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  1. Article ; Online: Recruiting a transcription factor in the liver to prevent atherosclerosis.

    Attie, Alan D

    The Journal of clinical investigation

    2021  Volume 131, Issue 22

    Abstract: Hypertriglyceridemia is associated with obesity, diabetes, and atherosclerosis. While lipoprotein lipase (LPL) hydrolyzes triglyceride (TG) cargo into remnant lipoproteins with atherogenic properties, how remnant lipoprotein clearance relates to ... ...

    Abstract Hypertriglyceridemia is associated with obesity, diabetes, and atherosclerosis. While lipoprotein lipase (LPL) hydrolyzes triglyceride (TG) cargo into remnant lipoproteins with atherogenic properties, how remnant lipoprotein clearance relates to atherosclerosis in people with diabetes remains unclear. In this issue of the JCI, Shimizu-Albergine et al. examined the effects of the basic leucine zipper transcription factor CREBH, which induces genes that activate LPL in mouse models of type I diabetes. Overexpression of a CREBH fragment reduced apolipoprotein C3 (APOC3) levels, which reduced plasma TGs. Notably, the TGs were lowered by a mechanism that was independent of LPL, and atherosclerosis was alleviated by enhanced lipoprotein remnant clearance as opposed to increased lipolysis of TG-rich lipoprotein precursors. A proinflammatory mechanism likely underlies the atherogenicity of remnant lipoproteins. These findings suggest that modifying CREBH expression in the liver may ameliorate atherosclerosis and, perhaps, other diabetes complications.
    MeSH term(s) Animals ; Apolipoprotein C-III ; Atherosclerosis/genetics ; Atherosclerosis/prevention & control ; Hyperlipidemias ; Liver ; Mice ; Transcription Factors ; Triglycerides
    Chemical Substances Apolipoprotein C-III ; Transcription Factors ; Triglycerides
    Language English
    Publishing date 2021-11-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI154677
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Sorting through the extensive and confusing roles of sortilin in metabolic disease.

    Mitok, Kelly A / Keller, Mark P / Attie, Alan D

    Journal of lipid research

    2022  Volume 63, Issue 8, Page(s) 100243

    Abstract: Sortilin is a post-Golgi trafficking receptor homologous to the yeast vacuolar protein sorting receptor 10 (VPS10). The VPS10 motif on sortilin is a 10-bladed β-propeller structure capable of binding more than 50 proteins, covering a wide range of ... ...

    Abstract Sortilin is a post-Golgi trafficking receptor homologous to the yeast vacuolar protein sorting receptor 10 (VPS10). The VPS10 motif on sortilin is a 10-bladed β-propeller structure capable of binding more than 50 proteins, covering a wide range of biological functions including lipid and lipoprotein metabolism, neuronal growth and death, inflammation, and lysosomal degradation. Sortilin has a complex cellular trafficking itinerary, where it functions as a receptor in the trans-Golgi network, endosomes, secretory vesicles, multivesicular bodies, and at the cell surface. In addition, sortilin is associated with hypercholesterolemia, Alzheimer's disease, prion diseases, Parkinson's disease, and inflammation syndromes. The 1p13.3 locus containing SORT1, the gene encoding sortilin, carries the strongest association with LDL-C of all loci in human genome-wide association studies. However, the mechanism by which sortilin influences LDL-C is unclear. Here, we review the role sortilin plays in cardiovascular and metabolic diseases and describe in detail the large and often contradictory literature on the role of sortilin in the regulation of LDL-C levels.
    MeSH term(s) Adaptor Proteins, Vesicular Transport ; Cholesterol, LDL ; Genome-Wide Association Study ; Humans ; Hypercholesterolemia ; Inflammation ; Protein Transport
    Chemical Substances Adaptor Proteins, Vesicular Transport ; Cholesterol, LDL ; sortilin (Z020Y8WIJ4)
    Language English
    Publishing date 2022-06-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1016/j.jlr.2022.100243
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 175: Show issues Location:
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  3. Book ; Conference proceedings: Molecular biology of atherosclerosis

