Acetyl-L-carnitine infusion increases glucose disposal in type 2 diabetic patients

Citation
A. Giancaterini et al., Acetyl-L-carnitine infusion increases glucose disposal in type 2 diabetic patients, METABOLISM, 49(6), 2000, pp. 704-708
Citations number
26
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
METABOLISM-CLINICAL AND EXPERIMENTAL
ISSN journal
00260495 → ACNP
Volume
49
Issue
6
Year of publication
2000
Pages
704 - 708
Database
ISI
SICI code
0026-0495(200006)49:6<704:AIIGDI>2.0.ZU;2-D
Abstract
Little information is available in the literature on the effect of L-carnit ine to improve glucose disposal in healthy control subjects and type 2 diab etic patients. No data are reported on the pharmacological properties of ac etyl-L-carnitine (ALC) in type 2 diabetes mellitus. The present study evalu ates glucose uptake and oxidation rates with either ALC or placebo administ ration in 18 type 2 diabetic patients. On different days, each patient rece ived both a primed-constant infusion of ALC (5 mg/kg body weight [BW] primi ng bolus and either 0.025, 0.1, or 1.0 mg/kg BW/min constant infusion) and a comparable placebo formulation. During the infusion period, continuous in direct calorimetric monitoring and a euglycemic-hyperinsulinemic clamp (EHC ) study were performed, The total end-clamp glucose tissue uptake (M value) was significantly increased by the administration of ALC (from 3.8 to 5.2 mg/kg/min, P = .006), and the dose dependence of this effect reached border line statistical significance (P = .037). The increase in the M/I ratio was also highly significant after ALC administration (from 3.9 to 5.8 x 10(-2) mg/kg/min/(mu UI/mL, P < .001), while no statistically significant effect was attributable to the different dosages. The increase in the M value was related to increased glucose storage (highly significant effect of ALC) rat her than increased glucose oxidation (no statistical significance). In conc lusion, the effect of ALC on glucose disposal has no relationship to the am ount administered. This could be due to an effect of ALC on the enzymes inv olved in both the glycolytic and gluconeogenetic pathways, and a possible r eversibility of glycogen synthase inhibition in diabetic subjects. Copyrigh t (C) 2000 by W.B. Saunders Company.