Редактирование: CRH

Corticoliberin precursor (Corticotropin-releasing factor) (CRF) (Corticotropin-releasing hormone)

==Publications==

{{medline-entry
|title=Roles of peptides and steroids in sleep disorders.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30754093
|abstract=A bidirectional interaction exists between the electrophysiological and neuroendocrine components of sleep. The first is represented by the nonrapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS) cycles, the latter by distinct patterns of the secretion of various hormones. Certain hormones (neuropeptides and steroids) play a specific role in sleep regulation. Changes in their activity contribute to the pathophysiology of sleep disorders. A reciprocal interaction of the peptides growth hormone-releasing hormone ([[GHRH]]) and corticotropin-releasing hormone ([[CRH]]) plays a key role in sleep regulation. [[GHRH]] promotes growth hormone secretion and, at least in males, NREMS, whereas [[CRH]] impairs NREMS, promotes REMS and stimulates the secretion of adrenocorticotropic hormone and cortisol. Changes in the [[CRH]]:[[GHRH]] ratio in favor of [[CRH]] contribute to impaired sleep, elevated cortisol secretion and blunted GH levels during depression and normal aging. However, in women, [[GHRH]] exerts [[CRH]]-like effects. Galanin, ghrelin and neuropeptide Y are other sleep-promoting peptides, whereas somatostatin impairs sleep. A decline of orexin activity causes narcolepsy. In addition to [[CRH]] overactivity, hypercortisolism appears to be involved in the pathophysiology of sleep- electroencephalogram (EEG) changes in depression. Various neuroactive steroids exert specific effects on sleep. The changes of sleep EEG in women after the menopause are related to the decline of estrogen and progesterone. Furthermore, sleep-EEG changes in dwarfism, acromegaly, Addison's disease, Cushing's disease, brain injury, sleep apnea syndrome, primary insomnia, prolactinoma and dementia appear to be related to changes in the activity of peptides and steroids.

|keywords=* aging
* depression
* insomnia
* narcolepsy
* neuropeptides
* sleep
* sleep disorders
* sleep endocrinology
* steroids
|full-text-url=https://sci-hub.do/10.1586/17446651.1.5.609
}}
{{medline-entry
|title=Novel molecular mechanisms for the adaptogenic effects of herbal extracts on isolated brain cells using systems biology.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30466987
|abstract=Adaptogens are natural compounds or plant extracts that increase adaptability and survival of organisms under stress. Adaptogens stimulate cellular and organismal defense systems by activating intracellular and extracellular signaling pathways and expression of stress-activated proteins and neuropeptides. The effects adaptogens on mediators of adaptive stress response and longevity signaling pathways have been reported, but their stress-protective mechanisms are still not fully understood. The aim of this study was to identify key molecular mechanisms of adaptogenic plants traditionally used to treat stress and aging-related disorders, i.e., Rhodiola rosea, Eleutherococcus senticosus, Withania somnifera, Rhaponticum carthamoides, and Bryonia alba. To investigate the underlying molecular mechanisms of adaptogens, we conducted RNA sequencing to profile gene expression alterations in T98G neuroglia cells upon treatment of adaptogens and analyzed the relevance of deregulated genes to adaptive stress-response signaling pathways using in silico pathway analysis software. At least 88 of the 3516 genes regulated by adaptogens were closely associated with adaptive stress response and adaptive stress-response signaling pathways (ASRSPs), including neuronal signaling related to corticotropin-releasing hormone, cAMP-mediated, protein kinase A, and CREB; pathways related to signaling involving [[CXCR4]], melatonin, nitric oxide synthase, [[GP6]], Gαs, MAPK, neuroinflammation, neuropathic pain, opioids, renin-angiotensin, AMPK, calcium, and synapses; and pathways associated with dendritic cell maturation and G-coupled protein receptor-mediated nutrient sensing in enteroendocrine cells. All samples tested showed