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Chronic Alcohol Consumption Results in Greater Damage to the Pancreas Than to the Liver in the Rats.

Lee SS, Hong OK, Ju A, Kim MJ, Kim BJ, Kim SR, Kim WH, Cho NH, Kang MI, Kang SK, Kim DJ, Yoo SJ - Korean J. Physiol. Pharmacol. (2015)

Bottom Line: There were no significant differences in body weight between the control and ethanol groups.In prediabetes rats, alcohol induced significant expression of ER stress markers in the pancreas; however, alcohol did not affect the 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.

View Article: PubMed Central - PubMed

Affiliation: 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.

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.

No MeSH data available.


Related in: MedlinePlus

ER stress of the liver in diabetic OLETF rats. (A) Representative Western blot analysis showing ER stress of the liver in the alcohol treatment group. (B) The result of A is expressed as the mean± SE of the relative band density from three independent experiments. ER, endoplasmic reticulum; OLETF, Otsuka Long-Evans Tokushima Fatty; D-O-C, early diabetes/OLETF rat/control diet; D-O-E, early diabetes/OLETF rat/ethanol diet (Lieber-DeCarli diet). *p<0.05 compared to control. Data are the mean of four independent experiments.
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Figure 4: ER stress of the liver in diabetic OLETF rats. (A) Representative Western blot analysis showing ER stress of the liver in the alcohol treatment group. (B) The result of A is expressed as the mean± SE of the relative band density from three independent experiments. ER, endoplasmic reticulum; OLETF, Otsuka Long-Evans Tokushima Fatty; D-O-C, early diabetes/OLETF rat/control diet; D-O-E, early diabetes/OLETF rat/ethanol diet (Lieber-DeCarli diet). *p<0.05 compared to control. Data are the mean of four independent experiments.

Mentions: The p-PERK, p-elF2α, ATF6, and IRE1α levels were significantly higher in the D-O-E group than in the D-O-C group; however, the p-JNK level was significantly lower (p<0.05). There were no significant differences in the GADD153 or Grp78 level (Fig. 4).


Chronic Alcohol Consumption Results in Greater Damage to the Pancreas Than to the Liver in the Rats.

Lee SS, Hong OK, Ju A, Kim MJ, Kim BJ, Kim SR, Kim WH, Cho NH, Kang MI, Kang SK, Kim DJ, Yoo SJ - Korean J. Physiol. Pharmacol. (2015)

ER stress of the liver in diabetic OLETF rats. (A) Representative Western blot analysis showing ER stress of the liver in the alcohol treatment group. (B) The result of A is expressed as the mean± SE of the relative band density from three independent experiments. ER, endoplasmic reticulum; OLETF, Otsuka Long-Evans Tokushima Fatty; D-O-C, early diabetes/OLETF rat/control diet; D-O-E, early diabetes/OLETF rat/ethanol diet (Lieber-DeCarli diet). *p<0.05 compared to control. Data are the mean of four independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4499642&req=5

Figure 4: ER stress of the liver in diabetic OLETF rats. (A) Representative Western blot analysis showing ER stress of the liver in the alcohol treatment group. (B) The result of A is expressed as the mean± SE of the relative band density from three independent experiments. ER, endoplasmic reticulum; OLETF, Otsuka Long-Evans Tokushima Fatty; D-O-C, early diabetes/OLETF rat/control diet; D-O-E, early diabetes/OLETF rat/ethanol diet (Lieber-DeCarli diet). *p<0.05 compared to control. Data are the mean of four independent experiments.
Mentions: The p-PERK, p-elF2α, ATF6, and IRE1α levels were significantly higher in the D-O-E group than in the D-O-C group; however, the p-JNK level was significantly lower (p<0.05). There were no significant differences in the GADD153 or Grp78 level (Fig. 4).

Bottom Line: There were no significant differences in body weight between the control and ethanol groups.In prediabetes rats, alcohol induced significant expression of ER stress markers in the pancreas; however, alcohol did not affect the 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.

View Article: PubMed Central - PubMed

Affiliation: 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.

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.

No MeSH data available.


Related in: MedlinePlus