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A key role for neuropeptide Y in lifespan extension and cancer suppression by dietary restriction

ABSTRACT: Key molecules that modulate the effect of dietary restriction (DR), a well-known laboratory intervention for longevity in organisms, remain elusive in mammals. We evaluated neuropeptide Y (Npy), which is involved in the physiological adaptation to energy deficits, for its role in the effects of DR. At 12 weeks of age, Npy-/- and WT mice were divided into the AL (ad libitum) and DR groups. The DR groups received a food allotment consisting of 70% of the mean daily food intake of the AL groups. Two replicates per genotype per feeding group.

ORGANISM(S): Mus musculus

SUBMITTER: Isao Shimokawa

PROVIDER: E-GEOD-42761 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A key role for neuropeptide Y in lifespan extension and cancer suppression by dietary restriction

Project description:Key molecules that modulate the effect of dietary restriction (DR), a well-known laboratory intervention for longevity in organisms, remain elusive in mammals. We evaluated neuropeptide Y (Npy), which is involved in the physiological adaptation to energy deficits, for its role in the effects of DR.

2013-02-28 | GSE42761 | GEO

Cancer anorexia: the role of serotonin in hypothalamic resistance of the neuropeptide Y system [A358_GEO_hypocells]

Project description:Anorexia is a common symptom among cancer patients and contributes to malnutrition and insufficient food intake. In cancer-induced anorexia, food intake regulation in the hypothalamus appears to be impaired. A negative energy balance persists and accelerates muscle wasting and malnutrition. Moreover, it strongly affects mortality and survival in these patients. Here, we show that the neuropeptide Y system (NPY) appears to fail to respond adequately to changes in energy balance during cancer cachexia. In addition, we investigate the connection between serotonin and NPY release in hypothalamic cell lines. Hypothalamic neuronal cells mHypoE-46 (serotonin sensitive cells) and mHypoA-2/12 (serotonin unresponsive cells) were used to study the effect of serotonin on messenger NPY expression and NPY excretion.

2014-10-31 | E-GEOD-57189 | biostudies-arrayexpress

Cancer anorexia: the role of serotonin in hypothalamic resistance of the neuropeptide Y system [A286_GEO_LLM]

Project description:Anorexia is a common symptom among cancer patients and contributes to malnutrition and insufficient food intake. In cancer-induced anorexia, food intake regulation in the hypothalamus appears to be impaired. A negative energy balance persists and accelerates muscle wasting and malnutrition. Moreover, it strongly affects mortality and survival in these patients. Here, we show that the neuropeptide Y system (NPY) appears to fail to respond adequately to changes in energy balance during cancer cachexia. In addition, we investigate the connection between serotonin and NPY release in hypothalamic cell lines. Lewis Lung tumour cells were intramuscularly inoculated 6w old male C57BL/6 mice. Body weight and food intake were measured 3 times a week. On day 10, 14 and 17 hypothalamus was dissected and used for gene expression profiling.

2014-10-31 | E-GEOD-57188 | biostudies-arrayexpress

Lifespan extension by diet restriction in DNA repair deficient progeroid Ercc1Δ/- mice [miRNA]

Project description:DNA repair-deficient Ercc1Δ/- mice show premature cell death, senescence and numerous accelerated aging features limiting lifespan to 4-6 month. Simultaneously they exhibit a ‘survival response’, which suppresses growth and enhances maintenance, resembling the anti-aging response induced by dietary restriction (DR). Here we report that subjecting these progeroid, dwarf mutants to actual dietary restriction (DR) resulted in the largest lifespan increase recorded in mammals. Thirty percent DR tripled median and maximal remaining lifespan, and drastically retarded numerous aspects of accelerated aging, e.g. DR animals retained 50% more neurons and maintained full motoric function. The DR response in Ercc1Δ/- mice resembled DR in wild type animals including reduced insulin signaling. Interestingly, ad libitum Ercc1Δ/- liver expression profiles showed preferential extinction of expression of long genes, consistent with genome-wide accumulation of stochastic, transcription-blocking lesions, which affect long genes more than short ones. DR largely prevented this decline of transcriptional output, indicating that DR prolongs genome function. Our findings strengthen the link between DNA damage and aging, establish Ercc1Δ/- mice as powerful model for identifying interventions to promote healthy aging, reveal untapped potential for reducing endogenous damage, provide new venues for understanding the molecular mechanism of DR, and suggest a counterintuitive DR-like therapy for human progeroid genome instability syndromes and DR-like interventions for preventing neurodegenerative diseases.

