Colon Involvement in Necrotizing Pancreatitis: Incidence, Risk Factors, and Outcomes.

Objective: To investigate the incidence, risk factors, and outcomes of colon involvement in patients with necrotizing pancreatitis.

Summary/background Data: Necrotizing pancreatitis is characterized by a profound inflammatory response with local and systemic implications. Mesocolic involvement can compromise colonic blood supply leading to ischemic complications; however, few data exist regarding this problem.

Does adiponectin upregulation attenuate the severity of acute pancreatitis in obesity?

Introduction: Obesity is an independent risk factor for severe acute pancreatitis, though the mechanisms underlying this association are unknown. The powerful anti-inflammatory adipokine adiponectin is decreased in obesity. We recently showed that the severity of pancreatitis in obese mice is inversely related to circulating adiponectin levels, and therefore hypothesized that adiponectin upregulation would attenuate the severity of pancreatitis in obese mice.

Acute pancreatitis in obesity: adipokines and dietary fish oil.

Background: Acute pancreatitis is a substantial clinical problem accounting for 240,000 hospital admissions yearly in the United States. Obesity is epidemic and is clearly an independent risk factor for increased severity of acute pancreatitis (AP). Adipose tissue is an endocrine organ that secretes a variety of metabolically active substances termed adipokines.

The burden of incisional hernia in necrotizing pancreatitis: how can we improve?

Background: Necrotizing pancreatitis (NP) patients frequently require pancreatic debridement, and have risk factors for incisional hernia (IH). However, no published data exist regarding the incidence of IH in NP. The aim of the current study was to define the incidence of and identify risk factors for developing IH after pancreatic debridement.

Leptin regulates gallbladder genes related to gallstone pathogenesis in leptin-deficient mice.

Background: Little is known about the genetic factors that cause alterations in gallbladder motility, cholesterol crystal nucleation, biliary lipids, and, ultimately, cholesterol gallstones. Obese, leptin-deficient (Lep(ob)) mice have large gallbladder volumes with decreased contraction in vitro and are predisposed to cholesterol crystal formation. Leptin administration to these mice causes weight loss and restores gallbladder function.

Steatocholecystitis: the influence of obesity and dietary carbohydrates.

Introduction: We have recently demonstrated that obese and lean mice fed a high fat diet have increased gallbladder wall fat and decreased gallbladder contractility, cholecystosteatosis. Animal and human data also suggest that diets high in refined carbohydrates lead to gallstone formation. However, no data are available on the role of dietary carbohydrates on gallbladder wall fat and inflammation.

Ezetimibe ameliorates cholecystosteatosis.

Background: Cholecystosteatosis is the accumulation of gallbladder wall fats leading to decreased gallbladder emptying. Ezetimibe inhibits intestinal fat absorption and prevents murine gallstone formation. However, the influence of ezetimibe on gallbladder emptying and cholecystosteatosis has not been studied.

High dietary carbohydrates decrease gallbladder volume and enhance cholesterol crystal formation.

Background: Animal and human data suggest that a diet high in refined carbohydrates leads to gallstone formation. However, no data are available on the role of dietary carbohydrates on gallbladder volume or on cholesterol crystal formation. Therefore, we tested the hypothesis that a high carbohydrate diet would alter gallbladder volume and enhance cholesterol crystal formation.

Cholecystosteatosis: an explanation for increased cholecystectomy rates.

Introduction: Over the past decade, obesity has become epidemic, and the number of cholecystectomies as well as the percentage with acalculous cholecystitis have increased. We have recently reported that congenitally obese mice and lean mice fed a high fat diet have increased gallbladder wall lipids and poor gallbladder emptying. Therefore, we tested the hypothesis that compared to patients with a normal gallbladder, patients with both acalculous and calculous cholecystitis would have increased gallbladder wall fat.

Resistin-like molecule alpha reduces gallbladder optimal tension.

Introduction: Insulin resistance is associated with increased gallbladder volume and impaired gallbladder emptying. Resistin and resistin-like molecule alpha (RELM-alpha) are adipose-derived hormones that are believed to mediate insulin resistance. Therefore, we tested the hypothesis that administration of resistin or RELM-alpha would cause insulin resistance and diminish gallbladder contractility.

Pioglitazone increases gallbladder volume in insulin-resistant obese mice.

Background: Both obesity and diabetes are associated with an increased incidence of gallstones. Recent animal and human data from our laboratory suggest that insulin resistance is associated with increased gallbladder volume and/or impaired gallbladder emptying. Pioglitazone is a thiazolidinedione that has been shown to improve insulin resistance.

Nonalcoholic Fatty gallbladder disease: the influence of diet in lean and obese mice.

The obesity epidemic has contributed to an increased prevalence of gallstones and a higher percentage of chronic acalculous cholecystitis. Obesity is associated with Type II diabetes and hyperlipidemia in murine models. In addition, we have previously demonstrated that serum glucose, insulin, cholesterol, and triglycerides correlated with gallbladder contractility in murine models.