Raw and processed metabolomics data from mouse tissues and patient fibroblasts with PARK7 (DJ-1) loss-of-function
Description
Parkinson’s disease (PD) is recognized as a systemic condition, with clinical features potentially modifiable by dietary intervention. Diets high in saturated fats and refined sugars significantly increase PD risk and exacerbate motor and non-motor symptoms, yet precise metabolic mechanisms are unclear. To investigate the interplay between diet and PD, we used a model of early-onset PD under chronic glycative stress induced by prolonged high-fat high-sucrose (HFHS) diet. We found this obesogenic diet drives loss of fat and muscle mass in early-onset PD mice, with a selective vulnerability of glycolytic myofibers. We show that PD mice and early-onset familial PD patients are under pervasive glycative stress with pathological accumulation of advanced glycation end products (AGEs), including two previously unknown glycerinyl-AGE markers. This dataset includes raw and processed metabolomics data from skeletal muscles (gastrocnemius and soleus) and plasma from adult male wildtype mice and littermates with global PARK7 (DJ-1) knockout fed a standard chow or a glycative stress-inducing high-fat high-sucrose diet (HFHS). Metabolites were profiled with reversed-phase ultrahigh-performance liquid chromatography (RP-UHPLC)-tandem mass spectrometry and hydrophilic interaction liquid chromatography (HILIC)-tandem mass spectrometry. Fibroblasts from healthy controls and patients with PARK7-related early-onset familial Parkinson's disease were measured with liquid chromatography-tandem mass spectrometry (LC-MS/MS). Data are from the paper "Pervasive glycative stress links metabolic imbalance and muscle atrophy in early-onset Parkinson’s disease" by de Mello, Berger, et al. (2025).
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