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We examined here whether high fat diet administered in young mice, compromised the attainment of articular cartilage thickness. Further, we sought to determine if low\u2010intensity vibration (LIV) could protect the retention of articular cartilage in a mouse model of diet\u2010induced obesity. Five\u2010week\u2010old, male, C57BL\/6 mice were separated into three groups (<jats:italic>n<\/jats:italic>\u2009=\u200910): Regular diet (RD), High fat diet (HF), and HF\u2009+\u2009LIV (HFv; 90\u2009Hz, 0.2g, 30\u2009min\/d, 5\u2009d\/w) administered for 6 weeks. Additionally, an extended HF diet study was run for 6 months (LIV at 15\u2009m\/d). Articular cartilage and subchondral bone morphology, and sulfated GAG content were quantified using contrast agent enhanced \u03bcCT and histology. Gene expression within femoral condyles was quantified using real\u2010time polymerase chain reaction. Contrary to our hypothesis, HF cartilage thickness was not statistically different from RD. However, LIV increased cartilage thickness compared to HF, and the elevated thickness was maintained when diet and LIV were extended into adulthood. RT\u2010PCR analysis showed a reduction of aggrecan expression with high fat diet, while application of LIV reduced the expression of degradative MMP\u201013. Further, long\u2010term HF diet resulted in subchondral bone thickening, compared to RD, providing early evidence of OA pathology\u2014LIV suppressed the thickening, such that levels were not significantly different from RD. These data suggest that dynamic loading, via LIV, protected the retention of cartilage thickness, potentially resulting in joint surfaces better suited to endure the risks of elevated loading that parallel obesity. \u00a9 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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