Impact of nitric oxide on metabolism in health and age-related disease

    Authors

    A. B. Knott;E. Bossy-Wetzel

    Comments

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    Abbreviated Journal Title

    Diabetes Obes. Metab.

    Keywords

    mitochondrial biogenesis; mitochondrial fission and fusion; nitric; oxide; PGC1-alpha; sirtuins; DYNAMIN-RELATED PROTEIN; DOMINANT OPTIC ATROPHY; PROMOTES MITOCHONDRIAL; BIOGENESIS; ENDOPLASMIC-RETICULUM STRESS; LINKED INSULIN-RESISTANCE; CYTOCHROME-C RELEASE; BROWN ADIPOSE-TISSUE; S-NITROSYLATION; ALZHEIMERS-DISEASE; SKELETAL-MUSCLE; Endocrinology & Metabolism

    Abstract

    Nitric oxide (NO) serves as a messenger molecule in a variety of physiological systems and also converts into toxic radical species that can damage cells through a process known as nitrosative stress. While the physiological roles of NO in blood vessel dilation, the nervous system and the immune system are well established, recent studies have begun to investigate the role of NO in metabolism and energy expenditure through modulation of mitochondria. NO appears to stimulate mitochondrial biogenesis in certain situations through activation of proteins such as peroxisome proliferator-activated receptor gamma (PPAR gamma) co-activator 1 alpha (PGC1-alpha). Because of this link between NO and mitochondrial biogenesis, the role of NO in certain aspects of metabolism, including exercise response, obesity, fat cell differentiation and caloric restriction, are the subject of increasing investigation. In addition to its role in mitochondrial biogenesis, NO also stimulates mitochondrial fragmentation, which can be caused by too much mitochondrial fission or inhibition of mitochondrial fusion and can result in bioenergetic failure. While the contribution of NO-mediated mitochondrial fragmentation to neurodegenerative diseases seems clear, the mechanisms by which NO causes fragmentation are uncertain and controversial. In this review, we discuss the role of NO in manipulation of mitochondrial biogenesis and dynamics and how these events contribute to human health- and age-related disease.

    Journal Title

    Diabetes Obesity & Metabolism

    Volume

    12

    Publication Date

    1-1-2010

    Document Type

    Review

    Language

    English

    First Page

    126

    Last Page

    133

    WOS Identifier

    WOS:000282375100017

    ISSN

    1462-8902

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