Author(s): Vickram1, Divya Dattaprasad2, Kashinath Rattihalli Thirumalarao3
Decreased cellular thiol levels seen in diabetes mellitus (DM) may be in part attributed to increased free radical generation. The free radical mediated oxidative stress has been implicated in the pathogenesis of DM and its complications. The relative deficiency or non-availability of insulin in DM affects the metabolism of biomolecules, specifically the carbohydrate metabolism. The insulin-mimicking actions of various thiols have been studied. In our previous study, we have documented that 3-mercapto-1-propanol (Thiopropanol), a low molecular weight thiol, at the dosage employed has increased glucose utilisation in alloxan-diabetic rat liver tissue probably by favouring utilisation of glucose through glycolysis and HMP pathway. It is known that insulin inhibits gluconeogenesis by inhibiting the key enzymes of the same and by controlling the channelling of amino acids for the glucose biosynthesis through gluconeogenic pathway. A study was undertaken to assess the effects of thiopropanol (TP) on amino acid turnover and the redox status in alloxan diabetic rat liver.
Male albino rats weighing 150-250 g were used. Diabetes was induced using alloxan monohydrate. Rats were divided into normal and diabetic groups. Levels of amino acid nitrogen (AAN), alanine, total thiol (-SH) groups, TBARS (Thiobarbituric acid reactive substances), and activities of alanine transaminase (ALT) and aspartate transaminase (AST) were estimated in liver specimens of normal, control-alloxan diabetic and TP-exposed-alloxan-diabetic rats.
The results showed a significant increase (p<0.001) in AAN levels, alanine levels, and total -SH groups concentration; and a significant decrease (p<0.001) in TBARS levels, ALT and AST activities in TP-exposed-alloxan diabetic liver slices as compared to control-alloxan diabetic liver slices.
Hence, it may be concluded that TP, at the concentration employed, inhibits gluconeogenesis from amino acids probably by lowering transaminases activity and suppresses free radical production probably by maintaining cellular reduced glutathione (G-SH) levels.