Abstract
PurposeKetone bodies, 3-hydroxybutyrate (3BOHB), and acetoacetate derive from increased free fatty acid beta-oxidation, thus reflecting marked insulin deprivation with or without decompensated diabetes. Objectives of this study were (1) to determine circulating levels of 3BOHB in patients with and without type 2 diabetes (T2DM), before and after an elective coronary angiography; (2) to detect 3BOHB modification during the procedure; (3) to study possible associations between 3BOHB and clinical parameters/outcomes.MethodsSixteen T2DM (72 ± 11 years) and 22 matched controls (71 ± 12 years) undergoing elective coronary angiography were enrolled. In all subjects, biohumoral parameters were determined at hospital admission. Point-of-care determinations of 3BOHB, glucose, and creatinine were performed, at 7 a.m, immediately before and after the procedure. The duration of the fasting period and of the procedure was recorded.ResultsT2DM had significantly higher fasting (0.538 ± 0.320 vs 0.255 ± 0.197 mM/l; p = 0.005) and pre-procedural (0.725 ± 0.429 vs 0.314 ± 0.205; p = 0.002) 3BOHB concentrations than controls. Similarly, absolute increment of 3BOHB from the morning value was significantly greater in T2DM (0.369 ± 0.252 vs 0.127 ± 0.135 in controls; p = 0.002). Significant correlations were observed between pre-procedure 3BOHB and glucose levels (r = 0.586; p < 0.0001) and between pre-procedure 3BOHB and fasting creatinine concentrations (r = 0.364; p = 0.029).ConclusionsAn overnight fasting period and a concomitantly stressful condition induce inappropriate 3BOHB increase in T2DM. Point-of-care capillary 3BOHB may be useful before any procedural/surgical intervention in these patients.
Highlights
Ketone bodies (KB), acetoacetate (AcAc) and 3-hydroxybutyrate (3BOHB), are metabolites produced by free fatty acid (FFA) beta-oxidation, and utilized by peripheral cells as an energy source [1, 2]
There has been a resurgent interest about these substrates, since ketoacidosis may be a rare complication of sodium-glucose co-transporter 2 (SGLT2) inhibitors [5]; it was shown that 3BOHB is an endogenous inhibitor of histone deacetylases (HDACs) and its metabolites, acetyl-CoA and succinyl-CoA, have themselves signalling activities [6]
The same authors suggested that severe chronic heart failure (CHF) is a ketosis-prone state determined by augmented supply of FFA, induced by increased stress hormone-related lipolysis [8]: after 20 h of fasting, the reported total KB
Summary
Ketone bodies (KB), acetoacetate (AcAc) and 3-hydroxybutyrate (3BOHB), are metabolites produced by free fatty acid (FFA) beta-oxidation, and utilized by peripheral cells as an energy source [1, 2]. Blood KB concentrations in healthy individuals are low, they can increase 100 folds during diabetic ketoacidosis [4]. There has been a resurgent interest about these substrates, since ketoacidosis may be a rare complication of sodium-glucose co-transporter 2 (SGLT2) inhibitors [5]; it was shown that 3BOHB is an endogenous inhibitor of histone deacetylases (HDACs) and its metabolites, acetyl-CoA and succinyl-CoA, have themselves signalling activities [6]. Several years ago Lommi and colleagues reported increased concentration of KB in chronic heart failure (CHF), in proportion to the severity of cardiac dysfunction and neurohormonal activation [7]. The same authors suggested that severe CHF is a ketosis-prone state determined by augmented supply of FFA, induced by increased stress hormone-related lipolysis [8]: after 20 h of fasting, the reported total KB
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