Abstract
Although the influence of diabetes on salivary glands is well studied, it still presents conflicting results. In this work, the regulation of the phosphofructokinase-1 enzyme (PFK-1) was studied utilizing the salivary glands of rats. Diabetes was induced by a single intraperitoneal injection of streptozotocin (60 mg/Kg of body weight) in rats (180-200 g). The animals were killed 30 days after the induction of diabetes and the submandibular and parotid salivary glands were used. Hyperglycemia was evaluated by blood sugar determination. The distribution of PFK-1 between the soluble and cytoskeleton fractions, the phosphate content of PFK-1, the content of fructose-2,6-bisphosphate and the activity of the PFK-2 enzyme were determined. The calculated relative glandular weight showed a higher value for the parotid gland in comparison with the control, but not for the submandibular gland. The activity of PFK-1 expressed per gland showed no variation between diabetic and control animals. However, considering the specific activity, the soluble enzyme presented a value 50% higher than that of the control and the cytoskeleton bound form increased by 84% compared to the control. For the parotid gland, no difference in the specific activity between diabetic and control animals was observed. On the other hand, the activity per gland of the soluble enzyme increased in the diabetic animals. The phosphate content of PFK-1 increased in the submandibular and parotid glands of diabetic rats. Both the content of fructose-2,6-bisphosphate and the active form of PFK-2 were reduced in the diabetic glands. In conclusion, the increase in the activity of PFK-1 observed in the salivary glands of rats with streptozotocin-induced diabetes does not seem to be due to its modulator fructose-2,6-bisphosphate.
Highlights
Diabetes mellitus is a metabolic disease that affects many organs and systems, including the oral cavity
It has been reported that diabetes decreases norepinephrine content, the density of adrenergic receptor and receptor-adenyl cyclase coupling in parotid glands[14], as well as salivary secretion closely associated with the lowered susceptibility of the muscarinic receptors[30]
The calculated relative glandular weight (RGW) of the submandibular gland (RGW = glandular weight x 100/body weight) showed no significant difference between diabetic and control rats (0.067 ± 0.005 and 0.070 ± 0.007, respectively), while for the parotid gland the RGW was statistically higher for the diabetic group (0.060 ± 0.001 and 0.030 ± 0.007 respectively for the diabetic and control groups)
Summary
Diabetes mellitus is a metabolic disease that affects many organs and systems, including the oral cavity. Some investigations have described the effects of experimental diabetes induced either by streptozotocin or alloxan in the structure and functions of the salivary glands of animals[2,24]. It was reported that isolated parotid gland from streptozotocin-induced diabetic rats presented a dose-dependent decrease in amylase release in response to noradrenaline when compared to control parotid gland[17]. The role of PFK-1 in the regulation of glycolysis has been established for a variety of cell types in various animals[29]. The activity of this enzyme is controlled by multiple positive and negative allosteric factors such as ATP, ADP, AMP, fructose-2,6bisphosphate (Fru-2,6-P2) and citrate. Similar to other glycolytic enzymes PFK-1 may be covalently modified by phosphorylation/ dephosphorylation as a form of regulation[18]
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