Biochemical Basis and Clinical Consequences of Glucolipotoxicity: A Primer

    Authors

    V. A. R. Srinivasan; V. A. Raghavan;S. Parthasarathy

    Comments

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    Abbreviated Journal Title

    Heart Fail. Clin.

    Keywords

    Glucolipotoxicity; Pancreatic beta-cell dysfunction; Insulin resistance; RAT PANCREATIC-ISLETS; DEPENDENT DIABETES-MELLITUS; INSULIN; GENE-TRANSCRIPTION; BETA-CELL DYSFUNCTION; FREE FATTY-ACIDS; ACTIVATED; SIGNALING PATHWAYS; AORTIC ENDOTHELIAL-CELLS; LOW-DENSITY LIPOPROTEINS; CORONARY-ARTERY-DISEASE; LONG-TERM EXPOSURE; Cardiac & Cardiovascular Systems

    Abstract

    Both glucose and fatty acids may have good/adaptive or toxic/maladaptive actions on the pancreatic beta cell, depending on their concentrations. Hyperglycemia, via metabolic intermediates, may result in multiple cellular effects that are toxic to the pancreatic beta cell and indeed other tissues. While free fatty acids may affect cellular processes beyond lipid metabolism by interacting with transcription factors, triglyceride rich lipoproteins are endothelial cell-toxic and facilitate atherogenesis. The paradigm of "glucolipotoxicity" espouses that increased glucose and fatty acid levels act synergistically in causing toxicity to pancreatic islets and other organs, a process that eventually leads to the multiple defects seen in the metabolic syndrome and diabetes mellitus.

    Journal Title

    Heart Failure Clinics

    Volume

    8

    Issue/Number

    4

    Publication Date

    1-1-2012

    Document Type

    Article

    Language

    English

    First Page

    501

    Last Page

    +

    WOS Identifier

    WOS:000310397100003

    ISSN

    1551-7136

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