving the release of PYY and signaling through Y2 receptor-expressing vagal afferent neurons to inhibit AgRP neurons. These findings unexpectedly reveal that AgRP neurons respond not just to calories, but to specific nutrients, and highlight how fructose engages a unique gut-brain pathway to communicate with AgRP neurons. - Source: PubMed
Publication date: 2026/06/10
McKnight Aaron Dde Araujo AlanHsu Fang-YuVargas-Elvira Alexandra GAcosta Alisha ASmith Miliani MIwueze Wisdomde Lartigue GuillaumeAlhadeff Amber L - Pregnancy and lactation trigger many metabolic adaptations, including increased food intake to support the energy demands of the growing foetus and then to provide nutrition through milk production after birth. Ghrelin, an orexigenic hormone, activates agouti related peptide (AgRP) neurons in the arcuate nucleus to promote food intake. Here, we investigated the hypothesis that increased sensitivity to ghrelin during pregnancy and lactation may contribute to elevated maternal food intake. Acute food intake was measured after a single dose of ghrelin or vehicle across reproductive states including virgin, pregnant (Day 8 and Day 15), lactating (Day 10) mice and dams 2 weeks after weaning. In vivo GCaMP fibre photometry of the AgRP neuron population was used to measure AgRP neuronal response to ghrelin. Unlike virgin mice, pregnant mice did not show an acute increase in food intake after ghrelin injection, while ghrelin-treated lactating mice showed a greater feeding response than virgin mice. After weaning, dams showed a similar increase in food intake to that seen in virgin mice. In contrast to the loss of feeding response to ghrelin, the expected increase in growth hormone (GH) in response to ghrelin was observed in both pregnancy and lactation. Across all of the reproductive states, a significant increase in AgRP neuron activity was observed in response to exogenous ghrelin administration, although the magnitude was slightly reduced in late pregnancy. Furthermore, the ghrelin-induced increase in c-Fos expression in AgRP neurons was similar in all reproductive states, indicating that AgRP neurons remained responsive to ghrelin despite the absence of a food-intake response to ghrelin during pregnancy. Interestingly, the expected drop in AgRP neuron activity in response to the presentation of food was absent during late pregnancy and lactation. The absence of a food consumption-mediated inhibition of AgRP neuron activity suggests that an attenuated response of the AgRP neurons to feedback signals associated with eating may contribute to increases in meal duration during pregnancy and lactation. Overall, these results indicate that ghrelin resistance develops during pregnancy, suggesting that ghrelin does not contribute to elevated food intake during pregnancy. In lactation, however, enhanced ghrelin sensitivity may contribute to elevated maternal food intake. These results also indicate that adaptations to ghrelin sensitivity in pregnancy and lactation are transient as 2 weeks after weaning our results are similar to the virgin state. - Source: PubMed
Murrell C LPerkinson M RAndrews Z BGrattan D RLadyman S R - Sleeve gastrectomy (SG) improves obesity-associated type 2 diabetes mellitus (T2DM) beyond mere weight loss. We investigated whether SG enhances systemic metabolic homeostasis by suppressing the Ghrelin-growth hormone secretagogue receptor (GHSR) axis, remodeling hypothalamic pro-opiomelanocortin (POMC) neuronal activity, and reprogramming CD4 T cell immunometabolism. - Source: PubMed
Publication date: 2026/06/08
Li XinZhang Ren-YiLiu Wei-Hui - The arcuate nucleus (ARC) and ventromedial hypothalamus (VMH) are highly specialized hypothalamic nuclei controlling appetite and energy expenditure. Here, we demonstrate that human VMH and ARC neurons can be generated from pluripotent stem cells by fine-tuned timing and duration of bone morphogenetic protein (BMP) exposure. We identified SHH/NKX2.1/FGF10/RAX/TBX3 posterior tuberal progenitors as the source of ARC cell types, including agouti-related peptide (AGRP)-, prepronociceptin (PNOC)-, growth-hormone-releasing hormone (GHRH)-, and thyrotropin-releasing hormone (TRH)-expressing neurons and β2-tanycytes. Differentiated ARC cultures showed high transcriptomic similarity to human ARC and responded to energy homeostasis-regulatory peptides including leptin, glucagon-like peptide 1 (GLP-1), ghrelin, and fibroblast growth factor 1 (FGF1). In contrast, anterior tuberal TBX3 progenitors generated VMH-associated neurons expressing NR5A1, SOX14, and GPR149. Strikingly, two transcriptionally distinct pro-opiomelanocortin (POMC) subpopulations emerged from these lineages, mapping spatially to either the ARC (POMC/TBX3/NR5A2) or the VMH (POMC/SOX14/NR5A1). This model provides a cellular platform to study human hypothalamic subtype specification and pathways involved in central appetite regulation. - Source: PubMed
Publication date: 2026/06/08
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