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      Thirteen weeks of supplementation of vitamin D and leucine-enriched whey protein nutritional supplement attenuates chronic low-grade inflammation in sarcopenic older adults: the PROVIDE study

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          Abstract

          Background

          A chronic low-grade inflammatory profile (CLIP) is associated with sarcopenia in older adults. Protein and Vitamin (Vit)D have immune-modulatory potential, but evidence for effects of nutritional supplementation on CLIP is limited.

          Aim

          To investigate whether 13 weeks of nutritional supplementation of VitD and leucine-enriched whey protein affected CLIP in subjects enrolled in the PROVIDE-study, as a secondary analysis.

          Methods

          Sarcopenic adults (low skeletal muscle mass) aged ≥ 65 years with mobility limitations (Short Physical Performance Battery 4–9) and a body mass index of 20–30 kg/m 2 were randomly allocated to two daily servings of active ( n = 137, including 20 g of whey protein, 3 g of leucine and 800 IU VitD) or isocaloric control product ( n = 151) for a double-blind period of 13 weeks. At baseline and after 13 weeks, circulating interleukin (IL)-8, IL-1 receptor antagonist (RA), soluble tumor-necrosis-factor receptor (sTNFR)1, IL-6, high-sensitivity C-reactive protein, pre-albumin and 25-hydroxyvitamin(OH)D were measured. Data-analysis included repeated measures analysis of covariance (corrected for dietary VitD intake) and linear regression.

          Results

          IL-6 and IL-1Ra serum levels showed overall increases after 13 weeks ( p = 0.006 and p < 0.001, respectively). For IL-6 a significant time × treatment interaction ( p = 0.046) was observed, with no significant change over time in the active group ( p = 0.155) compared to control (significant increase p = 0.012). IL-8 showed an overall significant decrease ( p = 0.03). The change in pre-albumin was a significant predictor for changes in IL-6 after 13 weeks.

          Conclusions

          We conclude that 13 weeks of nutritional supplementation with VitD and leucine-enriched whey protein may attenuate the progression of CLIP in older sarcopenic persons with mobility limitations.

          Electronic supplementary material

          The online version of this article (10.1007/s40520-019-01208-4) contains supplementary material, which is available to authorized users.

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          Most cited references38

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          Inflammatory markers in population studies of aging.

          To review findings from major epidemiologic studies regarding risk factors for and consequences of elevated markers of inflammation in older adults. Most large, current epidemiologic studies of older adults have measured serum interleukin-6 (IL-6), C-reactive protein (CRP) and tumor necrosis factor alpha (TNF-alpha) and some studies also include more extensive batteries of measures including soluble receptors. There are few defined risk factors for the modest elevations in inflammatory markers seen with aging. These include visceral adiposity, lower sex steroid hormones, smoking, depression and periodontal disease. Of the markers assessed, IL-6 is most robustly associated with incident disease, disability and mortality. Though correlated with age, the etiology of elevated inflammatory markers remains incompletely defined. Inflammation, especially IL-6 may be a common cause of multiple age-related diseases or a final common pathway by which disease leads to disability and adverse outcomes in older adults. Future research targeting inflammation should examine these pathways. Copyright © 2011. Published by Elsevier B.V.
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            Inflammatory mediators in the elderly.

            Ageing is accompanied by 2-4-fold increases in plasma/serum levels of inflammatory mediators such as cytokines and acute phase proteins. A wide range of factors seems to contribute to this low-grade inflammation, including an increased amount of fat tissue, decreased production of sex steroids, smoking, subclinical infections (e.g. asymptomatic bacteriuria), and chronic disorders such as cardiovascular diseases and Alzheimer's disease. Furthermore, there is some evidence that ageing is associated with a dysregulated cytokine response following stimulation. Several inflammatory mediators such as tumour necrosis factor-alpha and interleukin-6 have the potential to induce/aggravate risk factors in age-associated pathology, providing a positive feedback mechanism. Thus, it is possible that inflammatory mediators constitute a link between life style factors, infections and physiological changes in the process of ageing on the one hand and risk factors for age-associated diseases on the other. Consistent with this, inflammatory mediators are strong predictors of mortality independently of other known risk factors and co-morbidity in elderly cohorts. A direct pathogenetic role of inflammatory mediators would be highly likely if longevity was shown to be associated with cytokine polymorphisms regulating cytokine production. Several studies support indeed this hypothesis but, unfortunately, findings in this area are conflicting, which probably reflects the complexity of the effect of cytokine polymorphisms and their interaction with the lifestyle and sex.
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              1alpha,25-Dihydroxyvitamin d3 has a direct effect on naive CD4(+) T cells to enhance the development of Th2 cells.