    Attie, Alan D.

    proceedings of the Twentieth Steenbock Symposium held June 3 through June 5, 1990 ... Madison, Wisconsin, U.S.A

    1990  

    Event/congress Harry Steenbock Symposium (20, 1990, MadisonWis.)
    Author's details ed. by Alan D. Attie
    Keywords Atherosclerosis / congresses ; Arteriosklerose ; Molekularpathologie
    Subject Arterienverkalkung ; Atherosklerose ; Arteriosclerosis
    Size XVIII, 238 S. : Ill., graph. Darst.
    Edition 1. print.
    Publisher Elsevier
    Publishing place New York u.a.
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT003902580
    ISBN 0-444-01587-6 ; 978-0-444-01587-7
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    1991 A 4670 order for loan Magazin

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  4. Article ; Online: How do reducing equivalents increase insulin secretion?

    Attie, Alan D

    The Journal of clinical investigation

    2015  Volume 125, Issue 10, Page(s) 3754–3756

    Abstract: Glucose stimulation of insulin secretion in pancreatic β cells involves cell depolarization and subsequent opening of voltage-dependent Ca2+ channels to elicit insulin granule exocytosis. This pathway alone does not account for the entire magnitude of ... ...

    Abstract Glucose stimulation of insulin secretion in pancreatic β cells involves cell depolarization and subsequent opening of voltage-dependent Ca2+ channels to elicit insulin granule exocytosis. This pathway alone does not account for the entire magnitude of the secretory response in β cells. In this issue, Ferdaoussi, Dai, and colleagues reveal that insulin secretion is amplified by cytosolic isocitrate dehydrogenase-dependent transfer of reducing equivalents, which generates NADPH and reduced glutathione, which in turn activates sentrin/SUMO-specific protease-1 (SENP1). β Cell-specific deletion of Senp1 in murine models reduced the amplification of insulin exocytosis, resulting in impaired glucose tolerance. Further, their studies demonstrate that restoring intracellular NADPH or activating SENP1 improves insulin exocytosis in human β cells from donors with type 2 diabetes, suggesting a potential therapeutic target to augment insulin production.
    MeSH term(s) Animals ; Diabetes Mellitus, Type 2/physiopathology ; Endopeptidases/physiology ; Humans ; Insulin/metabolism ; Insulin Secretion ; Islets of Langerhans/metabolism ; Isocitrates/metabolism ; Male
    Chemical Substances Insulin ; Isocitrates ; Endopeptidases (EC 3.4.-)
    Language English
    Publishing date 2015-09-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI84011
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  5. Article: Systems genetics approach uncovers associations between host amylase locus, gut microbiome and metabolic traits in hyperlipidemic mice.

    Zhang, Qijun / Hutchison, Evan R / Pan, Calvin / Warren, Matthew F / Keller, Mark P / Attie, Alan D / Lusis, Aldons J / Rey, Federico E

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The molecular basis for how host genetic variation impacts gut microbial community and bacterial metabolic niches remain largely unknown. We leveraged 90 inbred hyperlipidemic mouse strains from the Hybrid Mouse Diversity Panel (HMDP), previously studied ...

    Abstract The molecular basis for how host genetic variation impacts gut microbial community and bacterial metabolic niches remain largely unknown. We leveraged 90 inbred hyperlipidemic mouse strains from the Hybrid Mouse Diversity Panel (HMDP), previously studied for a variety of cardio-metabolic traits. Metagenomic analysis of cecal DNA followed by genome-wide association analysis identified genomic loci that were associated with microbial enterotypes in the gut. Among these we detected a genetic locus surrounding multiple amylase genes that was associated with abundances of Firmicutes (
    Language English
    Publishing date 2024-03-03
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.28.582610
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The insulin centennial-100 years of milestones in biochemistry.

