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Belury M.A.,Ohio State University | Cole R.M.,Ohio State University | Bailey B.E.,Institute for Behavioral Medicine Research | Ke J.-Y.,Ohio State University | Kiecolt-Glaser J.K.,Institute for Behavioral Medicine Research
Molecular Nutrition and Food Research

Scope: Supplementation with linoleic acid (LA; 18:2Ω6)-rich oils increases lean mass and decreases trunk adipose mass in people. Erythrocyte fatty acids reflect the dietary pattern of fatty acid intake and endogenous metabolism of fatty acids. The aim of this study is to determine the relationship of erythrocyte LA, with aspects of body composition, insulin resistance, and inflammation. Additionally, we tested for relationships of oleic acid (OA) and the sum of long chain omega-three fatty acids (LC-Ω3-SUM), on the same outcomes. Methods and results: Men and women (N = 139) were evaluated for body composition, insulin resistance, and serum inflammatory markers, IL-6, and c-reactive protein (CRP) and erythrocyte fatty acid composition after an overnight fast. LA was positively related to appendicular lean mass/body mass index and inversely related to trunk adipose mass. Additionally, LA was inversely related to insulin resistance and IL-6. While there was an inverse relationship between OA or LC-Ω3-SUM with markers of inflammation, there were no relationships between OA or LC-Ω3-SUM with body composition or HOMA-IR. Conclusion: Higher erythrocyte LA was associated with improved body composition, insulin resistance, and inflammation. Erythrocyte OA or LC-Ω3-SUM was unrelated to body composition and insulin resistance. There is much controversy about whether all unsaturated fats have the same benefits for metabolic syndrome and weight gain. We sought to test the strength of the relationships between three unsaturated fatty acid in erythrocytes with measurements of body composition, metabolism, and inflammation in healthy adults. Linoleic acid, but not oleic acid or the sum of long-chain omega 3 fatty acids (w3), was associated with increased appendicular lean mass and decreased trunk adipose mass and insulin resistance. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. Source

Norman G.J.,Ohio State University | Karelina K.,Institute for Behavioral Medicine Research | Zhang N.,Institute for Behavioral Medicine Research | Cochran M.,Institute for Behavioral Medicine Research | And 2 more authors.
Psychosomatic Medicine

Objective: To examine the salubrious role of social interaction in modulating the development of allodynia (increased sensitivity to typically innocuous physical stimuli) and depressive-like behavior post peripheral nerve injury in mice. The determination of potential mechanisms that mediate social influences on the behavioral and physiological response to peripheral nerve injury. Methods: Mice were pair housed or socially isolated for 2 weeks before spared nerve injury (SNI). Animals were cannulated; socially isolated animals were centrally treated with oxytocin; and socially paired animals were centrally treated with an oxytocin receptor antagonist. Animals were subsequently monitored for the development of mechanical allodynia and depressive-like behavior, and tissue was collected for analysis of the central levels of the cytokine interleukin 1 beta (IL-1β). Results: Depressive-like behavior was assessed via the Porsolt forced swim test, developed only among socially isolated mice with nerve injury. Socially isolated mice with nerve injury also were the only experimental group to exhibit increased frontal cortex IL-1β gene expression on day 7 post injury. Moreover, central treatment of socially isolated mice with oxytocin, a neuropeptide associated with social bonding, attenuated the effects of SNI on depressive-like behavior and reduced frontal cortex IL-1β protein levels in socially isolated animals. Conversely, pair-housed animals treated with a selective oxytocin receptor antagonist developed depressive-like behavior equivalent to that of socially isolated animals and displayed increased IL-1β protein levels within the frontal cortex. CONCLUSION: These data suggest that social interaction significantly alters the affective and neuroinflammatory responses to SNI through a mechanism that could involve oxytocin. Copyright © 2010 by the American Psychosomatic Society. Source

Fonken L.K.,Institute for Behavioral Medicine Research | Gaudet A.D.,Institute for Behavioral Medicine Research | Gaudet A.D.,Ohio State University | Nelson R.J.,Institute for Behavioral Medicine Research | And 2 more authors.

Depressive disorders have complex and multi-faceted underlying mechanisms, rendering these disorders difficult to treat consistently and effectively. One under-explored therapeutic strategy for alleviating mood disorders is the targeting of microRNAs (miRs). miRs are small non-coding RNAs that cause sequestration/degradation of specific mRNAs, thereby preventing protein translation and downstream functions. miR-155 has validated and predicted neurotrophic factor and inflammatory mRNA targets, which led to our hypothesis that miR-155 deletion would modulate affective behaviors. To evaluate anxiety-like behavior, wildtype (wt) and miR-155 knockout (ko) mice (littermates; both male and female) were assessed in the open field and on an elevated plus maze. In both tests, miR-155 ko mice spent more time in open areas, suggesting they had reduced anxiety-like behavior. Depressive-like behaviors were assessed using the forced swim test. Compared to wt mice, miR-155 ko mice exhibited reduced float duration and increased latency to float. Further, although all mice exhibited a strong preference for a sucrose solution over water, this preference was enhanced in miR-155 ko mice. miR-155 ko mice had no deficiencies in learning and memory (Barnes maze) or social preference/novelty suggesting that changes in mood were specific. Finally, compared to wt hippocampi, miR-155 ko hippocampi had a reduced inflammatory signature (e.g., decreased IL-6, TNF-a) and female miR-155 ko mice increased ciliary neurotrophic factor expression. Together, these data highlight the importance of studying microRNAs in the context of anxiety and depression and identify miR-155 as a novel potential therapeutic target for improving mood disorders. © 2015 Elsevier Ltd. Source

Mays J.W.,Ohio State University | Mays J.W.,National Institute of Allergy and Infectious Diseases | Powell N.D.,Ohio State University | Hunzeker J.T.,Ohio State University | And 5 more authors.
Journal of Neuroimmunology

Social disruption stress (SDR) prior to primary influenza A virus (IAV) infection augments memory to IAV re-challenge in a T cell-specific manner. However, the effect of SDR on the primary anti-viral immune response has not been elucidated. In this study, SDR-infected (INF) mice terminated viral gene expression earlier and mounted an enhanced pulmonary IAV-specific CD8 +T cell response versus controls. Additionally, SDR-INF mice had a more pro-inflammatory lung profile prior to and during infection and an attenuated corticosterone response. These data demonstrate neuroendocrine modification of the lung microenvironment and increased antigen-specific T cell activation, clonal expansion and viral control in stress-exposed mice. © 2012 Elsevier B.V. Source

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