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      Effects of High-Fat Diet on Stress Response in Male and Female Wildtype and Prolactin Knockout Mice

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          Abstract

          Prolactin (PRL) is well characterized for its roles in initiation and maintenance of lactation, and it also suppresses stress-induced responses. Feeding a high-fat diet (HFD) disrupts activity of the hypothalamic-pituitary-adrenal (HPA) axis. Whether PRL regulates HPA axis activation under HFD feeding is not clear. Male and female wildtype (WT) and PRL knockout (KO) mice were fed either a standard low-fat diet (LFD) or HFD for 12 weeks. Circulating corticosterone (CORT) levels were measured before, during, and after mice were subjected to an acute restraint stress or remained in their home cages as no stress controls. HFD feeding increased leptin levels, but the increase was lower in KO than in WT mice. All stressed female groups and only LFD-fed stressed males had elevated CORT levels compared to their no stress same-sex counterparts regardless of genotype. These results indicated that HFD consumption blunted the HPA axis response to acute stress in males but not females. Additionally, basal hypothalamic CRH content was lower in HFD than LFD males, but was similar among female groups. Furthermore, although basal CORT levels were similar among KO and WT groups, CORT levels were higher in KO mice than their WT counterparts during stress, suggesting that loss of PRL led to greater HPA axis activation. Basal PRL receptor mRNA levels in the choroid plexus were higher in HFD than LFD same-sex counterparts, suggesting activation of central PRL’s action by HFD feeding in both males and females. Current results confirmed PRL’s roles in suppression of the stress-induced HPA axis activation. Although HFD feeding activated central PRL’s action in both sexes, only the male HPA axis was dampened by HFD feeding.

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          Most cited references 46

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          Central mechanisms of stress integration: hierarchical circuitry controlling hypothalamo–pituitary–adrenocortical responsiveness

          Appropriate regulatory control of the hypothalamo-pituitary-adrenocortical stress axis is essential to health and survival. The following review documents the principle extrinsic and intrinsic mechanisms responsible for regulating stress-responsive CRH neurons of the hypothalamic paraventricular nucleus, which summate excitatory and inhibitory inputs into a net secretory signal at the pituitary gland. Regions that directly innervate these neurons are primed to relay sensory information, including visceral afferents, nociceptors and circumventricular organs, thereby promoting 'reactive' corticosteroid responses to emergent homeostatic challenges. Indirect inputs from the limbic-associated structures are capable of activating these same cells in the absence of frank physiological challenges; such 'anticipatory' signals regulate glucocorticoid release under conditions in which physical challenges may be predicted, either by innate programs or conditioned stimuli. Importantly, 'anticipatory' circuits are integrated with neural pathways subserving 'reactive' responses at multiple levels. The resultant hierarchical organization of stress-responsive neurocircuitries is capable of comparing information from multiple limbic sources with internally generated and peripherally sensed information, thereby tuning the relative activity of the adrenal cortex. Imbalances among these limbic pathways and homeostatic sensors are likely to underlie hypothalamo-pituitary-adrenocortical dysfunction associated with numerous disease processes.
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            The role of neuropeptide Y in the antiobesity action of the obese gene product.

            Recently Zhang et al. cloned a gene that is expressed only in adipose tissue of the mouse. The obese phenotype of the ob/ob mouse is linked to a mutation in the obese gene that results in expression of a truncated inactive protein. Human and rat homologues for this gene are known. Previous experiments predict such a hormone to have a hypothalamic target. Hypothalamic neuropeptide Y stimulates food intake, decreases thermogenesis, and increases plasma insulin and corticosterone levels making it a potential target. Here we express the obese protein in Escherichia coli and find that it suppresses food intake and decreases body weight dramatically when administered to normal and ob/ob mice but not db/db (diabetic) mice, which are thought to lack the appropriate receptor. High-affinity binding was detected in the rat hypothalamus. One mechanism by which this protein regulated food intake and metabolism was inhibition of neuropeptide-Y synthesis and release.
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              What can we learn from rodents about prolactin in humans?