2016-09-09 | GSE77226 | GEO

Lifespan extension by diet restriction in DNA repair deficient progeroid Ercc1Δ/- mice [mRNA]

2016-09-09 | GSE77321 | GEO

Single-nuclei sequencing of the mouse hippocampus of dietary restricted mice

Project description:Dietary restriction (DR), reduced food intake while avoiding malnutrition, profoundly extends lifespan in most model and non-model organisms. Both chronic (i.e. life-long) and acute (i.e. late-onset) DR have been shown to improve cognitive performance in aged mice compared to animals with an unrestricted access to food (ad libitium feeding; AL). Yet so far, quantitative analyses of the molecular dynamics in the brain of DR fed animals have been limited. Here we performed single-nuclei sequencing (Nuc-seq) of whole hippocampus isolated from young (5 months) and old (24 months) AL fed animals, as well as old chronic DR (DR started at 3 months) and acute DR (aDR) mice.

2023-04-17 | GSE227515 | GEO

Proteomic analysis of dietary restriction in yeast reveals a role for Hsp26 in lifespan extension C4PR_LIV

Project description:Dietary restriction (DR) has been shown to increase lifespan in organisms ranging from yeast to mammals. This suggests that the underlying mechanisms may be evolutionarily conserved. Indeed, upstream signalling pathways, such as TOR, are strongly linked to DR-induced longevity in various organisms. However, the downstream effector proteins that ultimately mediate lifespan extension are less clear. To shed light on this, we used a proteomic approach on budding yeast. Our reasoning was that analysis of proteome-wide changes in response to DR might enable the identification of proteins that mediate its physiological effects, including lifespan extension. Of over 2500 proteins we identified by liquid chromatography-mass spectrometry, 183 were significantly altered in expression by at least 3-fold in response to DR. Most of these proteins were mitochondrial and/or had clear links to respiration and metabolism. Indeed, direct analysis of oxygen consumption confirmed that mitochondrial respiration was increased several-fold in response to DR. In addition, several key proteins involved in mating, including Ste2 and Ste6, were downregulated by DR. Consistent with this, shmoo formation in response to α-factor pheromone was reduced by DR, thus confirming the inhibitory effect of DR on yeast mating. Finally, we found that Hsp26, a member of the conserved small heat shock protein (sHSP) family, was upregulated by DR and that overexpression of Hsp26 extends yeast replicative lifespan. As overexpression of sHSPs in C. elegans and Drosophila has previously been shown to extend lifespan, our data on yeast Hsp26 suggest that sHSPs may be universally conserved effectors of longevity.

2022-02-17 | PXD025004 | Pride

Unprecedented life- and healthspan extension and genome preservation by diet restriction in DNA repair deficient progeroid Ercc1∆/- mice [RNA-seq]

Project description:In this study, we investigate the anti-aging response induced by dietary restriction (DR) on gene expression level. For this, we carried out Ribosomal RNA depleted Total RNA sequencing in 16 weeks old Ercc1∆/- ad libidum (AL), DR and wt mice.

2016-09-09 | GSE77494 | GEO

mTOR-neuropeptide Y signaling sensitizes nociceptors to drive neuropathic pain development

Project description:Neuropathic pain is a refractory condition that involves de novo protein synthesis in the nociceptive pathway. The mechanistic target of rapamycin (mTOR) is a master regulator of protein synthesis; however, mechanisms underlying its role in neuropathic pain remain elusive. Using spared nerve injury-induced neuropathic pain model, we found mTOR activation in large-diameter dorsal root ganglion (DRG) neurons and spinal microglia. However, selective ablation of mTOR in DRG neurons, rather than microglia, alleviated neuropathic pain. Combining transcriptomic profiling, electrophysiological recording and pharmacologic manipulations, we demonstrated that activated mTOR promoted neuropeptide Y (NPY) induction in mechanoreceptors and that NPY acted on Y2 receptors (Y2R) but not Y1R to enhance nociceptor excitability. Peripheral replenishment of NPY reversed pain alleviation upon mTOR removal, whereas Y2R antagonists prevented its function. Our findings reveal an unexpected link between mTOR and NPY in promoting nociceptor sensitization and neuropathic pain, through NPY/Y2R signaling-mediated intra-ganglionic transmission.

2022-09-01 | GSE184014 | GEO

Amygdala NPY circuits are critical for the development of accelerated obesity under chronic stress

Project description:Neuropeptide Y (NPY) exerts powerful feeding related functions in the hypothalamus. However, NPY is also present in extra-hypothalamic nuclei, however their influence on energy homeostasis is unclear. Here we uncover a previously unknown feeding stimulatory pathway that is activated under conditions of stress in combination with calorie dense food with NPY neurons in the central amygdala (CeA) being responsible for an exacerbated response to a combined stress and high fat diet intervention. CeA NPY neuron specific Npy overexpression mimics the obese phenotype seen in a stress/HFD model, which is prevented by the selective ablation of Npy. Using food intake and energy expenditure (EE) as readout we demonstrate that selective activation of CeA NPY neurons results in increased food intake and a decrease in EE, which requires the presence of NPY. Mechanistically it is the diminished insulin signalling capacity on CeA NPY neurons under stress combined with HFD conditions that leads to the exaggerated development of obesity.

2019-03-31 | GSE128413 | GEO

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