| It is hot topics that insulin resistance and pancreatic P cell dysfunction are two important parts of pathologic physiology in type 2 diabetes. Many studies have shown that the occurrence and development of insulin resistance is related to many factors, such as obesity, free fatty acids (FFA), corticosteroid, growth hormone, glucagon, and amylin and so on. It has been gradually realized that amylin might play an important role in the occurrence and development of insulin resistance and type 2 diabetes. Cooper, a member of Amylin Cooperation Group in USA, had put forward that amylin could induce the occurrence and development of type 2 diabetes as follows: (1)it could induce insulin resistance by antagonizing the action of insulin; (2)it might damage pancreatic tissue and the function of P cell by depositing in P cell.Studies have shown that hyperamylinemia can induce insulin resistance by glucose metabolism. However, recent studies have shown that amylin might play a role in lipid metabolism and it might be a mediator of amylin inducing insulin resistance, but the mechanism is not exactly demonstrated. So we designed this experiment on the basis of above-mentioned studies to discuss the role of amylin on glucose and lipid metabolism in rats and its possible effect on insulin resistance and type 2 diabetes mellitus.MethodsIn this experiment, a total of 20 SD rats (male, 240-275g) were raised with chow dietpurchased from the Center of Experimental Animal of Henan Province. A week later, the right carotid artery and left jugular vein of rats were cannulated, and rats were housed individually with food intake and body weight closely monitored.Before the experiment, rats were fasted for 16h and were randomly divided into 3 groups for being infused as follow: Group A, saline as a control; Group B, 5nmol/h amylin; Group C, 0.5nmol/h amylin. After the commencement of infusion, blood samples (0.6ml) were taken at 0, 30, 60, 120, and ISOmin point and were then snap frozen at -20 癈 for defecting the levels of serum lipids, glucose, and insulin. Homeostasis model assessment (HOMA) and Li's formula were used to evaluate insulin sensitivity index (ISI), and insulin resistance index (HOMA-IR) to make an inquiry into the relation of amylin and insulin resistance. The formula of ISI is 1/(FINS X FPG) and HOMA-IR is (FINS X FPG)/22.5.After a final blood sample was taken at ISOmin, rats were killed with pentobarbital sodium (50mg/kg). Red quadriceps muscle and liver were clamped and homogenized in sodium chloride solution. Then the homogenate was filtered and suitable portions of the filtrate stored in -20 癈 for determining FFA content.ResultsAnalysis of variance (ANOVA) with repeated measure showed that (1)the levels of glucose, insulin, FFA, ISI, and HOMA-IR differed greatly among different groups and at different time (P<0.01); (2)the level of triglycerid(TG) was not significant difference among different groups and at different time (P>0.05).The least significant difference (LSD) t test showed that: (1)serum glucose level increased at 30min and 1 80min period (P<0.05 vs. saline control) in Group B and C; FFA level was also significantly elevated at 60min (P<0.05 vs. control) and these elevations were sustained over 2h infusion period (P<0.05 vs. control) in Group B and C; insulin level was elevated at 30 min and 60 min period (P<0.01 vs. saline control) in Group B and C; ISI decreased significantly at 30min and 180min period in Group B(P<0.05 vs. control), and at 30min and 120min period in Group B(P<0.05 vs. control); HOMA-IR increased at 30min~ 180min period in Group B (P<0.05 vs. saline control) and at 30min and 120min period in Group C (P<0.05 vs. control); the above-mentioned indexes were all no difference betweenGroup B and C(P>0.05) (2)the levels of serum glucose, FFA, insulin, ISI, and HOMA-IR were all unaltered in Group A(P>0.05 vs. 0min); in Group B and C: glucose level was significantly higher at 30min and 180min period (P<0.05 vs. 0 min) with a peak at 30 min; FFA level was also...
|
PDF Full Text Request