Android fat distribution as predictor of severity in acute pancreatitis

Mery, Carlos M.; Rubio, Valeria; Duarte‐Rojo, Andrés; Suazo-Barahona, Jorge; Peláez-Luna, Mario; Milke, Pilar; Robles-Dı́az, Guillermo

doi:10.1159/000066099

Cited by 64 publications

(88 citation statements)

References 36 publications

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“…Ultimately, 8 studies were included in the analysis [2,3,4,5,6,7,8,9]. The detailed process is illustrated in figure 1.…”

Section: Resultsmentioning

confidence: 99%

“…Four studies involving 369 patients compared the severity and mortality of AP between normal-weight and overweight patients [2,3,4,5]. Overweight patients had more often SAP (OR 2.48, 95% CI 1.34–4.60) and a higher mortality rate (OR 3.81, 95% CI 1.22–11.83) than the normal-weight patients.…”

Section: Resultsmentioning

confidence: 99%

“…Accordingly, it is not clear whether overweight patients should be transferred early to a special center for severe AP (SAP). Some studies demonstrated no correlation between overweight and the prognosis of AP [2,3,4], while one study reported a tendency to a worse outcome in overweight patients and demonstrated that being overweight is correlated with the severity of AP [5]. …”

Section: Introductionmentioning

confidence: 99%

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Overweight Is an Additional Prognostic Factor in Acute Pancreatitis: A Meta-Analysis

Wang

Feng

et al. 2011

Pancreatology

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“…Ultimately, 8 studies were included in the analysis [2,3,4,5,6,7,8,9]. The detailed process is illustrated in figure 1.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Overweight Is an Additional Prognostic Factor in Acute Pancreatitis: A Meta-Analysis

Wang

Feng

et al. 2011

Pancreatology

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“…Obesity was recently proposed as a risk factor for acute pancreatitis [16]. Furthermore, several studies have shown that obesity is strongly associated with the onset of complications and increased mortality in patients with acute pancreatitis [8,18], and a decreased survival rate has been reported in genetically obese Zucker rats following induction of experimental acute pancreatitis [25]. These results suggest that obesity could accelerate pancreatitis in WBN/Kob-fatty rats.…”

Section: Discussionmentioning

confidence: 96%

The Influence of Dietary Restriction on the Development of Diabetes and Pancreatitis in Female WBN/Kob-Fatty Rats

et al. 2010

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Abstract:Original WBN/Kob male rats commonly develop chronic pancreatitis by the age of 3 months, while diabetes mellitus occurs at 9 months. In contrast, female rats of this strain do not show pancreatitis or diabetes. The WBN/Kob-fatty rat is a homozygous (fa/fa) congenic strain for the fa allele of the leptin receptor gene (Lepr). In WBN/Kob-fatty rats, both females and males provide a model of non-insulin-dependent diabetes with obesity. The leptin receptor fatty gene (Lepr fa ) induces obesity and hyperphagia. In the present study, we examined the effect of dietary restriction on pancreatitis and diabetes in female WBN/Kob-fatty rats. Five female fatty rats comprised a restricted feeding group with paired-feeding from 3 to 13 weeks of age, and five female lean rats comprised a control group with paired-feeding. At 13 weeks of age, two of the five female fatty rats of the control group developed diabetes mellitus, while no female fatty rats of the restricted feeding group developed diabetes mellitus. At this stage, pathological changes of the pancreas were observed in female fatty rats. All female fatty rats showed severe interlobular, intra-lobular and intra-islet fibrosis. In female fatty rats of the restricted feeding group, pathological changes of the pancreas were milder those of the free-feeding fatty group. Although dietary restriction could not completely prevent pancreatitis in female fatty rats, the development of diabetes was inhibited by its reduction of the severity of pancreatitis.

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“…In severe cases, progress to circulatory shock, acute lung injury, renal failure, and eventual death may occur (1). Despite some controversy, numerous studies have demonstrated that obesity is associated with increased risk of the severe form of AP and with development of life-threatening complications (2)(3)(4)(5)(6)(7)(8). However, the mechanism by which increased adiposity worsens AP remains unknown.…”

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confidence: 99%

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

Sennello¹,

Fayad²,

Pini³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Obesity is associated with increased severity of acute pancreatitis (AP). The cytokines IL-18 and IL-12 are elevated in patients with AP, and IL-18 levels are high in obesity. We aimed to develop a pathologically relevant model to study obesity-associated severe AP. Lean WT and obese leptin-deficient ob/ob mice received two injections of IL-12 plus IL-18. Survival, pancreatic inflammation, and biochemical markers of AP were measured. Dosing with IL-12 plus IL-18 induced 100% lethality in ob/ob mice; no lethality was observed in WT mice. Disruption of pancreatic exocrine tissue and acinar cell death as well as serum amylase and lipase levels were significantly higher in ob/ob than in WT mice. Edematous AP developed in WT mice, whereas obese ob/ob mice developed necrotizing AP. Adipose tissue necrosis and saponification were present in cytokine-injected ob/ob but not in WT mice. Severe hypocalcemia and elevated acute-phase response developed in ob/ob mice. The cytokine combination induced high levels of regenerating protein 1 and pancreatitis-associated protein expression in the pancreas of WT but not of ob/ob mice. To differentiate the contribution of obesity to that of leptin deficiency, mice received short-and long-term leptin replacement therapy. Shortterm leptin reconstitution in the absence of major weight loss did not protect ob/ob mice, whereas leptin deficiency in the absence of obesity resulted in a significant reduction in the severity of the pancreatitis. In conclusion, we developed a pathologically relevant model of AP in which obesity per se is associated with increased severity.cytokines ͉ inflammation ͉ obesity ͉ pancreas A cute pancreatitis (AP) is an inflammatory disorder that ranges from interstitial edema to confluent necrosis and hemorrhage. In severe cases, progress to circulatory shock, acute lung injury, renal failure, and eventual death may occur (1). Despite some controversy, numerous studies have demonstrated that obesity is associated with increased risk of the severe form of AP and with development of life-threatening complications (2-8). However, the mechanism by which increased adiposity worsens AP remains unknown.Leptin, a protein mainly produced by adipocytes, is a critical regulator of appetite (9). Leptin exerts important regulatory effects on inflammation (10). In the context of AP, the role of leptin remains controversial. In patients with AP, a correlation between serum leptin and disease severity has been reported by some investigators but not by others (11,12). Although in animal models administration of leptin decreases AP severity (13-16), more severe disease is present in leptin-deficient ob/ob and leptin receptordeficient db/db mice as well as leptin-receptor mutant fa/fa rats (17, 18). However, the differential effect of obesity versus leptin deficiency has not been fully investigated.IL-12 and IL-18 are two proinflammatory cytokines that drive the Th1 cell response, characterized by high levels of IFN-␥ (19). Both cytokines are mainly produced by monocytes/macrophages....

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Android fat distribution as predictor of severity in acute pancreatitis

Cited by 64 publications

References 36 publications

Overweight Is an Additional Prognostic Factor in Acute Pancreatitis: A Meta-Analysis

Overweight Is an Additional Prognostic Factor in Acute Pancreatitis: A Meta-Analysis

The Influence of Dietary Restriction on the Development of Diabetes and Pancreatitis in Female WBN/Kob-Fatty Rats

Interleukin-18, together with interleukin-12, induces severe acute pancreatitis in obese but not in nonobese leptin-deficient mice

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