Insulin Resistance in Late Pregnant Rats.
10.12701/yujm.1995.12.2.319
- Author:
Myung Heup CHUN
;
Yong Woon KIM
;
So Young PARK
;
Jong Yeon KIM
;
Suck Kang LEE
- Publication Type:Original Article
- Keywords:
Pregnancy;
Insulin resistance;
Insulin receptor;
Glycogen synthase;
Progesterone
- MeSH:
Animals;
Female;
Glucose;
Glucose Tolerance Test;
Glycogen;
Glycogen Synthase;
Humans;
Insulin Resistance*;
Insulin*;
Liver;
Membranes;
Pregnancy;
Progesterone;
Rats*;
Rats, Sprague-Dawley;
Receptor, Insulin
- From:Yeungnam University Journal of Medicine
1995;12(2):319-330
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The influence of normal late pregnancy on insulin action and insulin secretion was studied in the Sprague-Dawley female rats. On 20th day after mating, intravenous glucose tolerance test(IVGTI) was performed in non pregnant control and pregnant rats. As results of IVGTT, glucose disappearance rate was not significantly different in both groups, but secretory response of insulin was significantly(p<0.05) increased in pregnant rat. And the ratio of insulin/ .glucose was significantly higher in pregnant rats, which means existence of insulin resistance. These insulin resistance was overcomed by increased secretory response of pancreatic insulin. Insulinogenic index( A insulin/glucose - 5 min) was highly significantly (r=0.62, p<0.01) correlated with progesterone concentration. Glycogen level and amounts of "C-glucose incorporated into glycogen after IVGTT were significantly(p<0. 05) decreased in the liver, but were not changed significantly in soleus. Glycogen synthase activity of soleus and liver was not differ significantly in the both groups. Insulin binding at varying concentrations of insulin to crude membrane of pregnant liver was not significantly different from control. In conclusions, although these pregnant rats were normal glucose tolerance due to increased secretory response of insulin, that was correlated with progesterone concentration, pregnant rat had insulin resistance. The mechanisms of insulin resistance were not related to defect of insulin binding phase and glycogen synthase, but suggest pre-receptor and/or postreceptor phase.
