Abstract
There are several claims about the beneficial effects of supplementing L-glutamine to both type 1 and type 2 diabetes. The purpose of the present study was to provide detailed knowledge about the fate of this amino acid in the liver, the first organ that receives the compound when ingested orally. The study was done using the isolated perfused rat liver, an experimental system that preserves the microcirculation of the organ and that allows to measured several parameters during steady-state and pre steady-state conditions. L-Glutamine was infused in the portal vein (5 mM) and several parameters were monitored. Livers from type 1 diabetic rats showed an accelerated response to L-glutamine infusion. In consequence of this accelerated response livers from type 1 diabetic rats presented higher rates of ammonia, urea, glucose and lactate output during the first 25–30 minutes following L-glutamine infusion. As steady-state conditions approached, however, the difference between type 1 diabetes and control livers tended to disappear. Measurement of the glycogen content over a period of 100 minutes revealed that, excepting the initial phase of the L-glutamine infusion, the increased glucose output in livers from type 1 diabetic rats was mainly due to accelerated glycogenolysis. Livers from type 2 diabetic rats behaved similarly to control livers with no accelerated glucose output but with increased L-alanine production. L-Alanine is important for the pancreatic β-cells and from this point of view the oral intake of L-glutamine can be regarded as beneficial. Furthermore, the lack of increased glucose output in livers from type 2 diabetic rats is consistent with observations that even daily L-glutamine doses of 30 g do not increase the glycemic levels in well controlled type 2 diabetes patients.
Highlights
There are several claims about the beneficial effects of supplementing L-glutamine to both type 1 and type 2 diabetes [1,2,3,4,5]
The lack of increased glucose output in livers from type 2 diabetic rats is consistent with observations that even daily L-glutamine doses of 30 g do not increase the glycemic levels in well controlled type 2 diabetes patients
The results allow to conclude that a sudden load of L-glutamine in the portal vein can generate a temporarily increased glucose output in type 1 diabetes, which is probably due to enhanced gluconeogenesis during a period of 30 minutes
Summary
There are several claims about the beneficial effects of supplementing L-glutamine to both type 1 and type 2 diabetes [1,2,3,4,5]. L-Glutamine is the physiological precursor of L-arginine for the synthesis of nitric oxide (NOÁ), whose production in β-cells potentiates insulin secretion. L-glutamine combined with L-alanine constitute the main source of glutamate for the synthesis of GSH. The latter is important in helping to diminish the oxidative stress which contributes for maintaining inflammatory processes within the β-cells in diabetes. Besides improving the glucose profile L-glutamine has a positive effect on glucose oxidation and insulin resistance [5,9]. In streptozotocin-induced diabetes in rats, L-glutamine supplementation improved the plasma levels of transminases, fructosamine and the lipid profile [10]. The doses of L-glutamine that are administered with a meal may reach 30 g [4]. Doses of this magnitude will necessarily lead to high L-glutamine concentrations in the portal vein, the most important entry vessel of the liver
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