Activity, distribution and regulation of phosphofructokinase in salivary gland of rats with streptozotocin-induced diabetes

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.

Increased glycated calmodulin in the submandibular salivary glands of streptozotocin‐induced diabetic rats

“…Experimental animal models of diabetes induced by either alloxan or streptozotcin (STZ) have been used to study aspects of the pathophysiology of this disease. Previous papers from our laboratory showed that STZinduced diabetic rats had some biochemical parameters altered in the salivary glands [14][15][16] . It has been reported that a prolonged elevation of blood glucose in diabetes mellitus may be responsible for an overall increase in the degree of proteins glycation.…”

Alteration of Ca2+‐ATPase activity in the homogenate, plasma membrane and microsomes of the salivary glands of streptozotocin‐induced diabetic rats

“…[2][3][4][5][6] Experimental animal models of diabetes, induced either by alloxan or streptozotocin, have been used to study aspects of the pathophysiology of this disease. In salivary glands alterations in the glycolytic enzymes activities, 7,8 antioxidant parameters 9,10 of the salivary glands have been reported. It has been reported that a reduction in submandibular salivary flow rate of rats was associated with calcium signaling.…”

Metabolic remodeling triggered by salivation and diabetes in major salivary glands

“…In addition, it is widely known that several diseases could affect salivary gland function and saliva secretion. In particular, diabetes mellitus (DM) has been the focus of many studies using major salivary glands, attempting to elucidate the changes in the activity of some pivotal enzymes of the glycolytic pathway (hexokinase and phosphofructokinase 1) and glycogen (glycogen synthase and glycogen phosphorylase) metabolism …”