              1alpha,25-Dihydroxyvitamin D3 (vitD3) is an immunoregulatory hormone with beneficial effects on Th1 mediated autoimmune diseases. Although the inhibitory effects of vitD3 on macrophages and dendritic cells are well documented, any direct effects of vitD3 on Th cell development are not clearly defined. Using CD4(+)Mel14(+) T cells derived from mice on a BALB/c and a C57BL/6 genetic background we examined the effect of vitD3 on Th cell development. We demonstrated that vitD3 affects Th cell polarization by inhibiting Th1 (IFN-gamma production) and augmenting Th2 cell development (IL-4, IL-5, and IL-10 production). These effects were observed in cultures driven with splenic APC and Ag, as well as with anti-CD3 and anti-CD28 alone, indicating that CD4(+) cells can also be direct targets for vitD3. The enhanced Th2 development by vitD3 was found in both BALB/c and C57BL/6 mice. An increased expression of the Th2-specific transcription factors GATA-3 and c-maf correlated with the increased production of Th2 cytokines after vitD3 treatment. The vitD3-induced effects were largely mediated via IL-4, because neutralization of IL-4 almost completely abrogated the augmented Th2 cell development after vitD3 treatment. These findings suggest that vitD3 acts directly on Th cells and can, in the absence of APC, enhance the development of a Th2 phenotype and augment the expression of the transcription factors c-maf and GATA-3. Our findings suggest that the beneficial effects of vitD3 in autoimmune diseases and transplantation operate through prevention of strong Th1 responses via the action on the APC, while simultaneously directly acting on the T cell to enhance Th2 cell development.
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                Author and article information

                Contributors
                ivan.bautmans@vub.be
                Journal
                Aging Clin Exp Res
                Aging Clin Exp Res
                Aging Clinical and Experimental Research
                Springer International Publishing (Cham )
                1594-0667
                1720-8319
                2 May 2019
                2 May 2019
                2019
                : 31
                : 6
                : 845-854
                Affiliations
                [1 ]ISNI 0000 0001 2290 8069, GRID grid.8767.e, Frailty in Ageing Research Group (FRIA), , Vrije Universiteit Brussel (VUB), ; Laarbeeklaan 103, 1090 Brussels, Belgium
                [2 ]Nutricia Research, Nutricia Advanced Medical Nutrition, Utrecht, The Netherlands
                [3 ]ISNI 0000 0004 0435 165X, GRID grid.16872.3a, Department of Internal Medicine, Section of Gerontology and Geriatrics, , VU University Medical Center, ; Amsterdam, The Netherlands
                [4 ]ISNI 0000 0001 2190 4373, GRID grid.7700.0, Center of Geriatric Medicine, , Heidelberg University, ; Heidelberg, Germany
                [5 ]GRID grid.431204.0, Faculty of Sports and Nutrition, , Amsterdam University of Applied Sciences, ; Amsterdam, The Netherlands
                [6 ]ISNI 0000 0001 0462 7212, GRID grid.1006.7, Human Nutrition Research Centre, Institute of Cellular Medicine, , Newcastle University, ; Newcastle upon Tyne, UK
                [7 ]GRID grid.7841.a, Department of Experimental Medicine, Section of Medical Pathophysiology, Endocrinology and Human Nutrition, , “Sapienza” University of Rome, ; Rome, Italy
                [8 ]ISNI 0000 0004 1758 0937, GRID grid.10383.39, Department of Medicine and Surgery, Section of Geriatrics, , University of Parma, ; Parma, Italy
                [9 ]ISNI 0000 0001 2107 3311, GRID grid.5330.5, Friedrich-Alexander-Universität Erlangen-Nürnberg, ; Erlangen, Germany
                [10 ]ISNI 0000 0001 2351 3333, GRID grid.412354.5, Department of Public Health and Caring Nutrition Sciences/Clinical and Metabolism, Department of Geriatric Medicine, , Uppsala University Hospital, ; Uppsala, Sweden
                Author information
                http://orcid.org/0000-0002-6820-9586
                Article
                1208
                10.1007/s40520-019-01208-4
                6583678
                31049877
                6f0e80a3-8888-456f-ad3f-dbd5d364449a
                © The Author(s) 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 18 January 2019
                : 16 April 2019
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001720, Nutricia Research Foundation;
                Categories
                Original Article
                Custom metadata
                © Springer Nature Switzerland AG 2019

                vitamin d,leucine,whey proteins,dietary supplements,cytokines,aged

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