Obesity-induced chronic inflammation in high fat diet challenged C57BL/6J mice is associated with acceleration of age-dependent renal amyloidosis

• DOI: 10.1038/srep16474
• Publication Date: 2015-11-13T10:23:13Z
• Authors: Roel A. van der H...; Johan Bijzet; Wouter C. Meijers; Gopala K. Yakala; Robert Kleemann; Tri Q. Nguyen; Rudolf A. de Boer; Casper G. Schalkwijk; Bouke P. C. Hazen...; Uwe J. F. Tietge; Peter Heeringa
• Keywords: Amyloid (mycology); AA amyloidosis

Obesity-induced inflammation presumably accelerates the development of chronic kidney diseases. However, little is known about sequence these inflammatory events and their contribution to renal pathology. We investigated effects obesity on evolution age-dependent complications in mice conjunction with systemic low-grade (LGI). C57BL/6J susceptible develop sclerotic pathologies amyloid features kidney, were fed low (10% lard) or high-fat diets (45% for 24, 40 52 weeks. HFD-feeding induced overt adiposity, altered lipid insulin homeostasis, increased LGI adipokine release. also caused upregulation pro-inflammatory genes, infiltrating macrophages, collagen I protein, urinary albumin NGAL levels. severely aggravated structural changes kidney. Remarkably, enhanced deposition rather than sclerosis was observed. The degree amyloidosis correlated significantly body weight. Amyloid deposits stained positive serum A (SAA) whose plasma levels chronically elevated HFD mice. Our data indicate obesity-induced as a risk factor acceleration functional impairment mice, suggest that obesity-enhanced secretion SAA may be driving behind this process.