Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats

1 Departamento de Bioquímica, 2 Anatomopatología, y 3 Endocrinología, Instituto Nacional de Cardiología "Ignacio Chávez"; and 4 Unidad de Investigación, Instituto Nacional de Enfermedades Respiratorias, Secretaría de Salud, Mexico City 14080, Mexico Submitted 11 March 2004 ; accepted in final form 11 August 2004 The study investigated the mechanism by which glycine protects against increased circulating nonesterified fatty acids (NEFA), fat cell size, intra-abdominal fat accumulation, and blood pressure (BP) induced in male Wistar rats by sucrose ingestion. The addition of 1% glycine to the drinking water containing 30% sucrose, for 4 wk, markedly reduced high BP in sucrose-fed rats (SFR) (122.3 ± 5.6 vs. 147.6 ± 5.4 mmHg in SFR without glycine, P < 0.001). Decreases in plasma triglyceride (TG) levels (0.9 ± 0.3 vs. 1.4 ± 0.3 mM, P < 0.001), intra-abdominal fat (6.8 ± 2.16 vs. 14.8 ± 4.0 g, P < 0.01), and adipose cell size were observed in SFR treated with glycine compared with SFR without treatment. Total NEFA concentration in the plasma of SFR was significantly decreased by glycine intake (0.64 ± 0.08 vs. 1.11 ± 0.09 mM in SFR without glycine, P < 0.001). In control animals, glycine decreased glucose, TGs, and total NEFA but without reaching significance. In SFR treated with glycine, mitochondrial respiration, as an indicator of the rate of fat oxidation, showed an increase in the state IV oxidation rate of the -oxidation substrates octanoic acid and palmitoyl carnitine. This suggests an enhancement of hepatic fatty acid metabolism, i.e., in their transport, activation, or -oxidation. These findings imply that the protection by glycine against elevated BP might be attributed to its effect in increasing fatty acid oxidation, reducing intra-abdominal fat accumulation and circulating NEFA, which have been proposed as links between obesity and hypertension. obesity; mitochondrial oxygen uptake; fatty acid oxidation Address for reprint requests and other correspondence: M. El Hafidi, Departamento de Bioquímica, Instituto Nacional de Cardiología "Ignacio Chávez," Juan Badiano 1, Mexico City 14080, Mexico (E-mail: elhafidi{at}mail.ssa.gob.mx )