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  • 1
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    Suppression of oxidative stress by beta-hydroxybutyrate, an endogenous histone deacetylase inhibitor (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-12
    Description: Concentrations of acetyl-coenzyme A and nicotinamide adenine dinucleotide (NAD(+)) affect histone acetylation and thereby couple cellular metabolic status and transcriptional regulation. We report that the ketone body d-beta-hydroxybutyrate (betaOHB) is an endogenous and specific inhibitor of class I histone deacetylases (HDACs). Administration of exogenous betaOHB, or fasting or calorie restriction, two conditions associated with increased betaOHB abundance, all increased global histone acetylation in mouse tissues. Inhibition of HDAC by betaOHB was correlated with global changes in transcription, including that of the genes encoding oxidative stress resistance factors FOXO3A and MT2. Treatment of cells with betaOHB increased histone acetylation at the Foxo3a and Mt2 promoters, and both genes were activated by selective depletion of HDAC1 and HDAC2. Consistent with increased FOXO3A and MT2 activity, treatment of mice with betaOHB conferred substantial protection against oxidative stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3735349/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shimazu, Tadahiro -- Hirschey, Matthew D -- Newman, John -- He, Wenjuan -- Shirakawa, Kotaro -- Le Moan, Natacha -- Grueter, Carrie A -- Lim, Hyungwook -- Saunders, Laura R -- Stevens, Robert D -- Newgard, Christopher B -- Farese, Robert V Jr -- de Cabo, Rafael -- Ulrich, Scott -- Akassoglou, Katerina -- Verdin, Eric -- P30 DK026743/DK/NIDDK NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 DK056084/DK/NIDDK NIH HHS/ -- T32 AG000212/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2013 Jan 11;339(6116):211-4. doi: 10.1126/science.1227166. Epub 2012 Dec 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23223453" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Hydroxybutyric Acid/blood/*metabolism/pharmacology ; Acetylation ; Animals ; Caloric Restriction ; Catalase/metabolism ; Fasting ; Forkhead Transcription Factors/genetics ; HEK293 Cells ; Histone Deacetylase Inhibitors/blood/*metabolism/pharmacology ; Histone Deacetylases/genetics/*metabolism ; Histones/metabolism ; Humans ; Kidney/drug effects/*metabolism ; Lipid Peroxidation ; Metallothionein/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; *Oxidative Stress/genetics ; Promoter Regions, Genetic ; RNA, Small Interfering ; Superoxide Dismutase/metabolism ; Transcription, Genetic ; Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    p75 neurotrophin receptor regulates glucose homeostasis and insulin sensitivity (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-03-28
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 3
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    p75NTR regulates glucose metabolism [Medical Sciences] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-04-11
    Description: Insulin resistance is a key factor in the etiology of type 2 diabetes. Insulin-stimulated glucose uptake is mediated by the glucose transporter 4 (GLUT4), which is expressed mainly in skeletal muscle and adipose tissue. Insulin-stimulated translocation of GLUT4 from its intracellular compartment to the plasma membrane is regulated by small guanosine triphosphate hydrolases (GTPases) and is essential for the maintenance of normal glucose homeostasis. Here we show that the p75 neurotrophin receptor (p75NTR) is a regulator of glucose uptake and insulin resistance. p75NTR knockout mice show increased insulin sensitivity on normal chow diet, independent of changes in body weight. Euglycemic-hyperinsulinemic clamp studies demonstrate that deletion of the p75NTR gene increases the insulin-stimulated glucose disposal rate and suppression of hepatic glucose production. Genetic depletion or shRNA knockdown of p75NTR in adipocytes or myoblasts increases insulin-stimulated glucose uptake and GLUT4 translocation. Conversely, overexpression of p75NTR in adipocytes decreases insulin-stimulated glucose transport. In adipocytes, p75NTR forms a complex with the Rab5 family GTPases Rab5 and Rab31 that regulate GLUT4 trafficking. Rab5 and Rab31 directly interact with p75NTR primarily via helix 4 of the p75NTR death domain. Adipocytes from p75NTR knockout mice show increased Rab5 and decreased Rab31 activities, and dominant negative Rab5 rescues the increase in glucose uptake seen in p75NTR knockout adipocytes. Our results identify p75NTR as a unique player in glucose metabolism and suggest that signaling from p75NTR to Rab5 family GTPases may represent a unique therapeutic target for insulin resistance and diabetes.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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