significant effects on the expression of genes encoding neurohormones [[CRH]], GNRH, [[UCN]], G-protein-coupled and other transmembrane receptors [[TLR9]], [[PRLR]], [[CHRNE]], [[GP1BA]], [[PLXNA4]], a ligand-dependent nuclear receptor [[RORA]], transmembrane channels, transcription regulators [[FOS]], [[FOXO6]], [[SCX]], [[STAT5A]], [[ZFPM2]], [[ZNF396]], [[ZNF467]], protein kinases [[MAPK10]], [[MAPK13]], [[MERTK]], [[FLT1]], [[PRKCH]], [[ROS1]], [[TTN]]), phosphatases [[PTPRD]], [[PTPRR]], peptidases, metabolic enzymes, a chaperone (HSPA6), and other proteins, all of which modulate numerous life processes, playing key roles in several canonical pathways involved in defense response and regulation of homeostasis in organisms. It is for the first time we report that the molecular mechanism of actions of melatonin and plant adaptogens are alike, all adaptogens tested activated the melatonin signaling pathway by acting through two G-protein-coupled membrane receptors MT1 and MT2 and upregulation of the ligand-specific nuclear receptor [[RORA]], which plays a role in intellectual disability, neurological disorders, retinopathy, hypertension, dyslipidemia, and cancer, which are common in aging. Furthermore, melatonin activated adaptive signaling pathways and upregulated expression of [[UCN]], [[GNRH1]], [[TLR9]], [[GP1BA]], [[PLXNA4]], [[CHRM4]], [[GPR19]], [[VIPR2]], [[RORA]], [[STAT5A]], [[ZFPM2]], [[ZNF396]], [[FLT1]], [[MAPK10]], [[MERTK]], [[PRKCH]], and [[TTN]], which were commonly regulated by all adaptogens tested. We conclude that melatonin is an adaptation hormone playing an important role in regulation of homeostasis. Adaptogens presumably worked as eustressors ("stress-vaccines") to activate the cellular adaptive system by inducing the expression of ASRSPs, which then reciprocally protected cells from damage caused by distress. Functional investigation by interactive pathways analysis demonstrated that adaptogens activated ASRSPs associated with stress-induced and aging-related disorders such as chronic inflammation, cardiovascular health, neurodegenerative cognitive impairment, metabolic disorders, and cancer. This study has elucidated the genome-wide effects of several adaptogenic herbal extracts in brain cells culture. These data highlight the consistent activation of ASRSPs by adaptogens in T98G neuroglia cells. The extracts affected many genes playing key roles in modulation of adaptive homeostasis, indicating their ability to modify gene expression to prevent stress-induced and aging-related disorders. Overall, this study provides a comprehensive look at the molecular mechanisms by which adaptogens exerts stress-protective effects.
|mesh-terms=* Adaptation, Physiological
* Brain
* Bryonia
* Cell Line, Tumor
* Eleutherococcus
* Glioblastoma
* Humans
* Leuzea
* Longevity
* Neuroglia
* Plant Extracts
* Rhodiola
* Signal Transduction
* Systems Biology
* Withania
|keywords=* Adaptogen
* Melatonin
* Pathway analysis
* RNA sequencing
* Rhodiola
* Withania
|full-text-url=https://sci-hub.do/10.1016/j.phymed.2018.09.204
}}
{{medline-entry
|title=Caenorhabditis elegans respond to high-glucose diets through a network of stress-responsive transcription factors.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29990370
|abstract=High-glycemic-index diets, as well as a sedentary lifestyle are considered as determinant factors for the development of obesity, type 2 diabetes, and cardiovascular diseases in humans. These diets have been shown to shorten the life span of C. elegans in a manner that is dependent on insulin signaling, but the participation of other signaling pathways have not been addressed. In this study, we have determined that worms fed with high-glucose diets show alterations in glucose content and uptake, triglyceride content, body size, number of eggs laid, egg-laying defects, and signs of oxidative stress and accelerated aging. Additionally, we analyzed the participation of different key regulators of carbohydrate and lipid metabolism, oxidative stress and longevity such as SKN-1/NRF2, HIF-1/HIF1α, SBP-1/SREBP, [[CRH]]-1/CREB, CEP-1/p53, and DAF-16/FOXO, in the reduction of lifespan in glucose-fed worms.
