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      Transcriptional control of brown and beige fat development and function

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          Abstract

          Adipose tissue, once viewed as an inert organ of energy storage, is now appreciated to be a central node for the dynamic regulation of systemic metabolism. There are three general types of adipose tissue: white, brown, and brown-in-white or “beige” fat. All three types of adipose tissue communicate extensively with other organs in the body including skin, liver, pancreas, muscle, and brain to maintain energy homeostasis. When energy intake chronically exceeds energy expenditure, obesity and its comorbidities can develop. Thus, understanding the molecular mechanisms by which different types of adipose tissues develop and function could uncover new therapies for combating disorders of energy imbalance. In this article, we highlight recent findings on the transcriptional and chromatin-mediated regulation of brown and beige adipose tissue activity.

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          Peroxisome proliferator-activated receptor alpha mediates the adaptive response to fasting.

          S. Kersten, J. Seydoux, J Peters … (1999)
          Prolonged deprivation of food induces dramatic changes in mammalian metabolism, including the release of large amounts of fatty acids from the adipose tissue, followed by their oxidation in the liver. The nuclear receptor known as peroxisome proliferator-activated receptor alpha (PPARalpha) was found to play a role in regulating mitochondrial and peroxisomal fatty acid oxidation, suggesting that PPARalpha may be involved in the transcriptional response to fasting. To investigate this possibility, PPARalpha-null mice were subjected to a high fat diet or to fasting, and their responses were compared with those of wild-type mice. PPARalpha-null mice chronically fed a high fat diet showed a massive accumulation of lipid in their livers. A similar phenotype was noted in PPARalpha-null mice fasted for 24 hours, who also displayed severe hypoglycemia, hypoketonemia, hypothermia, and elevated plasma free fatty acid levels, indicating a dramatic inhibition of fatty acid uptake and oxidation. It is shown that to accommodate the increased requirement for hepatic fatty acid oxidation, PPARalpha mRNA is induced during fasting in wild-type mice. The data indicate that PPARalpha plays a pivotal role in the management of energy stores during fasting. By modulating gene expression, PPARalpha stimulates hepatic fatty acid oxidation to supply substrates that can be metabolized by other tissues.
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            Transcriptional control of brown fat determination by PRDM16.

            Patrick Seale, Shingo Kajimura, Wenli Yang … (2007)
            Brown fat cells are specialized to dissipate energy and can counteract obesity; however, the transcriptional basis of their determination is largely unknown. We show here that the zinc-finger protein PRDM16 is highly enriched in brown fat cells compared to white fat cells. When expressed in white fat cell progenitors, PRDM16 activates a robust brown fat phenotype including induction of PGC-1alpha, UCP1, and type 2 deiodinase (Dio2) expression and a remarkable increase in uncoupled respiration. Transgenic expression of PRDM16 at physiological levels in white fat depots stimulates the formation of brown fat cells. Depletion of PRDM16 through shRNA expression in brown fat cells causes a near total loss of the brown characteristics. PRDM16 activates brown fat cell identity at least in part by simultaneously activating PGC-1alpha and PGC-1beta through direct protein binding. These data indicate that PRDM16 can control the determination of brown fat fate.
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              A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction.

              K Clement, C. Vaisse, N Lahlou … (1998)
              The adipocyte-specific hormone leptin, the product of the obese (ob) gene, regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure. Leptin acts through the leptin receptor, a single-transmembrane-domain receptor of the cytokine-receptor family. In rodents, homozygous mutations in genes encoding leptin or the leptin receptor cause early-onset morbid obesity, hyperphagia and reduced energy expenditure. These rodents also show hypercortisolaemia, alterations in glucose homeostasis, dyslipidaemia, and infertility due to hypogonadotropic hypogonadisms. In humans, leptin deficiency due to a mutation in the leptin gene is associated with early-onset obesity. Here we describe a homozygous mutation in the human leptin receptor gene that results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains. In addition to their early-onset morbid obesity, patients homozygous for this mutation have no pubertal development and their secretion of growth hormone and thyrotropin is reduced. These results indicate that leptin is an important physiological regulator of several endocrine functions in humans.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101264860
                Journal ID (pubmed-jr-id): 32902
                Journal ID (nlm-ta): Obesity (Silver Spring)
                Journal ID (iso-abbrev): Obesity (Silver Spring)
                Title: Obesity (Silver Spring, Md.)
                ISSN (Print): 1930-7381
                ISSN (Electronic): 1930-739X
                Publication date Nihms-submitted: 24 September 2018
                Publication date (Print): January 2019
                Publication date PMC-release: 01 July 2019
                Volume: 27
                Issue: 1
                Pages: 13-21
                Affiliations
                [1 ]Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
                [2 ]Department of Cell and Developmental Biology, Smilow Center for Translational Research, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
                Author notes
                Correspondence should be addressed to: Patrick Seale, Perelman School of Medicine at the University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Blvd, Rm. 12-105, Philadelphia, PA, 19104. USA Tel: +1-215-573-8856 Fax: +1215-898-5408, sealep@ 123456pennmedicine.upenn.edu
                Article
                Manuscript ID: NIHMS1506778
                DOI: 10.1002/oby.22334
                PMC ID: 6309799
                PubMed ID: 30569639
                SO-VID: 38a8861b-cd67-4d11-afa8-2a17ea9a10ed
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                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

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                Subject: Article

                ScienceOpen disciplines: Medicine
                Keywords: thermogenesis,brown fat,beige fat,transcription,metabolism
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: thermogenesis, brown fat, beige fat, transcription, metabolism

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