ORIGINAL ARTICLE High-fat meals induce systemic cytokine release without evidence of endotoxemia-mediated cytokine production from circulating monocytes or myeloid dendritic cells Christopher L. Fogarty • Janne K. Nieminen • Lina Pera ¨neva • Mariann I. Lassenius • Aila J. Ahola • Marja-Riitta Taskinen • Matti Jauhiainen • Juha Kirveskari • Pirkko Pussinen • Sohvi Ho ¨rkko ¨ • Ville-Petteri Ma ¨kinen • Daniel Gordin • Carol Forsblom • Per-Henrik Groop • Outi Vaarala • Markku Lehto Received: 10 March 2014 / Accepted: 14 August 2014 Ó Springer-Verlag Italia 2014 Abstract Aims Dietary fats have been shown to promote the translocation of bacterial endotoxins from the gut into circulation, which may induce systemic inflammation and modulate the inflammatory response of circulating immune cells. The aim of this study was to determine the effect of the postprandial milieu on inflammation and the inflam- matory response of antigen presenting cells in the context of type 1 diabetes (T1D). Materials and methods Eleven patients with T1D and eleven nondiabetic controls were recruited as part of the FinnDiane study and given two fatty meals during 1 day. Cytokine responses in monocytes and myeloid dendritic cells (mDCs) as well as serum lipopolysaccharide activity levels, triglyceride concentrations and cytokine concen- trations were measured from fasting and postprandial blood samples. Results Postprandially, patients with T1D and controls showed significant increases in eight inflammatory cyto- kines (IL-6, TNF-a, IL-1b, IFN-a, IL-10, IFN-c, IL-12 and MIP-1b) without concomitant increase in serum LPS activity. Serum cytokine production was similar in both groups. No postprandial change was seen in the IL-6, TNF- a or IL-1b production of mDCs or monocytes. At fasting, diabetic mDCs exhibited higher LPS-induced IL-6 and IL- 1b production than controls. Conclusions Acute high-fat meals increase circulating cytokines but have no effect on serum lipopolysaccharide activity levels or cytokine production in circulating mDCs Managed by Massimo Porta. On behalf of the FinnDiane Study Group. Electronic supplementary material The online version of this article (doi:10.1007/s00592-014-0641-8) contains supplementary material, which is available to authorized users. C. L. Fogarty Á L. Pera ¨neva Á M. I. Lassenius Á A. J. Ahola Á D. Gordin Á C. Forsblom Á P.-H. Groop Á M. Lehto (&) Folkha ¨lsan Research Center, Biomedicum Helsinki (Room C317b), Haartmaninkatu 8, 00290 Helsinki, Finland e-mail: markku.lehto@helsinki.fi C. L. Fogarty Á L. Pera ¨neva Á M. I. Lassenius Á A. J. Ahola Á D. Gordin Á C. Forsblom Á P.-H. Groop (&) Á M. Lehto Division of Nephrology, Department of Medicine, Helsinki University Central Hospital, Biomedicum Helsinki (Room C318b), Haartmaninkatu 8, 00290 Helsinki, Finland e-mail: per-henrik.groop@helsinki.fi C. L. Fogarty Á L. Pera ¨neva Á M. I. Lassenius Á A. J. Ahola Á M.-R. Taskinen Á D. Gordin Á C. Forsblom Á P.-H. Groop Á M. Lehto Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland J. K. Nieminen Á O. Vaarala Immune Response Unit, Department of Vaccination and Immune Protection, National Institute for Health and Welfare, Helsinki, Finland M.-R. Taskinen Heart and Lung Center, Cardiovascular Research Group, HUCH, Helsinki, Finland M. Jauhiainen Public Health Genomics Unit, National Institute for Health and Welfare, Biomedicum, Helsinki, Finland J. Kirveskari Department of Bacteriology, HUSLAB, Helsinki, Finland P. Pussinen Institute of Dentistry, University of Helsinki, Helsinki, Finland 123 Acta Diabetol DOI 10.1007/s00592-014-0641-8