|mesh-terms=* Aging
* Animals
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Diet, Carbohydrate Loading
* Glucose
* Oviparity
* Oxidative Stress
* Stress, Physiological
* Transcription Factors
* Triglycerides

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6039004
}}
{{medline-entry
|title=Genome-wide association study and annotating candidate gene networks affecting age at first calving in Nellore cattle.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28994157
|abstract=We performed a genome-wide mapping for the age at first calving (AFC) with the goal of annotating candidate genes that regulate fertility in Nellore cattle. Phenotypic data from 762 cows and 777k SNP genotypes from 2,992 bulls and cows were used. Single nucleotide polymorphism (SNP) effects based on the single-step GBLUP methodology were blocked into adjacent windows of 1 Megabase (Mb) to explain the genetic variance. SNP windows explaining more than 0.40% of the AFC genetic variance were identified on chromosomes 2, 8, 9, 14, 16 and 17. From these windows, we identified 123 coding protein genes that were used to build gene networks. From the association study and derived gene networks, putative candidate genes (e.g., [[PAPPA]], [[PREP]], [[FER1L6]], [[TPR]], [[NMNAT1]], [[ACAD10]], [[PCMTD1]], [[CRH]], OPKR1, [[NPBWR1]] and NCOA2) and transcription factors (TF) (STAT1, [[STAT3]], [[RELA]], [[E2F1]] and EGR1) were strongly associated with female fertility (e.g., negative regulation of luteinizing hormone secretion, folliculogenesis and establishment of uterine receptivity). Evidence suggests that AFC inheritance is complex and controlled by multiple loci across the genome. As several windows explaining higher proportion of the genetic variance were identified on chromosome 14, further studies investigating the interaction across haplotypes to better understand the molecular architecture behind AFC in Nellore cattle should be undertaken.
|mesh-terms=* Aging
* Animals
* Breeding
* Cattle
* Female
* Fertility
* Gene Regulatory Networks
* Genome-Wide Association Study
* Genotype
* Phenotype
* Polymorphism, Single Nucleotide
* Quantitative Trait Loci
|keywords=* beef cattle
* gene function
* single-step
|full-text-url=https://sci-hub.do/10.1111/jbg.12299
}}
{{medline-entry
|title=A C. elegans Thermosensory Circuit Regulates Longevity through crh-1/CREB-Dependent flp-6 Neuropeptide Signaling.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27720609
|abstract=Sensory perception, including thermosensation, shapes longevity in diverse organisms, but longevity-modulating signals from the sensory neurons are largely obscure. Here we show that [[CRH]]-1/CREB activation by CMK-1/CaMKI in the AFD thermosensory neuron is a key mechanism that maintains lifespan at warm temperatures in C. elegans. In response to temperature rise and crh-1 activation, the AFD neurons produce and secrete the FMRFamide neuropeptide FLP-6. Both [[CRH]]-1 and FLP-6 are necessary and sufficient for longevity at warm temperatures. Our data suggest that FLP-6 targets the AIY interneurons and engages DAF-9 sterol hormone signaling. Moreover, we show that FLP-6 signaling downregulates ins-7/insulin-like peptide and several insulin pathway genes, whose activity compromises lifespan. Our work illustrates how temperature experience is integrated by the thermosensory circuit to generate neuropeptide signals that remodel insulin and sterol hormone signaling and reveals a neuronal-endocrine circuit driven by thermosensation to promote temperature-specific longevity.
|mesh-terms=* Animals
* Body Temperature
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Genes, Helminth
* Heat-Shock Response
* Hot Temperature
* Interneurons
* Intestinal Mucosa
* Longevity
* Models, Biological
* Mutation
* Neuropeptides
* Peptide Hormones
* Sensory Receptor Cells
* Signal Transduction
* Transcription Factors
* Transcription, Genetic

|full-text-url=https://sci-hub.do/10.1016/j.devcel.2016.08.021
}}
{{medline-entry
|title=Variation in the corticotropin-releasing hormone receptor 1 ([[CRH]]R1) gene modulates age effects on working memory.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25541005
|abstract=Decline in working memory (WM) functions during aging has been associated with hippocampal dysfunction mediated by age-related changes to the corticotropin-releasing hormone ([[CRH]]) system. Recent reports suggest that GG-homozygous individuals of single nucleotide polymorphisms (rs110402 and rs242924) in the [[CRH]] receptor 1 ([[CRH]]R1) gene show increased stress vulnerability and decreased BOLD responses in WM relevant regions. However, until now, no study investigated the interaction effects of variation in the [[CRH]]R1 gene and age on individual differences in WM. Here, young, middle-aged and old subjects (N = 466) were genotyped for rs110402 and rs242924 within the [[CRH]]R1 gene and an n-back task was used to investigate the hypothesis that vulnerable genotypes (GG-homozygotes) would show impaired WM functions