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      Lipid Processing in the Brain: A Key Regulator of Systemic Metabolism

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          Abstract

          Metabolic disorders, particularly aberrations in lipid homeostasis, such as obesity, type 2 diabetes mellitus, and hypertriglyceridemia often manifest together as the metabolic syndrome (MetS). Despite major advances in our understanding of the pathogenesis of these disorders, the prevalence of the MetS continues to rise. It is becoming increasingly apparent that intermediary metabolism within the central nervous system is a major contributor to the regulation of systemic metabolism. In particular, lipid metabolism within the brain is tightly regulated to maintain neuronal structure and function and may signal nutrient status to modulate metabolism in key peripheral tissues such as the liver. There is now a growing body of evidence to suggest that fatty acid (FA) sensing in hypothalamic neurons via accumulation of FAs or FA metabolites may signal nutritional sufficiency and may decrease hepatic glucose production, lipogenesis, and VLDL-TG secretion. In addition, recent studies have highlighted the existence of liver-related neurons that have the potential to direct such signals through parasympathetic and sympathetic nervous system activity. However, to date whether these liver-related neurons are FA sensitive remain to be determined. The findings discussed in this review underscore the importance of the autonomic nervous system in the regulation of systemic metabolism and highlight the need for further research to determine the key features of FA neurons, which may serve as novel therapeutic targets for the treatment of metabolic disorders.

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          AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy.

          D Hardie (2007)
          The SNF1/AMP-activated protein kinase (AMPK) family maintains the balance between ATP production and consumption in all eukaryotic cells. The kinases are heterotrimers that comprise a catalytic subunit and regulatory subunits that sense cellular energy levels. When energy status is compromised, the system activates catabolic pathways and switches off protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. Surprisingly, recent results indicate that the AMPK system is also important in functions that go beyond the regulation of energy homeostasis, such as the maintenance of cell polarity in epithelial cells.
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            Apolipoprotein E: structure and function in lipid metabolism, neurobiology, and Alzheimer's diseases.

            Apolipoprotein (apo) E is a multifunctional protein with central roles in lipid metabolism, neurobiology, and neurodegenerative diseases. It has three major isoforms (apoE2, apoE3, and apoE4) with different effects on lipid and neuronal homeostasis. A major function of apoE is to mediate the binding of lipoproteins or lipid complexes in the plasma or interstitial fluids to specific cell-surface receptors. These receptors internalize apoE-containing lipoprotein particles; thus, apoE participates in the distribution/redistribution of lipids among various tissues and cells of the body. In addition, intracellular apoE may modulate various cellular processes physiologically or pathophysiologically, including cytoskeletal assembly and stability, mitochondrial integrity and function, and dendritic morphology and function. Elucidation of the functional domains within this protein and of the three-dimensional structure of the major isoforms of apoE has contributed significantly to our understanding of its physiological and pathophysiological roles at a molecular level. It is likely that apoE, with its multiple cellular origins and multiple structural and biophysical properties, is involved widely in processes of lipid metabolism and neurobiology, possibly encompassing a variety of disorders of neuronal repair, remodeling, and degeneration by interacting with different factors through various pathways. Copyright © 2014 Elsevier Inc. All rights reserved.
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              UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals.

              The gut-derived hormone ghrelin exerts its effect on the brain by regulating neuronal activity. Ghrelin-induced feeding behaviour is controlled by arcuate nucleus neurons that co-express neuropeptide Y and agouti-related protein (NPY/AgRP neurons). However, the intracellular mechanisms triggered by ghrelin to alter NPY/AgRP neuronal activity are poorly understood. Here we show that ghrelin initiates robust changes in hypothalamic mitochondrial respiration in mice that are dependent on uncoupling protein 2 (UCP2). Activation of this mitochondrial mechanism is critical for ghrelin-induced mitochondrial proliferation and electric activation of NPY/AgRP neurons, for ghrelin-triggered synaptic plasticity of pro-opiomelanocortin-expressing neurons, and for ghrelin-induced food intake. The UCP2-dependent action of ghrelin on NPY/AgRP neurons is driven by a hypothalamic fatty acid oxidation pathway involving AMPK, CPT1 and free radicals that are scavenged by UCP2. These results reveal a signalling modality connecting mitochondria-mediated effects of G-protein-coupled receptors on neuronal function and associated behaviour.
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                Author and article information

                Contributors
                URI : http://frontiersin.org/people/u/412778
                URI : http://frontiersin.org/people/u/73427
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrinol.
                Frontiers in Endocrinology
                Frontiers Media S.A.
                1664-2392
                04 April 2017
                2017
                : 8
                : 60
                Affiliations
                [1] 1University of Colorado School of Medicine, Division of Endocrinology, Metabolism and Diabetes , Aurora, CO, USA
                [2] 2Department of Physiology, School of Medicine, Tulane University , New Orleans, LA, USA
                Author notes

                Edited by: Hubert Vaudry, University of Rouen, France

                Reviewed by: Alexandre Benani, Centre national de la recherche scientifique (CNRS), France; Miguel Lopez, Universidade de Santiago de Compostela, Spain; Christelle Le Foll, University of Zurich, Switzerland

                *Correspondence: Kimberley D. Bruce, kimberley.bruce@ 123456ucdenver.edu

                Specialty section: This article was submitted to Neuroendocrine Science, a section of the journal Frontiers in Endocrinology

                Article
                10.3389/fendo.2017.00060
                5378716
                28421037
                dcfb55ad-bd81-4c58-a49e-bc8d7a375a87
                Copyright © 2017 Bruce, Zsombok and Eckel.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 02 February 2017
                : 17 March 2017
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 142, Pages: 11, Words: 10913
                Funding
                Funded by: National Institutes of Health 10.13039/100000002
                Award ID: R01 DK089309, R01 DK099598
                Categories
                Endocrinology
                Review

                Endocrinology & Diabetes
                lipid metabolism,brain,liver,energy homeostasis,hypothalamus
                Endocrinology & Diabetes
                lipid metabolism, brain, liver, energy homeostasis, hypothalamus

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