Oral L-glutamine restores adenosine and glutathione content in the skeletal muscle and adipose tissue of insulin-resistant pregnant rats.

Abstract

Mishandling of lipid and glycogen has been documented as a feature of metabolic tissues in insulin resistance-related disorders. However, reports exist detailing that L-glutamine (GLN) protects non-adipose tissue against the deleterious effects of metabolic disorders. Therefore, we hypothesized that GLN would protect skeletal muscle and adipose tissue against the deleterious effects of lipid and glycogen mishandlings by increasing adenosine and glutathione levels in pregnant rats exposed to fructose (FRU)-enriched drinks. Pregnant Wistar rats weighing 150 to 180 g were randomly assigned to control, GLN, FRU, and FRU + GLN groups (six rats/group). The groups received vehicle (P.o.), glutamine (1 g/kg), FRU (10%; w/v), and FRU + GLN, respectively, for 19 d. Data show that FRU caused insulin resistance with corresponding increased blood glucose, circulating and pancreatic insulin levels, and lipid accumulation and glycogen depletion in skeletal muscle, but glycogen accumulation and a decreased lipid profile in adipose tissue. Adenosine and glutathione content decreased, whereas adenosine deaminase, xanthine oxidase, uric acid, and malondialdehyde concentrations increased in both tissues. In addition, glucose-6-phosphate dehydrogenase activity decreased in skeletal muscle but remained unaltered in adipose tissue. However, supplementation with GLN improved perturbed lipid and glycogen with a corresponding increase in adenosine and glutathione. The present results collectively indicate that lipid and glycogen mishandlings caused by high gestational FRU intake result in the depletion of adenosine and glutathione in skeletal muscle and adipose tissue. These findings also suggest that L-glutamine protects against skeletal muscle and adipose tissue dysmetabolism by enhancing adenosine and glutathione.