that might be magnified by increased [[CRH]] production with advancing age. Our results show an impact of genotype already in middle-age with significantly better performance in AT-carriers. Working memory performance in AT-carriers did not differ between young and middle-aged subjects, but was significantly impaired in old age. In GG-homozygotes, severe working memory dysfunction occurred already in middle age. Our data indicate that GG-homozygotes of [[CRH]]R1 rs110402 and rs242924 represent a genetically driven subtype of early WM impairments due to alterations in hippocampal [[CRH]]R1 activation. Early interventions that have proven effective in delaying cognitive decline appear to be particularly important for these subjects at risk for premature memory decline, who are in the prime of their personal and professional lives.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Female
* Genetic Testing
* Hippocampus
* Homozygote
* Humans
* Male
* Memory, Short-Term
* Middle Aged
* Neuropsychological Tests
* Polymorphism, Single Nucleotide
* Receptors, Corticotropin-Releasing Hormone
* Young Adult
|keywords=* Aging
* CRHR1 gene
* Hippocampus
* Working memory
|full-text-url=https://sci-hub.do/10.1016/j.jpsychires.2014.12.001
}}
{{medline-entry
|title=HPA axis and aging in depression: systematic review and meta-analysis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24495607
|abstract=One of the most consistent findings in the biology of depression is an altered activity of the hypothalamic-pituitary-adrenal (HPA) axis. However, data concerning this issue have never been examined with a focus on the older population. Here we present a systematic review and meta-analysis, based on studies investigating levels of cortisol, adrenocorticotropic hormone (ACTH) and corticotropin-releasing hormone ([[CRH]]) in depressed participants older than 60 and compared with healthy controls. We found 20 studies, for a total of 43 comparisons on different indices of HPA axis functioning. Depression had a significant effect (Hedges' g) on basal cortisol levels measured in the morning (0.89), afternoon (0.83) and night (1.39), but a smaller effect on cortisol measured continuously (0.51). The effect of depression was even higher on post-dexamethasone cortisol levels (3.22), whereas it was non-significant on morning ACTH and [[CRH]] levels. Subgroup analyses indicated that various methodological and clinical factors can influence the study results. Overall, older participants suffering from depression show a high degree of dysregulation of HPA axis activity, with differences compared with younger adults. This might depend on several mechanisms, including physical illnesses, alterations in the CNS and immune-endocrinological alterations. Further studies are needed to clarify the implications of altered HPA axis activity in older patients suffering from depression. Novel pharmacological approaches might be effective in targeting this pathophysiological feature, thus improving the clinical outcomes. 
|mesh-terms=* Adrenocorticotropic Hormone
* Aging
* Corticotropin-Releasing Hormone
* Depression
* Dexamethasone
* Humans
* Hydrocortisone
* Hypothalamo-Hypophyseal System
* Pituitary-Adrenal Function Tests
* Pituitary-Adrenal System
|keywords=* ACTH
* Antidepressant
* CRH
* Cortisol
* Depression
* Depressive symptoms
* Dexamethasone
* Elderly
* HPA axis
* Older adults
|full-text-url=https://sci-hub.do/10.1016/j.psyneuen.2013.12.004
}}
{{medline-entry
|title=Regulation of corticosterone secretion is modified by PFOS exposure at different levels of the hypothalamic-pituitary-adrenal axis in adult male rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24440345
|abstract=Perfluorooctane sulfonate (PFOS) is a fluorinated compound and a Persistent Organic Pollutant which can disrupt the endocrine system. This work was undertaken to evaluate the possible effects of PFOS exposure on the regulation of corticosterone secretion in adrenal and pituitary glands and at hypothalamic level in adult male rat, and to evaluate the possible morphological alterations induced by PFOS in this endocrine tissue. Adult male rats were orally treated with 0.5, 1.0, 3.0 and 6.0 mg of PFOS/kg/day for 28 days. Corticosterone, adrenocorticotropic hormone (ACTH) and corticotrophin-releasing hormone ([[CRH]]) secretion decreased in PFOS-treated rats. After PFOS exposure, relative expression of adrenocorticotropic hormone receptor (ACTHr) and proopiomelanocortin (POMC) genes was increased in adrenal and in pituitary glands, respectively; while relative expression of ACTHr and [[CRH]] genes decreased in hypothalamus with the doses of 0.5 and 1.0 mg/kg/day. PFOS treatment increased relative nitric oxide synthase 1 and 2 (NOS1 and NOS2) gene expression in the adrenal gland, and incremented superoxide dismutase activity. PFOS exposure induces a global inhibition of the hypothalamic-pituitary-adrenal (HPA) axis activity, and small morphological changes were observed in adrenal zona fasciculata cells.
