EFECTOS DE DIFERENTES FUENTES DE ÁCIDOS GRASOS N-3 (CHÍA, VEGETAL Y MARINA, ANIMAL) SOBRE COMPONENTES DEL SÍNDROME METABÓLICO EN MODELOS EXPERIMENTALES (RATAS/RATONES) / EFFECTS OF DIFFERENT SOURCES OF N-3 FATTY ACIDS (CHIA, VEGETAL AND MARINE, ANIMAL) ON METABOLIC SYNDROME COMPONENTS IN EXPERIMENTAL MODELS (RATS/MOUSES)

El síndrome metabólico (SM) constituye una constelación de factores interrelacionados que elevan el riesgo de padecer enfermedad cardiovascular y diabetes mellitus tipo 2. La composición de la dieta es crucial en la modificación de estos factores. Numerosos trabajos focalizaron su atención en fuentes de ácidos grasos n-3 de origen marino (animal) en el manejo de estos trastornos, pero más escasos y contemporáneos son aquellos de fuentes n-3 de origen vegetal.

Efectos de sustratos competitivos y de la insulina sobre la captación y el destino metabólico de la glucosa en corazón perfundido de ratas dislipémicas / Effects of competitive substrates ans insulin on glucose uptake and utilization in isolated perfused hearts of dyslipemic rats

Rats chronically fed (15 weeks) a sucrose-rich diet (SRD) developed hypertriglyceridemia (hyperTg), increased plasma free fatty acids (FFA), impaired glucose homeostasis and insulin insensitivity. An increase of Tg and glycogen (Gly) in heart muscle was also observed. HyperTg with altered glucose metabolism could have profound effects on myocardial glucose utilization. To test this hypothesis male Wistar rats were fed a semi-synthetic SRD (w/w: 62.5% sucrose, 8% corn-oil, 17% protein), and the control group (CD) received the same semi-synthetic diet, except that sucrose was replaced with starch for 90 days. At that time, the hearts from these animals were isolated and perfused for 30 min in the presence or absence of insulin (30 mU/ml). Levels of the exogenous substrates were similar to those found in the plasma of the animal in vivo in both dietary groups (glucose 8.5 mM, palmitate 0.8 mM in SRD and glucose 5-5 mM, palmitate 0.3 mM in CD). In the absence of insulin glucose uptake was reduced (40%) and lactate release was increased (50%) in SRD hearts. Glucose oxidation was depressed mainly due to both, an increase of PDH kinase and a decrease of 60% of PDHa (active form of PDHc). Insulin in the perfusion medium improved only glucose uptake. The results suggest that at least two different mechanisms might contribute to insulin resistance and to impaired glucose metabolism in the perfused hearts of dyslipemic SRD fed rats: 1) reduced basal and insulin-stimulated glucose uptake and its utilization and 2) increased availability and oxidation of lipids (low PDHa and PDH kinase activities), which in turn decreased glucose uptake and utilization. Thus, this experimental model may be useful to study how impaired glucose homeostasis, increased plasma FFA and hyperTg could contribute to heart tissue malfunction.