    Attie, Alan D / Tang, Qi-Qun / Bornfeldt, Karin E

    Journal of lipid research

    2021  Volume 62, Page(s) 100132

    MeSH term(s) Animals ; Biochemistry ; Blood Glucose/metabolism ; Humans ; Hyperglycemia/metabolism ; Insulin/metabolism ; Lipid Metabolism ; Lipids/chemistry
    Chemical Substances Blood Glucose ; Insulin ; Lipids
    Language English
    Publishing date 2021-10-28
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1016/j.jlr.2021.100132
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  7. Article ; Online: The insulin centennial-100 years of milestones in biochemistry.

    Attie, Alan D / Tang, Qi-Qun / Bornfeldt, Karin E

    The Journal of biological chemistry

    2021  Volume 297, Issue 5, Page(s) 101278

    MeSH term(s) Biochemistry/history ; History, 20th Century ; History, 21st Century ; Humans ; Insulin/history
    Chemical Substances Insulin
    Language English
    Publishing date 2021-10-28
    Publishing country United States
    Document type Editorial ; Historical Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2021.101278
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  8. Article ; Online: Introduction to the Thematic Review Series: Adipose Biology.

    Gupta, Rana K / Attie, Alan D

    Journal of lipid research

    2019  Volume 60, Issue 10, Page(s) 1646–1647

    MeSH term(s) Adipose Tissue/cytology ; Adipose Tissue/pathology ; Humans ; Obesity/pathology
    Language English
    Publishing date 2019-08-14
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 80154-9
    ISSN 1539-7262 ; 0022-2275
    ISSN (online) 1539-7262
    ISSN 0022-2275
    DOI 10.1194/jlr.IN119000337
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  9. Article ; Online: Insights into obesity and diabetes at the intersection of mouse and human genetics.

    Kebede, Melkam A / Attie, Alan D

    Trends in endocrinology and metabolism: TEM

    2014  Volume 25, Issue 10, Page(s) 493–501

    Abstract: Many of our insights into obesity and diabetes come from studies in mice carrying natural or induced mutations. In parallel, genome-wide association studies (GWAS) in humans have identified numerous genes that are causally associated with obesity and ... ...

    Abstract Many of our insights into obesity and diabetes come from studies in mice carrying natural or induced mutations. In parallel, genome-wide association studies (GWAS) in humans have identified numerous genes that are causally associated with obesity and diabetes, but discovering the underlying mechanisms required in-depth studies in mice. We discuss the advantages of studying natural variation in mice and summarize several examples where the combination of human and mouse genetics opened windows into fundamental physiological pathways. A noteworthy example is the melanocortin-4 receptor (MC4R) and its role in energy balance. The pathway was delineated by discovering the gene responsible for the Agouti mutation in mice. With more targeted phenotyping, we predict that additional pathways relevant to human pathophysiology will be discovered.
    MeSH term(s) Animals ; Diabetes Mellitus/genetics ; Diabetes Mellitus/physiopathology ; Genome-Wide Association Study ; Humans ; Mice ; Obesity/genetics ; Obesity/physiopathology ; Signal Transduction/genetics
    Language English
    Publishing date 2014-07-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2014.06.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Genetic Analysis of Obesity-Induced Diabetic Nephropathy in BTBR Mice.

    Keller, Mark P / O'Connor, Chris / Bitzer, Markus / Schueler, Kathryn L / Stapleton, Donald S / Emfinger, Christopher H / Broman, Aimee Teo / Hodgin, Jeffrey B / Attie, Alan D

    Diabetes

    2023  Volume 73, Issue 2, Page(s) 312–317

    MeSH term(s) Humans ; Mice ; Animals ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/pathology ; Leptin ; Diabetes Mellitus, Type 2/genetics ; Mice, Inbred C57BL ; Disease Models, Animal ; Mice, Inbred Strains ; Obesity/complications ; Obesity/genetics ; Mice, Obese
    Chemical Substances Leptin
    Language English
    Publishing date 2023-12-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db23-0444
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