Regulation of Homeostasis by Neuropeptide Y: Involvement in Food
Intake

Rabal, Maria del Pilar Marcos; Coveñas, Rafael

doi:10.2174/0929867328666211213114711

Cited by 12 publications

(9 citation statements)

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“…The orexigenic effect is expected to stimulate food intake in patients with cancer who lose appetite due to cachexia [ 53 ] and elderly individuals with sarcopenia based on poor nutritional status, which contributes to a loss of muscle mass [ 54 , 55 ]. Other endogenous neuropeptides, such as neuropeptide Y, ghrelin, and orexin, have orexigenic activity but are inactivated when administered orally [ 56 , 57 , 58 ]; however, p.o. rubiscolin-6 has been shown to evoke these effects.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Potential of Orally Administered Rubiscolin-6

Karasawa

Miyano

Yamaguchi

et al. 2023

IJMS

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Rubiscolins are naturally occurring opioid peptides derived from the enzymatic digestion of the ribulose bisphosphate carboxylase/oxygenase protein in spinach leaves. They are classified into two subtypes based on amino acid sequence, namely rubiscolin-5 and rubiscolin-6. In vitro studies have determined rubiscolins as G protein-biased delta-opioid receptor agonists, and in vivo studies have demonstrated that they exert several beneficial effects via the central nervous system. The most unique and attractive advantage of rubiscolin-6 over other oligopeptides is its oral availability. Therefore, it can be considered a promising candidate for the development of a novel and safe drug. In this review, we show the therapeutic potential of rubiscolin-6, mainly focusing on its effects when orally administered based on available evidence. Additionally, we present a hypothesis for the pharmacokinetics of rubiscolin-6, focusing on its absorption in the intestinal tract and ability to cross the blood–brain barrier.

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Section: Discussionmentioning

confidence: 99%

Therapeutic Potential of Orally Administered Rubiscolin-6

Karasawa

Miyano

Yamaguchi

et al. 2023

IJMS

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“…NPY is a 36-amino acid peptide neurotransmitter implicated in physiological processes such as energy homeostasis 36 , learning and memory 37,38 , acting on different types of Gi/o-coupled NPY receptors 39 . NPY also plays a role in regulating memory systems relevant to pathophysiology of post-traumatic stress disorder (PTSD) with therapeutic potential 40 , yet its brain-region- and cell-type-specific origin, spatiotemporal targeting and signaling mechanisms in fear memory remain ambiguous.…”

Section: Mainmentioning

confidence: 99%

Neuropeptide Y co-opts neuronal ensembles for memory lability and stability

Wu,

Gu,

Kong

et al. 2024

Preprint

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Memory engrams are formed by activity-dependent recruitment of distinct subsets of excitatory principal neurons (or neuronal ensembles) whereas inhibitory neurons pivot memory lability and stability (1-5). However, the molecular logic for memory engrams to preferentially recruit specific type of interneurons over other subtypes remains enigmatic. Using activity-dependent single-cell transcriptomic profiling6-8 in mice with training of cued fear memory and extinction, we discovered that neuropeptide Y (NPY)-expressing (NPY+) GABAergic interneurons in the ventral hippocampal CA1 (vCA1) region exert fast GABAergic inhibition to facilitate the acquisition of memory, but bifurcate NPY-mediated slow peptidergic inhibition onto distinct sub-ensembles underlying the extinction of single memory trace. Genetically encoded calcium and NPY sensors revealed that both calcium dynamics of NPY+ neurons and their NPY release in vCA1 ramp up as extinction learning progresses while behavioral state switches from "fear-on" to "fear-off". Bidirectional manipulations of NPY+ neurons or NPY itself demonstrated NPY is both necessary and sufficient to control the rate and degree of memory extinction by acting on two physically non-overlapping sub-ensembles composed of NPY1R- and NPY2R-expressing neurons. CRISPR/Cas9-mediated knockout of NPY2R or NPY1R further unravels that NPY co-opts its actions on these two sub-ensembles to gate early fast and late slow stages of extinction. These findings exemplify the intricate spatiotemporal orchestration of slow peptidergic inhibitions from single subtype of GABAergic interneurons to fine-tune engram lability verse stability of memory.

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“…Антагонисты рецепторов NPY тестируются в качестве препаратов Other problems of endocrinology против ожирения [27]. Периферическое введение антагониста NPY-рецептора предотвращает ожирение, вызванное «западной диетой» у мышей [28].…”

Section: хемореактомное исследование эффектов фонтурацетама: молекуля...unclassified

Phenylpiracetam: molecular mechanisms of effects in obesity

Gromova,

Torshin,

Lazebnik

2024

Medicinskij sovet

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Metabolic syndrome (MS), including hyperlipidemia and obesity, is a proven risk factor not only for cerebrovascular diseases. Obesity is a dangerous comorbid condition in patients, complicating cerebrovascular pathology, asthenic conditions, diabetes mellitus, liver disease, alcoholism and other diseases accompanied by dysmetabolic disorders. Fundamental and clinical studies of the nootropic fonturacetam (Actitropil) have shown that the drug can be used not only for a wide range of cerebrovascular diseases, asthenia, etc., but also for obesity. The mechanisms of action of fonturacetam in producing pharmacological effects that reduce excess appetite and prevent the accumulation of excess body weight were studied in chemoreactomic analysis. Regulation of the metabolic effectiveness of Phenylpiracetam is based on multi-level correction of target transmitters and receptors that control the metabolism of fats and carbohydrates (influence on leptin, cannabinoid receptors, adrenoreceptors, peroxisome receptors). Phenylpiracetam activates the adrenaline, adenosine, glucagon-like peptide, sphingosine phosphate and peroxisome proliferators (PPARG) receptors and inhibits the cannabinoid, opioid, histamine, glutamate, nociceptin, orexin, neuropeptide Y receptors. The resulting pharmacological properties indicate important pathophysiological effects of phenylpiracetam for the treatment of obesity. A decrease in the rate of fat mass gain when taking Phenylpiracetam is noted due to an improvement in the quality of night sleep. Chemoreactomic analysis of Actitropil indicated new molecular mechanisms of the pharmacological action of the molecule, which reduces excess appetite and prevents the accumulation of excess body weight. Phenylpiracetam (Actitropil) is distinguished by a balance of effectiveness, a high safety profile with no addiction to the drug and safety. Thus, Phenylpiracetam is a racetam that exhibits nootropic, antiasthenic and lipotropic effects.

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Regulation of Homeostasis by Neuropeptide Y: Involvement in Food Intake

Cited by 12 publications

References 0 publications

Therapeutic Potential of Orally Administered Rubiscolin-6

Therapeutic Potential of Orally Administered Rubiscolin-6

Neuropeptide Y co-opts neuronal ensembles for memory lability and stability

Phenylpiracetam: molecular mechanisms of effects in obesity

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