Diet, Diabetes, and Spine Health

The Diet and Diabetes Program focuses on understanding how diabetes and other systemic diseases involving chronic inflammatory conditions can accelerates painful spinal conditions. We also investigate how improved diet and other safe interventions that can improve spine health and reduce back pain.

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Spotlight Features

SEX-DEPENDENT EFFECTS OF DIETARY AGES ON VERTEBRAL BONE

The recently published manuscript in the Journal of Bone and Mineral Research demonstrated that a poor diet, high in advanced glycation end products can, independent of diabetic or overweight conditions, diminish vertebral microstructure, mechanical behaviors and fracture resistance in young female mice. This work suggests poor diet as a potential cause of accelerated spinal aging, especially in females.

Dietary Advanced Glycation End Products have Sex- and Age Dependent Effects on Vertebral Bone Microstructure and Mechanical Function in Mice. Illien-Jünger S, Palacio-Mancheno P, Kindschuh WF, Chen X, Sroga GE, Vashishth D, Iatridis JC. J Bone Miner Res. 2017 Nov 21. doi: 10.1002/jbmr.3321. [Epub ahead of print] PMID: 29160901

AGES  INDUCE ECTOPIC CALCIFICATIONS IN INTERVERTEBRAL DISCS

The published manuscript in the European Cells and Materials Journal demonstrated that advanced glycation end product accumulation is associated with endochondral ossification in IVDs and likely acts via the AGE/RAGE axis to induce hypertrophy and osteogenic differentiation in IVD cells.  This work suggests another mechanism for accelerated IVD degeneration including the initiation of structural defects.

AGEs induce ectopic endochondral ossification in intervertebral discs. Illien-Jünger S, Torre OM, Kindschuh WF, Chen X, Laudier DM, Iatridis JC. Eur Cell Mater. 2016 Nov 18;32:257-270. PMID: 27858401

CHRONIC AGE INJESTION INDUCED DISC DEGENERATION

The published manuscript in PLOS ONE Journal demonstrated that chronic exposure to dietary AGEs promoted age-accelerated IVD degeneration and vertebral alterations involving ectopic calcification, which occurred in parallel with insulin resistance; these changes were prevented by reducing the intake of dietary AGE. This work suggests an important role for chronic AGE ingestion in alterations to spinal tissues known to occur with chronic diabetic conditions.

Chronic ingestion of advanced glycation end products induces degenerative spinal changes and hypertrophy in aging pre-diabetic mice. Illien-Jünger S, Lu Y, Qureshi SA, Hecht AC, Cai W, Vlassara H, Striker GE, Iatridis JC. PLoS One. 2015 Feb 10;10(2):e0116625. doi: 10.1371/journal.pone.0116625. eCollection 2015. PMID: 25668621

Collaborator: Illien-Junger Laboratory

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