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Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro

BACKGROUND: Specific bio-active dietary compounds modulate numerous metabolic processes in adipose tissue (AT), including pre-adipocyte proliferation and differentiation. AT dysfunction, rather than an increased fat mass per se, is strongly associated with the development of insulin resistance and i...

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Autores principales: Warnke, Ines, Jocken, Johan W. E., Schoop, Rotraut, Toepfer, Christine, Goralczyk, Regina, Schwager, Joseph
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5117626/
https://www.ncbi.nlm.nih.gov/pubmed/27895698
http://dx.doi.org/10.1186/s12986-016-0143-5
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author Warnke, Ines
Jocken, Johan W. E.
Schoop, Rotraut
Toepfer, Christine
Goralczyk, Regina
Schwager, Joseph
author_facet Warnke, Ines
Jocken, Johan W. E.
Schoop, Rotraut
Toepfer, Christine
Goralczyk, Regina
Schwager, Joseph
author_sort Warnke, Ines
collection PubMed
description BACKGROUND: Specific bio-active dietary compounds modulate numerous metabolic processes in adipose tissue (AT), including pre-adipocyte proliferation and differentiation. AT dysfunction, rather than an increased fat mass per se, is strongly associated with the development of insulin resistance and is characterized by impaired adipogenesis, hypertrophic adipocytes, inflammation, and impairments in substrate metabolism. A better understanding of mechanisms underlying AT dysfunction may provide new strategies for the treatment of obesity-associated metabolic diseases. Here we evaluated the role of (all-E)-lycopene (Lyc), eicosapentaenoic acid (EPA) or trans-resveratrol (Res) and combinations thereof on human white adipocyte function. METHODS: In-vitro differentiating human pre-adipocytes were treated with EPA, Lyc and Res or their combinations for 14 days. The effects on intracellular lipid droplet (LD) accumulation, secreted anti- and pro-inflammatory cyto-/adipokines (e.g. adiponectin, IL-6, IL-8/CXCL-8 and MCP-1/CCL2) and on gene expression of markers of adipocyte differentiation and substrate metabolism (e.g. PPAR-gamma, C/EBP-alpha, GLUT-4, FAS, ATGL, HSL, and PLIN-1) were measured by fluorescent microscopy (Cellomics™), multi-parametric LiquiChip® technology and quantitative RT-PCR, respectively. RESULTS: Treatment of differentiating adipocytes for 14 days with the combination of Lyc/Res and EPA/Res resulted in significantly inhibited LD formation (~ -25 and -20%, respectively) compared to the effects of the single compounds. These morphological changes were accompanied by increased mRNA levels of the adipogenic marker PPAR-gamma and the lipase ATGL and by decreased expression levels of lipogenic markers (LPL, FAS, GLUT-4) and the LD-covering protein PLIN-1. In addition, a blunted adipocyte secretion of pro-inflammatory cytokines (IL-6 and MCP-1) and adiponectin was observed following treatment with these compounds. CONCLUSION: The combination of the dietary bio-actives Lyc and EPA with Res might influence adipocyte function by affecting the balance between adipogenic, lipogenic and lipolytic gene expression, resulting in a reduced LD storage and a less inflammatory secretion profile. Taken together, our results indicate that combinations of dietary compounds may be beneficial for the prevention and treatment of metabolic disorders via effects on human white adipocyte function. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12986-016-0143-5) contains supplementary material, which is available to authorized users.
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spelling pubmed-51176262016-11-28 Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro Warnke, Ines Jocken, Johan W. E. Schoop, Rotraut Toepfer, Christine Goralczyk, Regina Schwager, Joseph Nutr Metab (Lond) Research BACKGROUND: Specific bio-active dietary compounds modulate numerous metabolic processes in adipose tissue (AT), including pre-adipocyte proliferation and differentiation. AT dysfunction, rather than an increased fat mass per se, is strongly associated with the development of insulin resistance and is characterized by impaired adipogenesis, hypertrophic adipocytes, inflammation, and impairments in substrate metabolism. A better understanding of mechanisms underlying AT dysfunction may provide new strategies for the treatment of obesity-associated metabolic diseases. Here we evaluated the role of (all-E)-lycopene (Lyc), eicosapentaenoic acid (EPA) or trans-resveratrol (Res) and combinations thereof on human white adipocyte function. METHODS: In-vitro differentiating human pre-adipocytes were treated with EPA, Lyc and Res or their combinations for 14 days. The effects on intracellular lipid droplet (LD) accumulation, secreted anti- and pro-inflammatory cyto-/adipokines (e.g. adiponectin, IL-6, IL-8/CXCL-8 and MCP-1/CCL2) and on gene expression of markers of adipocyte differentiation and substrate metabolism (e.g. PPAR-gamma, C/EBP-alpha, GLUT-4, FAS, ATGL, HSL, and PLIN-1) were measured by fluorescent microscopy (Cellomics™), multi-parametric LiquiChip® technology and quantitative RT-PCR, respectively. RESULTS: Treatment of differentiating adipocytes for 14 days with the combination of Lyc/Res and EPA/Res resulted in significantly inhibited LD formation (~ -25 and -20%, respectively) compared to the effects of the single compounds. These morphological changes were accompanied by increased mRNA levels of the adipogenic marker PPAR-gamma and the lipase ATGL and by decreased expression levels of lipogenic markers (LPL, FAS, GLUT-4) and the LD-covering protein PLIN-1. In addition, a blunted adipocyte secretion of pro-inflammatory cytokines (IL-6 and MCP-1) and adiponectin was observed following treatment with these compounds. CONCLUSION: The combination of the dietary bio-actives Lyc and EPA with Res might influence adipocyte function by affecting the balance between adipogenic, lipogenic and lipolytic gene expression, resulting in a reduced LD storage and a less inflammatory secretion profile. Taken together, our results indicate that combinations of dietary compounds may be beneficial for the prevention and treatment of metabolic disorders via effects on human white adipocyte function. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12986-016-0143-5) contains supplementary material, which is available to authorized users. BioMed Central 2016-11-21 /pmc/articles/PMC5117626/ /pubmed/27895698 http://dx.doi.org/10.1186/s12986-016-0143-5 Text en © The Author(s). 2016 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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Warnke, Ines
Jocken, Johan W. E.
Schoop, Rotraut
Toepfer, Christine
Goralczyk, Regina
Schwager, Joseph
Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro
title Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro
title_full Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro
title_fullStr Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro
title_full_unstemmed Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro
title_short Combinations of bio-active dietary constituents affect human white adipocyte function in-vitro
title_sort combinations of bio-active dietary constituents affect human white adipocyte function in-vitro
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5117626/
https://www.ncbi.nlm.nih.gov/pubmed/27895698
http://dx.doi.org/10.1186/s12986-016-0143-5
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