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Ullrich, S. ; Gerst, F. ; Wagner, R. ; Panse, M.* ; Siegel-Axel, D. ; Machann, J. ; Stefan, N. ; Sipos, B.* ; Fend, F.* ; Nadalin, S.* ; Königsrainer, A.* ; Häring, H.-U.

Islet architecture and inflammation in human fatty pancreas.

Vortrag: ADA Kongress USA, 09-14 June 2016, New Orleans, USA. (2016)
Tissue inflammation and visceral fat deposits precede and accelerate the development of T2DM in humans. However, relative insulin deficiency is the ultimate cause for disease outbreak. Multiple observations suggest that adiposis exacerbates tissue inflammation, compromising insulin sensitivity and cellular functions. Whether pancreatic steatosis is deleterious for insulin secretion is still under discussion. This study attempts to quantify de degree of steatosis in human pancreatic tissue and its impact on islet architecture. Pancreatic resections from 58 patients were analysed using immunohistological and biometric methods. In addition, the expression pattern within the islets isolated by laser capture microscopy was estimated using RNA-Affymetrix. In 70% of the subjects,  differentiated adipocytes were identified by oil red staining of large lipid-containing vacuoles and by adiponectin staining of cytosolic vesicles. Most adipocytes infiltrate the exocrine parenchyma, only few locate within islets. In spite of adipocytes infiltration, the main fraction of the islets stain positive for insulin. Glucagon positive cells are found in the periphery and pervade the islets. Somatostatin positive cells are much less abundant and scattered throughout the islets. A capillary network is spread throughout the tissue, in the islets and in close contact to adipocytes. The quantification of the CD68-positive immune cells indicated an increased infiltration into islets neighbouring adipocytes. The expression analysis in islets of 17 patients with HbA1c between 4.6 to 9.4 reveals measurable levels of the immune cell chemo-attractants MCP-1 and CXCL12, while the mRNA levels of the pro-inflammatory cytokines IL-1beta and IFNgamma do not exceed background values. Of note, we found no correlation between expression levels of cytokines and HbA1c. In conclusion, the analysis of 17 tissue samples suggests that pancreatic steatosis may accentuate islet immune cell infiltration without triggering inflammation and alterations of islet architecture.
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Publikationstyp Sonstiges: Vortrag
Konferenztitel ADA Kongress USA
Konferzenzdatum 09-14 June 2016
Konferenzort New Orleans, USA
Institut(e) Institute for Diabetes Research and Metabolic Diseases (IDM)