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Kidney Week

Abstract: SA-PO071

Leveraging Metabolomics to Detect Global Alterations in the Renal Cortices of Formoterol Treated Mice

Session Information

  • AKI: Mechanisms - III
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Thompson, Austin D., The University of Arizona, Tucson, Arizona, United States
  • Schnellmann, Rick G., The University of Arizona, Tucson, Arizona, United States

Acute kidney injury (AKI) is defined as a sudden and rapid decline in renal function and is often accompanied by a persistent reduction in mitochondrial function and vascular/tubular injury/necrosis. AKI is a public health concern with no FDA-approved treatments. Stimulation of mitochondrial biogenesis (MB) via the b2-adrenergic receptor agonist formoterol (FORM) has been demonstrated in murine studies to accelerate renal recovery, promote MB, and restore mitochondrial homeostasis post-AKI. Albeit, the renal metabolic alterations induced by FORM, remain unknown. Thus, we used global metabolomics to assess metabolic changes in the mouse renal cortex treated with FORM.


Male 8-week-old C57B/6J mice were administered 0.3mg/kg of FORM or normal saline every 24h over a 60h period (n=6/group). Kidneys were harvested and snap frozen in liquid nitrogen. Renal cortex samples were analyzed by Metabolon via multi-mass spectrometry analysis. After mass normalization, log-transformation, and imputation, Welch’s two-sample t-test was used to identify metabolites that differed significantly between treatment groups. A p-value of p≤0.05 and a false discovery rate of q<0.10 were used to identify global metabolite changes and correct for multiple comparisons.


Total, 914 biochemicals (BC) were detected in the global metabolomic dataset. Of these BCs, we identified 165 BCs statistically different in FORM-treated mice compared to saline controls, 89 BCs increased, and 76 BCs decreased. FORM-treated mice had elevated 3-hydroxybutyrate and reduced free fatty acids, endocannabinoid, and lysoplasmalogen, which is indicative of increased mitochondrial b-oxidation and reduced inflammation. A decrease in glycolysis was identified by reduced lactate and elevated dihydroxyacetone phosphate (DHAP). This was accompanied by elevated amino acid metabolism, in accord with Mechanistic Target of Rapamycin Kinase Complex 1 (MTORC1) activation by DHAP. Lastly, we observed an increase in antioxidant pathways via elevated gamma-glutamyl amino acids and nicotinate/nicotinamide.


These data reveal that global metabolomics can identify 165 metabolic alterations in the renal cortices of FORM-treated mice. This approach will allow us to identify and monitor metabolic changes during AKI and other kidney diseases, and the effects of drugs stimulating repair/recovery.


  • Veterans Affairs Support