Quercetin exhibits a wide range of
biological functions. The first aim of the present work was to analyze the effects of
quercetin on fat accumulation in adipose tissue and
glycemic control in rats. Any potential involvement of muscle
fatty acid oxidation in its effect on
glycemic control was also assessed. Animals were fed a high-fat high-
sucrose diet either supplemented with
quercetin (30 mg/kg
body weight/day), or not supplemented, for 6 weeks. One week before killing, a
glucose tolerance test was carried out. Muscle
triacylglycerol content, serum
glucose,
insulin,
fructosamine and
free fatty acids were measured, and homeostatic model assessment for
insulin resistance (HOMA-IR) was calculated. The activities of lipogenic
enzymes and
lipoprotein lipase in adipose tissue,
carnitine palmitoyl transferase-1b (CPT-1b) and
citrate synthase in skeletal muscle, and the expression of several genes, ACO, CD36, CPT-1b,
PPAR-α, PGC-1α, UCP3, TFAM and COX-2 in skeletal muscle were analyzed.
Quercetin caused no significant reduction in
body weight or adipose tissue sizes. However,
fructosamine, basal
glucose and
insulin, and consequently HOMA-IR, were significantly reduced by
quercetin. No changes were observed in the activity of lipogenic
enzymes and
lipoprotein lipase. Muscle
triacylglycerol content was similar in both experimental groups. The expression of ACO, CD36, CPT-1b,
PPAR-α, PGC-1α, UCP3, TFAM and COX-2 remained unchanged. It can be concluded that
quercetin is more effective as an anti-diabetic than as an anti-
obesity biomolecule. The improvement in
insulin resistance induced by this
flavonoid is not mediated by a delipidating effect in skeletal muscle.