Impact of Insulin - Induced Hypoglycemia on some Plasma Markers of Skeletal Muscles and Heart Damage in Adult Male Rats: Relation to Oxidative Stress and Plasma Epinephrine | ||||
Bulletin of Egyptian Society for Physiological Sciences | ||||
Article 15, Volume 31, Issue 1, December 2011, Page 211-224 PDF (210.33 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/besps.2011.35983 | ||||
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Authors | ||||
Manal Kamal* ; Asmaa Hassan | ||||
Department of Medical Physiology, Faculty of Medicine, Assiut University, Assiut, Egypt | ||||
Abstract | ||||
Objective: Hypoglycemic damage to the central nervous system is well known complication of insulin therapy. Little is known about the effect of insulin induced hypoglycemia on peripheral tissues as skeletal muscles and heart. In the present study the effect of acute and recurrent insulin- induced hypoglycemia on plasma creatine kinase (CK) and Lactate dehydrogenase (LDH); markers of skeletal muscles and heart damage was studied. Oxidative stress in those tissues and plasma epinephrine levels after hypoglycemia were also evaluated to elucidate the mechanism of hypoglycemic effect on those tissues. Methods: The study consisted of 50 adult male rats divided into three groups: (1) Control group. (2) Acute insulininduced hypoglycemia group (AHG): injected with human insulin (humulin) intraperitoneal (ip) in a dose of 10 U/kg, food was then withheld for 6 hours. (3) Recurrent insulin-induced hypoglycemia group (RHG): received recurrent ip injection with 10 U/kg humulin once per day for three consecutive days, food is given after 2 hours and in the fourth day they received the same dose of insulin, then food was withheld for 6 hours. Blood glucose was measured before and 30, 60, 90 and 120 min after the injection. Plasma levels of CK, LDH were estimated before and 6 hours after the injection. Epinephrine levels were measured before and 90 min after the injection. Animals were sacrificed by decapitation 6 h after the injection for measurement of malondialdehyde (MDA) and total antioxidant capacity (T-AOC) in skeletal muscle and heart tissue homogenate. Results: it was found that acute and recurrent insulin induced hypoglycemia caused elevated levels of plasma CK, LDH, increase lipid peroxidations (MDA) together with decrease in T-AOC in skeletal muscle and heart tissue homogenate. The plasma epinephrine levels in response to hypoglycemia were significantly more in AHG group and RHG group at day 1 than control. It was also demonstrated that recurrent insulin induced hypoglycemia resulted in more increase in the levels of plasma CK, LDH and MDA with more decrease in T-AOC and blood glucose levels compared to acute insulin hypoglycemia rats. There was also revealed lower epinephrine levels in response to recurrent hypoglycemia at day 4 compared to control. Conclusions: our findings indicate that acute and recurrent insulin induced hypoglycemia caused skeletal muscle and heart damage. This damage may be attributed to increased oxidative stress revealed in those tissues. This damaging effect is more following recurrent hypoglycemia which may be related to the lower epinephrine levels in response to recurrent hypoglycemia detected in this group. That resulted in more decrease in blood glucose and therefore more damaging effects to those tissues. | ||||
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