

HV: National Institute of Health/National Institute of Diabetes and Digestive and Kidney Diseases (NIH/NIDDK RO1 AG023188).
#Dmg spine center skin#
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedĭata Availability: All relevant data are within the paper.įunding: Funding provided by JCI: National Institute of Health/National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIH/NIAMS R01AR051146). Received: ApAccepted: DecemPublished: February 10, 2015Ĭopyright: © 2015 Illien-Jünger et al. (2015) Chronic Ingestion of Advanced Glycation End Products Induces Degenerative Spinal Changes and Hypertrophy in Aging Pre-Diabetic Mice. This study described a new mouse model for diet-induced spinal degeneration, and results were in support of the hypothesis that chronic AGE ingestion could be a factor contributing to a pre-diabetic state, ectopic calcifications in spinal tissues, and musculoskeletal complications that are more generally known to occur with chronic diabetic conditions.Ĭitation: Illien-Jünger S, Lu Y, Qureshi SA, Hecht AC, Cai W, Vlassara H, et al.

Overall, chronic exposure to dietary AGEs promoted age-accelerated IVD degeneration and vertebral alterations involving ectopic calcification which occurred in parallel with insulin resistance, and which were prevented with dMG- diet. IVD morphology of dMG+ mice exhibited ectopic calcification, hypertrophic differentiation and glycosaminoglycan loss relative to dMG- mice. Vertebrae of dMG+ mice displayed increased cortical-thickness and cortical-area, greater MG-AGE accumulation and ectopic calcification in vertebral endplates. dMG+ mice exhibited a pre-diabetic phenotype, as they were insulin resistant but not hyperglycemic. methylglyoxal-derivatives (MG)) on IVD and vertebral pathologies in aging C57BL6 mice that were fed isocaloric diets with standard (dMG+) or reduced amounts of MG derivatives (dMG- containing 60-70% less dMG). This study investigated the role of specific AGE precursors (e.g. There is little information about potential effects of AGE rich diet on spinal pathology, which may be a contributing cause for back pain which is common in obese and diabetic individuals. Modern diets contain high levels of advanced glycation end products (AGEs), cyto-toxic components which are known contributors to obesity, diabetes and accelerated aging pathologies. Obese and diabetic individuals are at increased risk for back pain and musculoskeletal complications. Intervertebral disc (IVD) degeneration and pathological spinal changes are major causes of back pain, which is the top cause of global disability.
