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Sources of Funding: AUA Research Scholar

Introduction

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.

Funding

AUA Research Scholar