Agrp siRNA_Lentivectors
- Known as:
- Agrp siRNA_Lentivectors
- Catalog number:
- i064820b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Agrp siRNA_Lentivectors
Related genes to: Agrp siRNA_Lentivectors
- 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 siRNA_Lentivectors
Related articles to: Agrp siRNA_Lentivectors
- Dual declines in cognitive status and physical performance increase dementia risk but shared biological mechanisms between processes remain unclear. We investigated plasma proteomic signatures underlying dual decline in older adults from the Invecchiare in Chianti cohort (n = 774; age ≥ 60). Group-based trajectory models with up to 15 years of data on cognitive status (global Mini-Mental State Examination scores) and 4-m gait speed identified three trajectories that included no decline, physical decline, or dual decline groups. At baseline, 1301 plasma proteins were measured with aptamer-based proteomics (SomaScan). Adjusted multinomial regressions identified proteins associated with group membership. Additional analyses included Reactome functional enrichment and partial least squares discriminant analysis (PLS-DA). Collectively, eight proteins were associated with differences across trajectory groups. Higher PI3, GDF15, TFF3, CCL15, TNNT2, and AGRP were associated with greater odds of dual decline, whereas higher CKM and GHR were linked to lower odds. PLS-DA confirmed and extended these findings. The top discriminators by variable-importance were PTN, TFF3, GDF15, IGFBP-2, and CHRDL1. Hierarchical clustering found PTN, IGFBP-2, PI3, GDF15, and TFF3 formed a coherent module. Functional enrichment highlighted overrepresentation of regulation of IGF transport and uptake by IGF binding proteins across decline trajectories and exploratory enrichment of post-translational protein phosphorylation and diseases of homeostasis. Older adults with dual declines showed a proteomic profile marked by cellular stress, inflammation, barrier injury, reduced IGF-1 bioavailability, and cardiovascular-metabolic strain. These findings support system-level hypotheses of dual decline and warrant replication, longitudinal proteomics, and evaluation of module-level markers. - Source: PubMed
Publication date: 2026/06/16
Rathbun Alan MChen ChixiangTian QuTanaka ToshikoFerrucci LuigiShardell Michelle D - 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