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1k), suggesting that CAR T cells from LTR preferentially shunt HK glycolytic metabolites to the pentose phosphate pathway (PPP) rather than glycolysis, and by CPT1A could convert long-chain fatty acids into acylcarnitines for shuttling into the mitochondrial matrix for subsequent oxidation, previously associated with increased basal and maximal mitochondrial respiration 5,6,7,8

Background and aims: The complex metabolic network mediating the coupling of glucose to insulin release in pancreatic beta cells, is still not fully understood

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Availability of data and materials The data that support the findings are available from the Exercise and Biochemical Nutritional Laboratory (EBNL) in the Department of Human Performance of Baylor University and the grant sponsor, being the Function Research Group of Kyowa Hakko Bio Co., Ltd