|mesh-terms=* Adrenocorticotropic Hormone
* Aging
* Alkanesulfonic Acids
* Animals
* Corticosterone
* Dose-Response Relationship, Drug
* Fluorocarbons
* Hypothalamo-Hypophyseal System
* Male
* Pituitary-Adrenal System
* Rats
* Rats, Sprague-Dawley
|keywords=* Corticosterone
* Histopathology
* Hypothalamic–pituitary–adrenal axis
* Oxidative stress
* PFOS
|full-text-url=https://sci-hub.do/10.1016/j.toxlet.2014.01.003
}}
{{medline-entry
|title=Differential contribution of CBP:CREB binding to corticotropin-releasing hormone expression in the infant and adult hypothalamus.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23768074
|abstract=Corticotropin-releasing hormone ([[CRH]]) contributes crucially to the regulation of central and peripheral responses to stress. Because of the importance of a finely tuned stress system, [[CRH]] expression is tightly regulated in an organ- and brain region-specific manner. Thus, in the hypothalamus, [[CRH]] is constitutively expressed and this expression is further enhanced by stress; however, the underlying regulatory mechanisms are not fully understood. The regulatory region of the crh gene contains several elements, including the cyclic-AMP response element (CRE), and the role of the CRE interaction with the cyclic-AMP response element binding protein (CREB) in [[CRH]] expression has been a focus of intensive research. Notably, whereas thousands of genes contain a CRE, the functional regulation of gene expression by the CRE:CREB system is limited to ∼100 genes, and likely requires additional proteins. Here, we investigated the role of a member of the CREB complex, CREB binding protein (CBP), in basal and stress-induced [[CRH]] expression during development and in the adult. Using mice with a deficient CREB-binding site on CBP, we found that CBP:CREB interaction is necessary for normal basal [[CRH]] expression at the mRNA and protein level in the nine-day-old mouse, prior to onset of functional regulation of hypothalamic [[CRH]] expression by glucocorticoids. This interaction, which functions directly on crh or indirectly via regulation of other genes, was no longer required for maintenance of basal [[CRH]] expression levels in the adult. However, CBP:CREB binding contributed to stress-induced [[CRH]] expression in the adult, enabling rapid [[CRH]] synthesis in hypothalamus. CBP:CREB binding deficiency did not disrupt basal corticosterone plasma levels or acute stress-evoked corticosterone release. Because dysregulation of [[CRH]] expression occurs in stress-related disorders including depression, a full understanding of the complex regulation of this gene is important in both health and disease.
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Corticosterone
* Corticotropin-Releasing Hormone
* Cyclic AMP Response Element-Binding Protein
* Hypothalamus
* Male
* Mice
* Paraventricular Hypothalamic Nucleus
* Restraint, Physical
* Stress, Physiological
* Stress, Psychological

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869921
}}
{{medline-entry
|title=Stress responsiveness of the hypothalamic-pituitary-adrenal axis: age-related features of the vasopressinergic regulation.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23486926
|abstract=The hypothalamic-pituitary-adrenal (HPA) axis plays a key role in adaptation to environmental stresses. Parvicellular neurons of the hypothalamic paraventricular nucleus secrete corticotrophin releasing hormone ([[CRH]]) and arginine vasopressin ([[AVP]]) into pituitary portal system; [[CRH]] and [[AVP]] stimulate adrenocorticotropic hormone (ACTH) release through specific G-protein-coupled membrane receptors on pituitary corticotrophs, [[CRH]]R1 for [[CRH]] and V1b for [[AVP]]; the adrenal gland cortex secretes glucocorticoids in response to ACTH. The glucocorticoids activate specific receptors in brain and peripheral tissues thereby triggering the necessary metabolic, immune, neuromodulatory, and behavioral changes to resist stress. While importance of [[CRH]], as a key hypothalamic factor of HPA axis regulation in basal and stress conditions in most species, is generally recognized, role of [[AVP]] remains to be clarified. This review focuses on the role of [[AVP]] in the regulation of stress responsiveness of the HPA axis with emphasis on the effects of aging on vasopressinergic regulation of HPA axis stress responsiveness. Under most of the known stressors, [[AVP]] is necessary for acute ACTH secretion but in a context-specific manner. The current data on the [[AVP]] role in regulation of HPA responsiveness to chronic stress in adulthood are rather contradictory. The importance of the vasopressinergic regulation of the HPA stress responsiveness is greatest during fetal development, in neonatal period, and in the lactating adult. Aging associated with increased variability in several parameters of HPA function including basal state, responsiveness to stressors, and special testing. Reports on the possible role of the [[AVP]]/V1b receptor system in the increase of HPA axis hyperactivity with aging are contradictory and requires further research. Many contradictory results may be due to age and species differences in the HPA function of rodents and primates.

