Antecedent long term ethanol consumption in combination with different diets alters the severity of experimental acute pancreatitis in rats.

Rämö, O. J.

doi:10.1136/gut.28.1.64

Cited by 21 publications

(6 citation statements)

References 11 publications

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“…59,60 Furthermore, various combinations of ethanol and a high-fat diet worsen both caerulein-and bile acid-induced experimental acute pancreatitis. [61][62][63] Finally, the excessive ethanol consumption that often occurs in human alcoholic pancreatitis may be accompanied by decreased nutritious food intake, leading to malnourishment and an increase in fatty acid metabolism.…”

Section: Discussionmentioning

confidence: 99%

The Role of Phosphate in Alcohol-Induced Experimental Pancreatitis

et al. 2021

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See Covering the Cover synopsis on page 741.BACKGROUND & AIMS: Heavy alcohol consumption is a common cause of acute pancreatitis; however, alcohol abuse does not always result in clinical pancreatitis. As a consequence, the factors responsible for alcohol-induced pancreatitis are not well understood. In experimental animals, it has been difficult to produce pancreatitis with alcohol. Clinically, alcohol use predisposes to hypophosphatemia, and hypophosphatemia has been observed in some patients with acute pancreatitis. Because of abundant protein synthesis, the pancreas has high metabolic demands, and reduced mitochondrial function leads to organelle dysfunction and pancreatitis. We proposed, therefore, that phosphate deficiency might limit adenosine triphosphate synthesis and thereby contribute to alcoholinduced pancreatitis. METHODS: Mice were fed a lowphosphate diet (LPD) before orogastric administration of ethanol. Direct effects of phosphate and ethanol were evaluated in vitro in isolated mouse pancreatic acini. RESULTS: LPD reduced serum phosphate levels. Intragastric administration of ethanol to animals maintained on an LPD caused severe pancreatitis that was ameliorated by phosphate repletion. In pancreatic acinar cells, low-phosphate conditions increased susceptibility to ethanol-induced cellular dysfunction through decreased bioenergetic stores, specifically affecting total cellular adenosine triphosphate and mitochondrial function. Phosphate supplementation prevented ethanol-associated cellular injury. CONCLUSIONS: Phosphate status plays a critical role in predisposition to and protection from alcoholinduced acinar cell dysfunction and the development of acute alcohol-induced pancreatitis. This finding may explain why pancreatitis develops in only some individuals with heavy alcohol use and suggests a potential novel therapeutic approach to pancreatitis. Finally, an LPD plus ethanol provides a new model for studying alcohol-associated pancreatic injury.

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Section: Discussionmentioning

confidence: 99%

The Role of Phosphate in Alcohol-Induced Experimental Pancreatitis

et al. 2021

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“…Letko et al 54 used the same model to test the various modes of ethanol administration and found that it did not influence the development of acute pancreatitis. A number of other studies have found that ethanol can sensitize acinar cells to CCK‐induced procarboxypeptidase A 1 processing in vitro and can sensitize to various forms of acute pancreatitis in vivo 61–64. In this way, ethanol is thought to increase stimulation‐dependent induction of acute pancreatitis, and thus may be important in ethanol toxicity in the pancreas.…”

Section: Non‐invasive Models Of Acute Pancreatitismentioning

confidence: 96%

Review of experimental animal models of acute pancreatitis

Cuthbertson

Christophi

2006

HPB

134

105

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The underlying mechanisms involved in the pathogenesis of acute pancreatitis are ill understood. The mortality rate of this disease has not significantly improved over the past few decades. Current treatment options are limited, and predominantly aimed at supportive therapy. A key feature of severe acute pancreatitis is the presence of extensive tissue necrosis with both local and systemic manifestations of inflammatory response syndromes. A better understanding of the underlying pathophysiology of severe acute pancreatitis may lead to more targeted therapeutic options, potentially leading to improved survival. Animal models of acute pancreatitis are therefore an essential investigative tool for these aims to be achieved. This review discusses the suitability of recent non-invasive models of acute pancreatitis such as hormone-induced, alcohol-induced, immune-mediated, diet-induced, gene knockout and L-arginine; and invasive models including closed duodenal loop, antegrade pancreatic duct perfusion, biliopancreatic duct injection, combination of secretory hyperstimulation with minimal intraductal bile acid exposure, vascular-induced, ischaemia/reperfusion and duct ligation.

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“…47 Animal models document associations with high protein and fat diets in the development of AP. [48][49][50][51] Further potential evidence for the role of high-fat diets in the development of AP comes from the results of a study evaluating ketogenic diets in the management of idiopathic epilepsy. 3 In that study 3/9 dogs fed a ketogenic diet (57% fat, 5.8% NFE, 25% crude protein; as dry matter) developed pancreatitis whereas only 2/31 dogs fed the control diet (16% crude fat, 54% NFE, 25% crude protein; as dry matter) developed pancreatitis.…”

Section: Dietary Factorsmentioning

confidence: 99%

New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice

Cridge

Lim

Algül

et al. 2022

Veterinary Internal Medicne

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While most cases of pancreatitis in dogs are thought to be idiopathic, potential risk factors are identified. In this article we provide a state‐of‐the‐art overview of suspected risk factors for pancreatitis in dogs, allowing for improved awareness and detection of potential dog‐specific risk factors, which might guide the development of disease prevention strategies. Additionally, we review important advances in our understanding of the pathophysiology of pancreatitis and potential areas for therapeutic manipulation based thereof. The outcome of pathophysiologic mechanisms and the development of clinical disease is dependent on the balance between stressors and protective mechanisms, which can be evaluated using the critical threshold theory.

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Antecedent long term ethanol consumption in combination with different diets alters the severity of experimental acute pancreatitis in rats.

Abstract: SUMMARY The effect of fat rich (F), protein rich (P) and carbohydrate rich (C) diets

Cited by 21 publications

References 11 publications

The Role of Phosphate in Alcohol-Induced Experimental Pancreatitis

The Role of Phosphate in Alcohol-Induced Experimental Pancreatitis

Review of experimental animal models of acute pancreatitis

New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice

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