Systemic pH modifies ketone body production rates and lipolysis in humans.

Abstract

To investigate whether changes in systemic pH influence ketone body production or utilization, total ketone body (TK) kinetics were measured with [3-14C]acetoacetate and D-beta-[1,3-13C2]hydroxybutyrate tracers in overnight fasted subjects during metabolic alkalosis (NaHCO3 infusion) or acidosis [NH4Cl ingestion or arginine (Arg)-HCl infusion]. Somatostatin, with insulin, glucagon, and growth hormone replacement, was infused in all studies. Blood pH and HCO3- (mM) increased from baseline (0-30 min) to 180-210 min by 0.08 +/- 0.02 and 7 +/- 1 with NaHCO3 and decreased by 0.08 +/- 0.2 and 7 +/- 1 or 5 +/- 1 with NH4Cl or Arg-HCl (all P less than 0.005). Over this period blood TK (microM) differed between the NaHCO3 (+198 +/- 65) and both NH4Cl (-90 +/- 53) and Arg-HCl (-154 +/- 55) (P less than 0.05). These changes resulted from parallel alterations in TK production rate of appearance (Ra TK, mumol.kg-1.min-1), because changes from baseline in Ra 14C TK also differed between NaHCO3 (+1.9 +/- 0.8) and NH4Cl (-1.0 +/- 0.6) and Arg-HCl (-2.0 +/- 0.5) (P less than 0.05). Ra TK calculated with single- or dual-tracer techniques were similar. Blood free fatty acids (FFA) increased with NaHCO3, and FFA and glycerol decreased with NH4Cl and Arg-HCl, suggesting that FFA availability mediated the pH effects on hepatic ketogenesis. These results demonstrate that modest changes in systemic pH modify FFA availability and TK production rates.

Single pyruvate intake induces blood alkalization and modification of resting metabolism in humans

“…The rate of lipolysis is controlled by several factors [11,12]; one of the most well-known factors is pH [13]. It has been demonstrated that plasma FFA concentration decreases during acidosis, whereas alkalosis results in an increase in plasma FFA [14,15]. Recently, the buffering properties of NaP have been widely reviewed [16].…”

Effects of Glucagon-Like Peptide 1 (7–36 Amide) on Glucose Kinetics during Somatostatin-Induced Suppression of Insulin Secretion in Healthy Men

“…To overcome GLP-1-induced hormonal changes, somatostatin was infused during all studies, while insulin, glucagon and growth hormone were replaced in basal amounts (pancreatic clamp) [9]. Glucose clamping was performed at 8 mmol/l taking into account the glucose dependence of GLP-1 effects and imitating mild hyperglycemia during restricted insulin availability.…”

Effects of glucagon‐like peptide 1 (7–36 amide) on whole‐body protein metabolism in healthy man

“…[1-13 C]-Leucine infusions were used to measure leucine flux and oxidation as parameters of whole-body protein breakdown and catabolism [15], and indirect calorimetry yielded energy expenditure data. In order to differentiate between insulin-mediated and direct GLP-1 effects, similar experiments were performed during somatostatin infusion blocking pancreatic hormone secretion (pancreatic clamp) [16]. Considering the glucose dependence of the GLP-1 effects, all the experiments were performed during hyperglycaemic glucose clamping.…”