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Urine Glucose Excretion Attenuates the Association Between Lipid Accumulation Product and Serum Uric Acid in Subjects with Prediabetes.

ABSTRACT: PurposeObesity is known to be strongly associated with hyperuricemia. Moreover, the impact of urine glucose excretion (UGE) on serum uric acid (UA) levels has gained much more attention in recent years. Yet concern is raised about whether UGE influences the relationship between obesity and hyperuricemia. The aim of this study was to assess the effect of UGE on the association between lipid accumulation product (LAP), a novel marker of visceral adipose accumulation, and UA in subjects with prediabetes.Materials and MethodsData were obtained from a cross-sectional study. A total of 3645 subjects with prediabetes were included in the present study. The separate and joint associations of LAP and UGE with hyperuricemia were examined using logistic regression analyses.ResultsLAP was positively associated with UA in both genders. Subgroup analysis based on UGE revealed that the association was strongest in subjects with low UGE (r = 0.328, p < 0.001), whereas the positive association was weakened, but still remained significant in subjects with moderate and high UGE. High LAP was significantly associated with an increased odds ratio for hyperuricemia after adjustment for potential confounders in the overall population (OR = 2.07, 95% CI: 1.66–2.58, p < 0.001). However, a downward trend in odds ratios for hyperuricemia was observed across UGE categories. In addition, the joint association analysis confirmed that the relationship between LAP and hyperuricemia was attenuated by UGE.ConclusionThe positive association between LAP and UA appears to be attenuated by UGE, indicating that promoting UGE may be an effective strategy for controlling UA levels, especially for people with obesity who are at increased risk for hyperuricemia.

SUBMITTER: Chen J

PROVIDER: S-EPMC7335310 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Project description:Background:The role of the kidney in glucose homeostasis has gained global interest. Kidneys are innervated by renal nerves, and renal denervation animal models have shown improved glucose regulation. We hypothesized that stimulation of renal nerves at kilohertz frequencies, which can block propagation of action potentials, would increase urine glucose excretion. Conversely, we hypothesized that low frequency stimulation, which has been shown to increase renal nerve activity, would decrease urine glucose excretion. Methods:We performed non-survival experiments on male rats under thiobutabarbital anesthesia. A cuff electrode was placed around the left renal artery, encircling the renal nerves. Ureters were cannulated bilaterally to obtain urine samples from each kidney independently for comparison. Renal nerves were stimulated at kilohertz frequencies (1-50 kHz) or low frequencies (2-5 Hz), with intravenous administration of a glucose bolus shortly into the 25-40-min stimulation period. Urine samples were collected at 5-10-min intervals, and colorimetric assays were used to quantify glucose excretion and concentration between stimulated and non-stimulated kidneys. A Kruskal-Wallis test was performed across all stimulation frequencies (??=?0.05), followed by a post-hoc Wilcoxon rank sum test with Bonferroni correction (??=?0.005). Results:For kilohertz frequency trials, the stimulated kidney yielded a higher average total urine glucose excretion at 33 kHz (+?24.5%; n?=?9) than 1 kHz (-?5.9%; n?=?6) and 50 kHz (+?2.3%; n?=?14). In low frequency stimulation trials, 5 Hz stimulation led to a lower average total urine glucose excretion (-?40.4%; n?=?6) than 2 Hz (-?27.2%; n?=?5). The average total urine glucose excretion between 33 kHz and 5 Hz was statistically significant (p?<?0.005). Similar outcomes were observed for urine flow rate, which may suggest an associated response. No trends or statistical significance were observed for urine glucose concentrations. Conclusion:To our knowledge, this is the first study to investigate electrical stimulation of renal nerves to modulate urine glucose excretion. Our experimental results show that stimulation of renal nerves may modulate urine glucose excretion, however, this response may be associated with urine flow rate. Future work is needed to examine the underlying mechanisms and identify approaches for enhancing regulation of glucose excretion.

Project description:BackgroundBreast cancer resistance protein (BCRP) and multidrug resistance protein 4 (MRP4) are involved in uric acid excretion in humans and mice. Despite evidence suggesting that renal proximal tubular epithelial cells participate in uric acid excretion in chickens, the roles of BCRP and MRP4 therein remain unclear. This study evaluated the relationship between BCRP and MRP4 expression and renal function in chickens.ResultsSixty laying hens were randomly divided into four treatment groups: a control group (NC) fed a basal diet; a sulfonamide-treated group (SD) fed the basal diet and supplemented with sulfamonomethoxine sodium via drinking water (8 mg/L); a fish meal group (FM) fed the basal diet supplemented with 16% fishmeal; and a uric acid injection group (IU) fed the basal diet and intraperitoneally injected with uric acid (250 mg/kg body weight). The results showed that serum uric acid, creatinine, and blood urea nitrogen levels were significantly higher in the SD and IU, but not FM, than in the NC groups. Renal tubular epithelial cells in the SD and IU groups were damaged. Liver BCRP and MRP4 mRNA and protein levels were significantly decreased in the SD and IU groups, but slightly increased in the FM group. In the SD group, BCRP and MRP4 were significantly increased in the ileum and slightly increased in the kidney. In the FM group, BCRP and MRP4 were significantly increased in the kidney and slightly increased in the ileum. In the IU group, BCRP and MRP4 were significantly increased in the kidney and ileum. BCRP and MRP4 expression in the jejunum was not affected by the treatments.ConclusionTogether, these results demonstrate that BCRP and MRP4 are involved in renal and intestinal uric acid excretion in chickens and that BCRP is positively related to MRP4 expression. Further, impairment of renal function results in an increase in serum uric acid as well as a compensatory increase in BCRP and MRP4 in the ileum; however, under normal renal function, renal BCRP and MRP4 are the main regulators of uric acid excretion.

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Urine Glucose Excretion Attenuates the Association Between Lipid Accumulation Product and Serum Uric Acid in Subjects with Prediabetes.

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