Resistin-Like Molecule Alpha Reduces Gallbladder Optimal Tension

Al-Azzawi, Hayder H.; Mathur, Abhishek; Lu, Da-Yong; Swartz-Basile, Deborah A.; Nakeeb, Attila; Pitt, Henry A.

doi:10.1007/s11605-006-0039-1

Cited by 16 publications

(8 citation statements)

References 27 publications

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“…In addition, recent reports that overweight Crohn's disease patients (body mass index >24) develop more severe disease (as indicated by more frequent anoperineal complications, a marked year-by-year disease activity and require earlier surgical intervention), compared with lean patients (35, 36). In agreement with our data, a recent study by Al-Azzawi et al demonstrated that prolonged administration of intraperitoneal Relm-α (but not resistin), significantly increased insulin resistance that is associated with decreased gallbladder tension (37). Thus, while Relm-α and resistin share similar structure and expression pattern, they may have distinct roles under different settings.…”

Section: Discussionsupporting

confidence: 93%

Resistin-Like Molecule α Decreases Glucose Tolerance during Intestinal Inflammation

Munitz

Seidu

Cole

et al. 2009

The Journal of Immunology

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Resistin-like molecule α (Relm-α) is a secreted cysteine-rich protein belonging to a newly defined family of proteins, including resistin, Relm-β, and Relm-γ. Resistin was initially defined based on its insulin resistance activity, but the family members are highly up-regulated in various inflammatory states, especially those involving intestinal inflammation. In this study, we report the role of Relm-α at baseline and following an experimental model of colitis. Relm-α was readily detected in the serum at baseline (4–5 ng/ml), and its level was regulated by energy uptake. Retnla−/− mice had decreased baseline circulating leptin levels, but displayed normal glucose, glucose clearance, and insulin levels. Following exposure to the oral innate trigger dextran sodium sulfate (DSS), a nonredundant proinflammatory role for Relm-α was uncovered as Retnla−/− mice were markedly protected from DSS-induced disease activity and histopathological features. Relm-α regulated eosinophil-directed cytokines (e.g., IL-5, CCL11/eotaxin-1, and CCL5/RANTES) and IL-17 ex vivo. Consistently, DSS-treated Retnla−/− mice displayed substantially decreased eosinophil accumulation and decreased phosphorylation of NF-κB, ERK1/2, and p38 in macrophages and eosinophils. Following DSS exposure, serum level of Relm-α was up-regulated, and DSS-treated Retnla−/− mice were markedly protected from hyperglycemia induced by glucose injection independent of changes in insulin levels. Retnla−/− mice were protected from increases in gut hormone serum levels of gastric inhibitory polypeptide and peptide YY that were induced following DSS treatment. These findings demonstrate a central proinflammatory role for Relm-α in the regulation of colonic inflammation and a novel link between colonic injury, glucose tolerance, and energy intake.

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Section: Discussionsupporting

confidence: 93%

Resistin-Like Molecule α Decreases Glucose Tolerance during Intestinal Inflammation

Munitz

Seidu

Cole

et al. 2009

The Journal of Immunology

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“…[28][29][30][31] These inflammatory changes predispose to GD by impairing the muscle cell function of the gallbladder wall resulting from increased insulin resistance, and by impairing absorptive and secretive functions of the gallbladder. [32][33][34] Our results support this theory as FGV was found to be increased in patients with NAFLD, possibly due to the decreased absorptive function of gallbladder. A recent study by Pellegrinelli et al 33 has indeed shown that inflammation caused by human adipocytes causes decreased expression of contractile proteins in myotubes.…”

supporting

confidence: 81%

Impaired Gallbladder Motility and Increased Gallbladder Wall Thickness in Patients with Nonalcoholic Fatty Liver Disease

Çolak

Bozbey

Erim

et al. 2016

J Neurogastroenterol Motil

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Background/AimsNonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver disease worldwide. Along with the increase in the incidence of NAFLD and associated obesity, an increase in gallbladder disease (GD) has been noted. This has led to the identification of a new disease entity called fatty GD. There is a gap in the literature on the dynamics of gallbladder function in patients with NAFLD. MethodsAn observational case-control study, a total of 50 patients with biopsy proven NAFLD without gallbladder stone/sludge and 38 healthy comparison subjects were enrolled. Fasting, postprandial gallbladder volumes (PGV), gallbladder ejection fraction (GEF), and fasting gallbladder wall thickness (FGWT) were measured by real-time 2-dimensional ultrasonography. ResultsFasting gallbladder wall thickness, fasting gallbladder volumes and PGV were significantly higher in patients with NAFLD than control subjects (P < 0.001, P = 0.006, and P < 0.001, respectively). Gallbladder ejection fraction was significantly lower in the NAFLD group than the controls (P = 0.008). The presence of NAFLD was an independent predictor for GEF, PGV, and FGWT. Also, steatosis grade was an independent predictor for GEF, and GEF was significantly lower in the nonalcoholic steatohepatitis (NASH) subgroup than the controls. ConclusionsGallbladder dysfunction and increase in gallbladder wall thickness exists in asymptomatic (without stone/sludge and related symptoms) patients with NAFLD and are useful in identifying fatty GD. Measurement of these variables in NAFLD patients may be useful in identifying those at higher risk for GD.

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“…Furthermore, hepatic insulin resistance in a mouse model has been identified as the molecular link between MS and risk of cholesterol gallstones, by way of its ability to increase biliary cholesterol secretion [28]. Increased hepatic cholesterol secretion, supersaturation of bile and gallbladder dysmotility are all exacerbated with conditions of the MS, providing the ideal setting for the development of gallstones [73]. Interestingly, an alarmingly high prevalence of the MS is observed in societies where ‘westernized’ nutrition prevails and its dietary constituents, e.g.…”

Section: Lifestyle Factorsmentioning

confidence: 99%

Gallstones: Environment, Lifestyle and Genes

Stokes

Krawczyk

Lammert³

2011

Dig Dis

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Gallstone disease represents one of the most common and costly gastroenterological disorders. In Germany, 0.25% of the population undergo cholecystectomy per year, and cholelithiasis incurs annual medical expenses of more than USD 6.5 billion in the United States. The paradigm of environmental risk factors for gallstones has lately been challenged by genetic studies in experimental models and humans. The analysis of more than 40,000 Swedish twin pairs with gallstones demonstrated that genetic factors account for 25% of the phenotypic variance. Since then, studies employing genome-wide association analysis, case-control cohorts and analysis of sib-pairs in families with gallstones have expanded our knowledge of ‘gallstone genes’. Indeed, gallstone disease phenotypes are likely to result from the complex interaction of genetic factors, chronic overnutrition with carbohydrates, depletion of dietary fibre and other not fully defined environmental factors including physical inactivity and infections. This hypothesis is supported by the profound increases of cholesterol gallstone prevalence rates in Native Americans, post-war European countries and current urban centres in East Asia, all of which were associated with ‘westernized’ nutrition. Herein, we summarise the spectrum of environmental and genetic risk factors which should pave the way to ‘personalised’ strategies for the prevention and therapy of gallstones.

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Resistin-Like Molecule Alpha Reduces Gallbladder Optimal Tension

Cited by 16 publications

References 27 publications

Resistin-Like Molecule α Decreases Glucose Tolerance during Intestinal Inflammation

Resistin-Like Molecule α Decreases Glucose Tolerance during Intestinal Inflammation

Impaired Gallbladder Motility and Increased Gallbladder Wall Thickness in Patients with Nonalcoholic Fatty Liver Disease

Gallstones: Environment, Lifestyle and Genes

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