MP12-01 INCREASED URINARY EXCRETION OF GLYCOLATE AND OXALATE IN OBESE AND DIABETIC MICE MODELS

You have accessJournal of UrologyStone Disease: Basic Research & Pathophysiology I1 Apr 2017MP12-01 INCREASED URINARY EXCRETION OF GLYCOLATE AND OXALATE IN OBESE AND DIABETIC MICE MODELS Kyle Wood, John Knight, Dean Assimos, and Ross Holmes Kyle WoodKyle Wood More articles by this author , John KnightJohn Knight More articles by this author , Dean AssimosDean Assimos More articles by this author , and Ross HolmesRoss Holmes More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2017.02.423AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Obesity and diabetes have both been shown to be risk factors for nephrolithiasis. Both diseases are associated with increased urinary excretion of oxalate (Uox). Our objective was to study endogenous production of oxalate in diabetic and obese mouse models on controlled diets. METHODS Three male mouse models of obesity and diabetes (KKAy n=3, Akita n=8, ob/ob n=3) were placed on controlled ultra-low oxalate diets and compared to matched control mice. 24 hour urines were collected and analyzed. Total body fat and lean body mass were also measured in the ob/ob and control mice with DEXA scans. Statistical analysis was performed using t-test. RESULTS KKAy, Akita, and ob/ob weighed 198%, 58%, 56% more compared to control mice, respectively. On an ultra-low oxalate diet, when compared to control, KKay, Akita, and ob/ob mice had increased 24 hour urinary oxalate (µg/mg Cr, 164%, 223%, 241% respectively, more than control mice, p<0.05). 24 hour urinary glycolate (Ugl, µg/mg Cr) levels were 234%, 174% higher in the Akita, and ob/ob mice, respectively, compared to control mice (p<0.001). The KKAy mice had the same Ugl as control mice. The ob/ob mice had decreased lean body mass compared to controls (20.1 g vs 22.6 g, p=0.04),but had increased body fat (27.7 g vs 3.6 g, p=0.0001). For ob/ob mice and control mice, increasing urinary oxalate correlated with increasing urinary glycolate (r=0.82, p=0.05). CONCLUSIONS These findings suggest that obesity may increase endogenous oxalate synthesis via pathways linked to glycolate production. Further studies are needed to determine if this is occurring in the fat compartment or whether signaling from this area upregulates endogenous oxalate synthesis. This model system may be an ideal method of assessing such responses. © 2017FiguresReferencesRelatedDetails Volume 197Issue 4SApril 2017Page: e145 Advertisement Copyright & Permissions© 2017MetricsAuthor Information Kyle Wood More articles by this author John Knight More articles by this author Dean Assimos More articles by this author Ross Holmes More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...