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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

The islet area in the pancreas of OLETF rats. The size of the islets was quantified and analyzed. (A) Islet area data in 16-week-old OLETF rats (prediabetes). (B) Islet area data in 22-week-old OLETF rats (diabetes). Data represent mean±SE. Pd-O-C, prediabetic OLETF rat-control diet; Pd-O-E, prediabetic-OLETF rat-ethanol diet; D-O-C, diabetic OLETF rat-control diet; D-O-E, diabetic OLETF rat-ethanol diet. There were no statistically significant differences between the control group and ethanol group.
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Figure 9: The islet area in the pancreas of OLETF rats. The size of the islets was quantified and analyzed. (A) Islet area data in 16-week-old OLETF rats (prediabetes). (B) Islet area data in 22-week-old OLETF rats (diabetes). Data represent mean±SE. Pd-O-C, prediabetic OLETF rat-control diet; Pd-O-E, prediabetic-OLETF rat-ethanol diet; D-O-C, diabetic OLETF rat-control diet; D-O-E, diabetic OLETF rat-ethanol diet. There were no statistically significant differences between the control group and ethanol group.

Mentions: The pancreatic islets were smaller in the Pd-O-C group than in the Pd-O-E group, and smaller in the D-O-E group than in the D-O-C group. However, there were no statistically significant differences between the control group and ethanol group (Figs. 8 and 9).


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)

The islet area in the pancreas of OLETF rats. The size of the islets was quantified and analyzed. (A) Islet area data in 16-week-old OLETF rats (prediabetes). (B) Islet area data in 22-week-old OLETF rats (diabetes). Data represent mean±SE. Pd-O-C, prediabetic OLETF rat-control diet; Pd-O-E, prediabetic-OLETF rat-ethanol diet; D-O-C, diabetic OLETF rat-control diet; D-O-E, diabetic OLETF rat-ethanol diet. There were no statistically significant differences between the control group and ethanol group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 9: The islet area in the pancreas of OLETF rats. The size of the islets was quantified and analyzed. (A) Islet area data in 16-week-old OLETF rats (prediabetes). (B) Islet area data in 22-week-old OLETF rats (diabetes). Data represent mean±SE. Pd-O-C, prediabetic OLETF rat-control diet; Pd-O-E, prediabetic-OLETF rat-ethanol diet; D-O-C, diabetic OLETF rat-control diet; D-O-E, diabetic OLETF rat-ethanol diet. There were no statistically significant differences between the control group and ethanol group.
Mentions: The pancreatic islets were smaller in the Pd-O-C group than in the Pd-O-E group, and smaller in the D-O-E group than in the D-O-C group. However, there were no statistically significant differences between the control group and ethanol group (Figs. 8 and 9).

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