|keywords=* V1b receptors
* aging
* hypothalamic–pituitary–adrenal axis
* stress
* vasopressin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3594837
}}
{{medline-entry
|title=Effects of aging on hypothalamic-pituitary-adrenal (HPA) axis activity and reactivity in virgin male and female California mice (Peromyscus californicus).
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23458287
|abstract=Life history theory posits that organisms face a trade-off between current and future reproductive attempts. The physiological mechanisms mediating such trade-offs are still largely unknown, but glucocorticoid hormones are likely candidates as elevated, post-stress glucocorticoid levels have been shown to suppress both reproductive physiology and reproductive behavior. Aged individuals have a decreasing window in which to reproduce, and are thus predicted to invest more heavily in current as opposed to future reproduction. Therefore, if glucocorticoids are important in mediating the trade-off between current and future reproduction, aged animals are expected to show decreased hypothalamic-pituitary-adrenal (HPA) axis responses to stressors and to stimulation by corticotropin-releasing hormone ([[CRH]]), and enhanced responses to glucocorticoid negative feedback, as compared to younger animals. We tested this hypothesis in the monogamous, biparental California mouse by comparing baseline and post-stress corticosterone levels, as well as corticosterone responses to dexamethasone (DEX) and [[CRH]] injections, between old (∼18-20months) and young (∼4months) virgin adults of both sexes. We also measured gonadal and uterine masses as a proxy for investment in potential current reproductive effort. Adrenal glands were weighed to determine if older animal had decreased adrenal mass. Old male mice had lower plasma corticosterone levels 8h after DEX injection than did young male mice, suggesting that the anterior pituitary of older males is more sensitive to DEX-induced negative feedback. Old female mice had higher body-mass-corrected uterine mass than did young females. No other differences in corticosterone levels or organ masses were found between age groups within either sex. In conclusion, we did not find strong evidence for age-related change in HPA activity or reactivity in virgin adult male or female California mice; however, future studies investigating HPA activity and reproductive outcomes in young and old breeding adults would be illuminating.
|mesh-terms=* Adrenal Glands
* Aging
* Animals
* Corticosterone
* Corticotropin-Releasing Hormone
* Female
* Hypothalamo-Hypophyseal System
* Male
* Mice
* Peromyscus
* Pituitary-Adrenal System

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640751
}}
{{medline-entry
|title=[Study on establishment of kidney deficient aging model and comparison with D-galactose induced aging model].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23234144
|abstract=To establish a kidney deficient aging model (KDAM), assess it in antioxidant capacity, HPAT axis function and bone metabolism, and compare with D-galactose aging model. Aging rat model was established by injecting D-galactose solution, meanwhile dexamethasone solution was injected to establish kidney deficient aging model. Then these models were evaluated by serum MDA (malondialdehyde) and GSH-Px (glutathione peroxidase), liver SOD (superoxide dismutase), adrenal, thymus and spleen index, CD4( ), CD8( ), and serum COR (cortisol), BGP (bone Gla-protein), plasma ACTH (adrenocorticotropic hormone) and [[CRH]] (corticotropin-releasing hormone). Compared with the normal group, the aging model group and the kidney deficient aging group showed significant decrease in liver SOD activity (P < 0.01 on average) and significant increase in serum MDA content (P < 0.01 on average) , and the kidney deficient aging group revealed remarkable decline in plasma ACTH content (P < 0.05). Compared with the normal group and the aging model group, the kidney deficient aging model group's weight, serum GSH-Px decreased (P < 0.01, P < 0.05), adrenal index decreased (P < 0.05, P < 0.01), serum COR decreased (P < 0.05 on average), plasma [[CRH]] increased (P < 0.05, P < 0.01), serum BGP content significantly decreased (P < 0.01 on average), value of CD4( ), CD8( ) decreased (P < 0.05, P < 0.01), CD4( )/CD8( ) increased, but without significant difference. The kidney deficient aging model shows significant decrease in antioxidant capacity, dysfunction of HPAT axis disorder and abnormal bone metabolism. However, D-galactose aging model only shows a significant difference in antioxidant capacity.
|mesh-terms=* Aging
* Animals
* Antioxidants
* Disease Models, Animal
* Galactose
* Humans
* Kidney
* Kidney Diseases
* Liver
* Male
* Malondialdehyde
* Oxidative Stress
* Rats
* Rats, Sprague-Dawley
* Superoxide Dismutase


}}