Therefore, the response to ischemia/reperfusion encompassed several aspects of energy metabolism with signatures in both plasma and kidney tissue. Among this group of chemicals were clear distinctions between kidney cortex and kidney medulla. Glucose, free fatty acids, and amino acids serve as potential cellular energy sources under different conditions. Glucose metabolism is largely reflected by the activity of glycolysis/ gluconeogenesis and the TCA cycle while the free fatty acids contribute to energy metabolism via fatty acid beta-oxidation and the TCA cycle. Under relatively extreme fasting conditions, amino acids from the protein breakdown also can contribute to the TCA cycle. In this study, complex changes over time and Cefepime Dihydrochloride Monohydrate across matrices were observed for intermediates in these pathways. For glucose metabolism, the kidney cortex and the plasma samples showed early decreases in both glucose, and the metabolite of pyruvate, lactate, but recovery to near-sham levels by the 1 week reperfusion time. The intermediates in the TCA cycle, including succinate and malate showed a similar pattern in the plasma but not in the kidney cortex. This pattern of change suggests a transient decrease in the use of glucose for energy metabolism in the kidney cortex and perhaps with systemic effects such that a similar change also registered in the plasma. By contrast, kidney medulla showed a slower decrease over time from sham to 1 week reperfusion in glycolysis and TCA cycle activity. Together, these changes supported a delayed energy metabolism response but longer-term negative energy status in the kidney medulla following renal IRI. In all three matrices, the TCA cycle intermediate and fatty acid biosynthetic precursor, citrate, showed a unique pattern of generally Estradiol increasing levels from sham through the ischemia/ reperfusion time course. Notably, previous reports have suggested that elevated citrate levels in urine correlate with reperfusion injury. Accumulating citrate levels may be indicative of a block to TCA cycle progression and may contribute to the reduced glucose metabolism as well.