              Prolactin (PRL) is a 23-kDa protein hormone that binds to a single-span membrane receptor, a member of the cytokine receptor superfamily, and exerts its action via several interacting signaling pathways. PRL is a multifunctional hormone that affects multiple reproductive and metabolic functions and is also involved in tumorigenicity. In addition to being a classical pituitary hormone, PRL in humans is produced by many tissues throughout the body where it acts as a cytokine. The objective of this review is to compare and contrast multiple aspects of PRL, from structure to regulation, and from physiology to pathology in rats, mice, and humans. At each juncture, questions are raised whether, or to what extent, data from rodents are relevant to PRL homeostasis in humans. Most current knowledge on PRL has been obtained from studies with rats and, more recently, from the use of transgenic mice. Although this information is indispensable for understanding PRL in human health and disease, there is sufficient disparity in the control of the production, distribution, and physiological functions of PRL among these species to warrant careful and judicial extrapolation to humans.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                28 November 2016
                2016
                : 11
                : 11
                Affiliations
                [1 ]Department of Biology, Physiology and Neuroscience, Miami University, Oxford, Ohio, United States of America
                [2 ]Cell, Molecular, and Structural Biology, Miami University, Oxford, Ohio, United States of America
                Brock University, CANADA
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                • Conceptualization: MK KH JMJ PC HS.

                • Data curation: MK KH JMJ PC HS.

                • Formal analysis: MK KH JMJ PC HS.

                • Funding acquisition: JMJ PC HS.

                • Investigation: MK KH JMJ PC HS.

                • Methodology: MK KH JMJ PC HS.

                • Project administration: MK KH JMJ PC HS.

                • Resources: MK JMJ PC HS.

                • Supervision: JMJ PC HS.

                • Validation: MK KH JMJ PC HS.

                • Visualization: MK JMJ PC HS.

                • Writing – original draft: MK KH JMJ PC HS.

                • Writing – review & editing: MK KH JMJ PC HS.

                Article
                PONE-D-16-27668
                10.1371/journal.pone.0166416
                5125580
                27893788
                © 2016 Kalyani et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Page count
                Figures: 5, Tables: 0, Pages: 17
                Product
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/100000062, National Institute of Diabetes and Digestive and Kidney Diseases;
                Award ID: DK046479
                Award Recipient :
                Funded by: funder-id http://dx.doi.org/10.13039/100000062, National Institute of Diabetes and Digestive and Kidney Diseases;
                Award ID: DK090823
                Award Recipient :
                This work was supported by National Institutes of Health DK046479 (JJ and PC) and DK090823 (HS), https://www.niddk.nih.gov/Pages/default.aspx.
                Categories
                Research Article
                Biology and Life Sciences
                Biochemistry
                Hormones
                Peptide Hormones
                Leptin
                Research and Analysis Methods
                Model Organisms
                Animal Models
                Mouse Models
                Biology and Life Sciences
                Anatomy
                Brain
                Choroid Plexus
                Medicine and Health Sciences
                Anatomy
                Brain
                Choroid Plexus
                Biology and Life Sciences
                Ecology
                Community Ecology
                Trophic Interactions
                Ecology and Environmental Sciences
                Ecology
                Community Ecology
                Trophic Interactions
                Biology and Life Sciences
                Nutrition
                Diet
                Medicine and Health Sciences
                Nutrition
                Diet
                Biology and Life Sciences
                Physiology
                Physiological Parameters
                Body Weight
                Medicine and Health Sciences
                Physiology
                Physiological Parameters
                Body Weight
                Biology and Life Sciences
                Biochemistry
                Lipids
                Fats
                Biology and Life Sciences
                Anatomy
                Endocrine System
                Pituitary Gland
                Medicine and Health Sciences
                Anatomy
                Endocrine System
                Pituitary Gland
                Biology and Life Sciences
                Anatomy
                Nervous System
                Neuroanatomy
                Pituitary Gland
                Medicine and Health Sciences
                Anatomy
                Nervous System
                Neuroanatomy
                Pituitary Gland
                Biology and Life Sciences
                Neuroscience
                Neuroanatomy
                Pituitary Gland
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                All relevant data are within the paper.

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