Chronic Alcohol Consumption Results in Greater Damage to the Pancreas Than to the Liver in the Rats.
10.4196/kjpp.2015.19.4.309
- Author:
Seong Su LEE
1
;
Oak Kee HONG
;
Anes JU
;
Myung Jun KIM
;
Bong Jo KIM
;
Sung Rae KIM
;
Won Ho KIM
;
Nam Han CHO
;
Moo Il KANG
;
Sung Koo KANG
;
Dai Jin KIM
;
Soon Jib YOO
Author Information
1. Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Bucheon St. Mary's Hospital, The Catholic University of Korea, Bucheon 420-717, Korea. sjyoo@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Alcohol;
Endoplasmic reticulum stress;
OLETF rat
- MeSH:
Alcohol Drinking*;
Animals;
Body Weight;
Diet;
Eating;
Endoplasmic Reticulum;
Endoplasmic Reticulum Stress;
Ethanol;
Fasting;
Glucose;
Glucose Tolerance Test;
Liver*;
Models, Animal;
Pancreas*;
Prediabetic State;
Rats*;
Rats, Inbred OLETF
- From:The Korean Journal of Physiology and Pharmacology
2015;19(4):309-318
- CountryRepublic of Korea
- Language:English
-
Abstract:
Alcohol consumption increases the risk of type 2 diabetes. However, its effects on prediabetes or early diabetes have not been studied. We investigated endoplasmic reticulum (ER) stress in the pancreas and liver resulting from chronic alcohol consumption in the prediabetes and early stages of diabetes. We separated Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a type-2 diabetic animal model, into two groups based on diabetic stage: prediabetes and early diabetes were defined as occurrence between the ages of 11 to 16 weeks and 17 to 22 weeks, respectively. The experimental group received an ethanol-containing liquid diet for 6 weeks. An intraperitoneal glucose tolerance test was conducted after 16 and 22 weeks for the prediabetic and early diabetes groups, respectively. There were no significant differences in body weight between the control and ethanol groups. Fasting and 120-min glucose levels were lower and higher, respectively, in the ethanol group than in the control group. In prediabetes rats, alcohol induced significant expression of ER stress markers in the pancreas; however, alcohol did not affect the liver. In early diabetes rats, alcohol significantly increased most ER stress-marker levels in both the pancreas and liver. These results indicate that chronic alcohol consumption increased the risk of diabetes in prediabetic and early diabetic OLETF rats; the pancreas was more susceptible to damage than was the liver in the early diabetic stages, and the adaptive and proapoptotic pathway of ER stress may play key roles in the development and progression of diabetes affected by chronic alcohol ingestion.
