Glucagon secretion during the development of insulin-secreting tumors induced by streptozotocin and nicotinamide.
Serial oral glucose tolerance tests in rats treated with streptozotocin and nicotinamide showed that blood glucose levels after glucose loading were suppressed significantly 7 months after treatment as compared to those of earlier stages. Post-glucose plasma insulin levels were significantly elevated at the 9th to 12th month and concomitantly fasting plasma glucagon levels rose significantly. At that time pancreatic islet cell tumors were demonstrated in all of the rats in this experiment. Post-glucose plasma glucagon levels, however, did not show remarkable changes throughout the observation. In spite of hyperinsulinemia, post-glucose plasma glucagon levels of tumor-bearing rats were significantly lower than those of body weight adjusted controls. It is inferred from the study that secretory activity of pancreatic A-cells of tumor-bearing rats is restrained by excess insulin released from islet cell tumors.
D007516:Adenoma, Islet Cell / Q000139:chemically induced / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D005934:Glucagon / Q000378:metabolism*; D005951:Glucose Tolerance Test; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D009374:Neoplasms, Experimental / Q000139:chemically induced / Q000378:metabolism; D009536:Niacinamide; D010190:Pancreatic Neoplasms / Q000139:chemically induced / Q000378:metabolism*; D051381:Rats; D013311:Streptozocin
D001786:Blood Glucose; D007328:Insulin; D009536:Niacinamide; D013311:Streptozocin; D005934:Glucagon