The very first article of Froukje Vanweert as first author has been published titled “Elevated plasma branched-chain amino acid levels correlate with type 2 diabetes-related metabolic disturbances”. The full article can be found online: https://doi.org/10.1210/clinem/dgaa751
Read the abstract below:
CONTEXT: Patients with type 2 diabetes (T2DM) have elevated plasma branched-chain amino acid levels (BCAA). The underlying cause is however not known. Low mitochondrial oxidation of BCAA could contribute to higher plasma BCAA levels.
OBJECTIVE: We aimed to investigate ex vivo muscle mitochondrial oxidative capacity and in vivo BCAA oxidation measured by whole-body leucine oxidation rates in patients with T2DM, first-degree relatives (FDR) and control participants (CON) with overweight or obesity.
DESIGN AND SETTING: An observational, community-based study was conducted.
PARTICIPANTS: Fifteen patients with T2DM, thirteen FDR and seventeen CON were included (age between 40-70 years and BMI ranging from 27-35 kg/m 2).
MAIN OUTCOME MEASURES: High-resolution respirometry was used to examine ex vivo mitochondrial oxidative capacity in permeabilized muscle fibers. A subgroup of five T2DM and five CON underwent hyperinsulinemic-euglycemic clamps combined with 1- 13C leucine-infusion to determine whole-body leucine oxidation.
RESULTS: Total BCAA levels were higher in patients with T2DM compared to CON, but not in FDR, and correlated negatively with muscle mitochondrial oxidative capacity (r = -0.44, p<0.001). Consistently, whole-body leucine oxidation rate was lower in patients with T2DM vs. CON under basal conditions (0.202 ± 0.049 vs. 0.275 ± 0.043 μmol kg -1 min -1, p<0.05) and tended to be lower during high insulin infusion (0.326 ± 0.024 vs. 0.382 ± 0.013 μmol kg -1 min -1, p=0.075).
CONCLUSIONS: In patients with T2DM, a compromised whole-body leucine oxidation rate supports our hypothesis that higher plasma BCAA levels may at least originate partly from a low mitochondrial oxidative capacity.