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|Title:||Ferroportin Expression in Adipocytes Does Not Contribute to Iron Homeostasis or Metabolic Responses to a High Calorie Diet.|
|Authors:||Britton, Laurence;Jaskowski, Lesley-Anne;Bridle, Kim;Secondes, Eriza;Wallace, Daniel;Santrampurwala, Nishreen;Reiling, Janske;Miller, Gregory;Mangiafico, Salvatore;Andrikopoulos, Sofianos;Subramaniam, V Nathan;Crawford, Darrell|
|Affiliation:||Gallipoli Medical Research Institute, Greenslopes Private Hospital, Greenslopes, Queensland, Australia|
The University of Queensland, Herston, Queensland, Australia..
Department of Gastroenterology, Princess Alexandra Hospital, Queensland, Australia
QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia
Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Kelvin Grove, Queensland, Australia
Department of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands
Envoi Pathology, Kelvin Grove, Queensland, Australia..
Department of Medicine, Austin Health, the University of Melbourne, Heidelberg, Victoria, Australia
|Citation:||Cellular and molecular gastroenterology and hepatology 2018; 5(3): 319-331|
|Abstract:||Iron has an increasingly recognized role in the regulation of adipose tissue function, including the expression of adipokines involved in the pathogenesis of nonalcoholic fatty liver disease. The cellular iron exporter, ferroportin, has been proposed as being a key determinant of adipocyte iron homeostasis. We studied an adipocyte-specific ferroportin (Fpn1) knockout mouse model, using anAdipoq-Cre recombinase drivenFpn1deletion and fed mice according to the fast food diet model of nonalcoholic steatohepatitis. We showed successful selective deletion ofFpn1in adipocytes, but found that this did not lead to increased adipocyte iron stores as measured by atomic absorption spectroscopy or histologically quantified iron granules after staining with 3,3'-diaminobenzidine-enhanced Perls' stain. Mice with adipocyte-specificFpn1deletion did not show dysregulation of adiponectin, leptin, resistin, or retinol-binding protein-4 expression. Similarly, adipocyte-specificFpn1deletion did not affect insulin sensitivity during hyperinsulinemic-euglycemic clamp studies or lead to histologic evidence of increased liver injury. We have shown, however, that the fast food diet model of nonalcoholic steatohepatitis generates an increase in adipose tissue macrophage infiltration with crown-like structures, as seen in human beings, further validating the utility of this model. Ferroportin may not be a key determinant of adipocyte iron homeostasis in this knockout model. Further studies are needed to determine the mechanisms of iron metabolism in adipocytes and adipose tissue.|
|Subjects:||AAS, atomic absorption spectroscopy|
ANOVA, analysis of variance
AUC, area under the curve
EFP, epididymal fat pad
FKO, ferroportin knockout
Ferroportin Flox, Fpn1fl/fl
HIC, hepatic iron concentration
NAFLD, nonalcoholic fatty liver disease
NASH, nonalcoholic steatohepatitis
Nonalcoholic Fatty Liver Disease
PCR, polymerase chain reaction
RBP-4, retinol binding protein-4
Tfr1, transferrin receptor-1
bp, base pair
cDNA, complementary DNA
mRNA, messenger RNA
|Appears in Collections:||Journal articles|
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