Chronic Alcohol Intake Increases the Severity of Pancreatitis Induced by Acute Alcohol Administration, Hyperlipidemia and Pancreatic Duct Obstruction in Rats

Grauvogel, Juergen; Daemmrich, T.D.; Ryschich, Eduard; Gebhard, Martha-Maria; Werner, Jens

doi:10.1159/000288707

Cited by 12 publications

(9 citation statements)

References 50 publications

(58 reference statements)

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“…5C ). The alcohol-induced up-regulation and down-regulation of these parameters were previously reported [ 21 , 22 ], indicating that our experimental plan was feasible.…”

Section: Resultssupporting

confidence: 61%

Alcohol-induced Hyperlipidemia Is Ameliorated by Orally Administered DWP208, a Sodium Succinate Form of ZYM201

Cho

Choi

Park

et al. 2014

Korean J Physiol Pharmacol

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DWP208 is a sodium succinate form of ZYM-201 which is a triterpenoid glycoside isolated from Sanguisorba officinalis, a medicinal plant prescribed for various diseases, such as duodenal ulcers and bleeding in East Asian counties. We demonstrated that this compound is able to normalize the altered lipid metabolism induced by hyperglycemia and a high fat diet. In this study, we determined whether hyperlipidemic conditions induced with chronically treated alcohol can also be restored by DWP208. Similar to our previous results, orally administered DWP208 (1 to 10 mg/kg) also ameliorated the hyperlipidemia that was induced by alcohol. This compound reversed the alcohol-induced hyperlipidemia including (i) up-regulated hyperlipidemic parameters such as low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), atherosclerotic index (AI), triglyceride, and total cholesterol, and (ii) down-regulated hyperlipidemic parameters such as absolute body weight, superoxide dismutase (SOD) activity, and high-density lipoprotein (HDL) in serum and liver. According to our data, the ameliorative activity of DWP208 is due to its indirect anti-oxidative activity as a result of which lipid peroxide and hydroxyl radical levels were reduced and the activity of SOD was enhanced. Therefore, our data strongly suggest that DWP208 can be used as a remedy against alcohol-induced hyperlipidemia.

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“…5C ). The alcohol-induced up-regulation and down-regulation of these parameters were previously reported [ 21 , 22 ], indicating that our experimental plan was feasible.…”

Section: Resultssupporting

confidence: 61%

Alcohol-induced Hyperlipidemia Is Ameliorated by Orally Administered DWP208, a Sodium Succinate Form of ZYM201

Cho

Choi

Park

et al. 2014

Korean J Physiol Pharmacol

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show abstract

“…We designed this experimental animal study to be similar to the clinical state because young adults and adolescents at risk for prediabetes and early diabetes are likely to be chronic alcohol drinkers. In this study, OLETF rats were separated into prediabetic and early diabetic groups and treated with chronic alcohol consumption by the pair-fed method [ 19 20 21 ]. The average calculated amounts of alcohol consumption in prediabetes and early diabetes were 10.62 and 10.33 g/kg/day.…”

Section: Discussionmentioning

confidence: 99%

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

Lee

Hong

et al. 2015

Korean J Physiol Pharmacol

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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.

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“…Further FAEE hydrolysis which takes place in mitochondria leads to the release of free fatty acids and an increase in toxic effects [76]. Suggestions come from an in vitro model, confirmed in an in vivo animal study in which ethanol feeding exacerbated pancreatitis due to hyperlipidemia [80]. This is important in light of studies showing that humans dying from alcohol intoxication have high levels of FAEEs in the pancreas [81].…”

Section: Environmental Factors and Their Role In Alcoholic Pancreatitismentioning

confidence: 96%

What Do We Currently Know about the Pathophysiology of Alcoholic Pancreatitis: A Brief Review

et al. 2020

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Background: Alcoholic pancreatitis is a serious medical concern worldwide and remains to be one of the common causes of pancreatic disease. Summary: While alcohol consumption causes direct damage to pancreatic tissue, only a small percentage of active drinkers will develop pancreatitis. An explanation of this phenomenon is probably that alcohol increases pancreatic vulnerability to damage; however, the simultaneous presence of additional risk factors and pancreatic costressors is required to increase the risk of pancreatitis and its complications caused by alcohol misuse. Recently, a number of important genetic as well as environmental factors influencing the risk of alcoholic pancreatitis have been described. Key Messages: In brief, this review reports established factors for the development of alcoholic pancreatitis and summarizes recent progress made in basic and clinical research.

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Chronic Alcohol Intake Increases the Severity of Pancreatitis Induced by Acute Alcohol Administration, Hyperlipidemia and Pancreatic Duct Obstruction in Rats

Cited by 12 publications

References 50 publications

Alcohol-induced Hyperlipidemia Is Ameliorated by Orally Administered DWP208, a Sodium Succinate Form of ZYM201

Alcohol-induced Hyperlipidemia Is Ameliorated by Orally Administered DWP208, a Sodium Succinate Form of ZYM201

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

What Do We Currently Know about the Pathophysiology of Alcoholic Pancreatitis: A Brief Review

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