For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
28
views
116
references
 Top references
cited by
80
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      0
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Endocrine-disrupting chemicals and fatty liver disease

      Author(s): , , ,
      Publication date Created:
      Publication date (Print):
      Journal: Nature Reviews Endocrinology
      Publisher: Springer Nature

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          In this Review, Foulds et al. posit that endocrine-disrupting chemicals are an unappreciated driver of the development and progression of nonalcoholic fatty liver disease. Experimental animal studies supporting this association are discussed, together with the challenges of establishing a causal link in humans.

          Related collections

          Most cited references116

          • Record: found
          • Abstract: found
          • Article: not found

          Hepatocyte-specific deletion of SIRT1 alters fatty acid metabolism and results in hepatic steatosis and inflammation.

          Aparna Purushotham, Thaddeus Schug, Qing Fang Xu … (2009)
          Hepatic metabolic derangements are key components in the development of fatty liver, insulin resistance, and atherosclerosis. SIRT1, a NAD+-dependent protein deacetylase, is an important regulator of energy homeostasis in response to nutrient availability. Here we demonstrate that hepatic SIRT1 regulates lipid homeostasis by positively regulating peroxisome proliferators-activated receptor alpha (PPARalpha), a nuclear receptor that mediates the adaptive response to fasting and starvation. Hepatocyte-specific deletion of SIRT1 impairs PPARalpha signaling and decreases fatty acid beta-oxidation, whereas overexpression of SIRT1 induces the expression of PPARalpha targets. SIRT1 interacts with PPARalpha and is required to activate PPARalpha coactivator PGC-1alpha. When challenged with a high-fat diet, liver-specific SIRT1 knockout mice develop hepatic steatosis, hepatic inflammation, and endoplasmic reticulum stress. Taken together, our data indicate that SIRT1 plays a vital role in the regulation of hepatic lipid homeostasis and that pharmacological activation of SIRT1 may be important for the prevention of obesity-associated metabolic diseases.
          Article 0 comments Cited 364 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Epigenetic inheritance at the agouti locus in the mouse.

            H. D. Morgan, H. Sutherland, D I Martin … (1999)
            Epigenetic modifications have effects on phenotype, but they are generally considered to be cleared on passage through the germ line in mammals, so that only genetic traits are inherited. Here we describe the inheritance of an epigenetic modification at the agouti locus in mice. In viable yellow ( A(vy)/a) mice, transcription originating in an intra-cisternal A particle (IAP) retrotransposon inserted upstream of the agouti gene (A) causes ectopic expression of agouti protein, resulting in yellow fur, obesity, diabetes and increased susceptibility to tumours. The pleiotropic effects of ectopic agouti expression are presumably due to effects of the paracrine signal on other tissues. Avy mice display variable expressivity because they are epigenetic mosaics for activity of the retrotransposon: isogenic Avy mice have coats that vary in a continuous spectrum from full yellow, through variegated yellow/agouti, to full agouti (pseudoagouti). The distribution of phenotypes among offspring is related to the phenotype of the dam; when an A(vy) dam has the agouti phenotype, her offspring are more likely to be agouti. We demonstrate here that this maternal epigenetic effect is not the result of a maternally contributed environment. Rather, our data show that it results from incomplete erasure of an epigenetic modification when a silenced Avy allele is passed through the female germ line, with consequent inheritance of the epigenetic modification. Because retrotransposons are abundant in mammalian genomes, this type of inheritance may be common.
            Article 0 comments Cited 337 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Anatomical profiling of nuclear receptor expression reveals a hierarchical transcriptional network.

              Angie L Bookout, Yangsik Jeong, Michael Downes … (2006)
              In multicellular organisms, the ability to regulate reproduction, development, and nutrient utilization coincided with the evolution of nuclear receptors (NRs), transcription factors that utilize lipophilic ligands to mediate their function. Studying the expression profile of NRs offers a simple, powerful way to obtain highly relational information about their physiologic functions as individual proteins and as a superfamily. We surveyed the expression of all 49 mouse NR mRNAs in 39 tissues, representing diverse anatomical systems. The resulting data set uncovers several NR clades whose patterns of expression indicate their ability to coordinate the transcriptional programs necessary to affect distinct physiologic pathways. Remarkably, this regulatory network divides along the following two physiologic paradigms: (1) reproduction, development, and growth and (2) nutrient uptake, metabolism, and excretion. These data reveal a hierarchical transcriptional circuitry that extends beyond individual tissues to form a meganetwork governing physiology on an organismal scale.
              Article 0 comments Cited 306 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Title: Nature Reviews Endocrinology
                Abbreviated Title: Nat Rev Endocrinol
                Publisher: Springer Nature
                ISSN (Print): 1759-5029
                ISSN (Electronic): 1759-5037
                Publication date Created: May 19 2017
                Publication date (Print): May 19 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nrendo.2017.42
                PMC ID: 5657429
                PubMed ID: 28524171
                SO-VID: 407befca-f508-4514-97e8-94fa95db8858
                Copyright © © 2017
                History

                Data availability:

                Comments

                Comment on this article