ACUTE BOUT OF EXERCISE INDUCED PROLONGED MUSCLE GLUCOSE TRANSPORTER-4 TRANSLOCATION AND DELAYED COUNTER-REGULATORY HORMONE RESPONSE IN TYPE 1 DIABETES.

Acute bout of exercise induced prolonged muscle glucose transporter-4 translocation and delayed counter-regulatory hormone response in type 1 diabetes.

Acute bout of exercise induced prolonged muscle glucose transporter-4 translocation and delayed counter-regulatory hormone response in type 1 diabetes.

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Previous studies have demonstrated that an acute bout Dog Toys of aerobic exercise induces a subsequent delayed onset of hypoglycemia among patients with type 1 diabetes.However, the mechanisms of exercise-induced hypoglycemia in type 1 diabetes are still unclear.Streptozotocin (STZ) was injected to 6-week-old male Wistar rats, and three days after STZ injection, animals were randomly assigned into 2 groups: STZ with insulin only (STZ) and STZ with insulin and exercise (STZ+EX).Normal Wistar rats with exercise were used as control (CON+EX).

Insulin was intraperitoneally injected (0.5 U/kg) to both STZ groups (-0.5 h), and a bout of aerobic exercise (15 m/min for 30 min) was conducted at euglycemic conditions (0 h).Blood was collected at 0, 1, 3, and 5 h after exercise from the carotid artery.

While the blood glucose level was stable during the post-exercise period (0-5 h) in the STZ and CON+EX groups, it decreased significantly only in Relora the STZ+EX group at 3 h.Plasma glucagon, adrenalin, and noradrenalin levels significantly increased at 1 h in the STZ group, whereas significant hormonal responses were observed at 5 h in the STZ+EX group.In skeletal muscle glucose metabolism-related pathway, the level of glucose transporter-4 (GLUT-4) translocation was significantly higher at 1 h in the CON and STZ groups.However, in the STZ+EX group, these activations were maintained by 5 h, indicating a sustained glucose metabolism in the STZ+EX group.

A single bout of aerobic exercise induced a delayed onset of hypoglycemia in STZ-treated rats.A prolonged enhancement of GLUT-4 translocation and delayed counter-regulatory hormone responses may have contributed to the induction of hypoglycemia.

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