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Pancreatic cancer: branched-chain amino acids as putative key metabolic regulators?

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    0553167 - FGÚ 2022 RIV NL eng J - Článek v odborném periodiku
    Rossmeislová, L. - Gojda, J. - Smolková, Katarína
    Pancreatic cancer: branched-chain amino acids as putative key metabolic regulators?
    Cancer and Metastasis Reviews. Roč. 40, č. 4 (2021), s. 1115-1139. ISSN 0167-7659. E-ISSN 1573-7233
    Grant CEP: GA MZd(CZ) NV19-01-00101
    Institucionální podpora: RVO:67985823
    Klíčová slova: PDAC * cancer cachexia * insulin resistance * adipose tissue * BCAA metabolism
    Obor OECD: Endocrinology and metabolism (including diabetes, hormones)
    Impakt faktor: 9.264, rok: 2020
    Způsob publikování: Omezený přístup
    https://doi.org/10.1007/s10555-021-10016-0

    Branched-chain amino acids (BCAA) are essential amino acids utilized in anabolic and catabolic metabolism. While extensively studied in obesity and diabetes, recent evidence suggests an important role for BCAA metabolism in cancer. Elevated plasma levels of BCAA are associated with an increased risk of developing pancreatic cancer, namely pancreatic ductal adenocarcinoma (PDAC), a tumor with one of the highest 1-year mortality rates. The dreadful prognosis for PDAC patients could be attributable also to the early and frequent development of cancer cachexia, a fatal host metabolic reprogramming leading to muscle and adipose wasting. We propose that BCAA dysmetabolism is a unifying component of several pathological conditions, i.e., obesity, insulin resistance, and PDAC. These conditions are mutually dependent since PDAC ranks among cancers tightly associated with obesity and insulin resistance. It is also well-established that PDAC itself can trigger insulin resistance and new-onset diabetes. However, the exact link between BCAA metabolism, development of PDAC, and tissue wasting is still unclear. Although tissue-specific intracellular and systemic metabolism of BCAA is being intensively studied, unresolved questions related to PDAC and cancer cachexia remain, namely, whether elevated circulating BCAA contribute to PDAC etiology, what is the biological background of BCAA elevation, and what is the role of adipose tissue relative to BCAA metabolism during cancer cachexia. To cover those issues, we provide our view on BCAA metabolism at the intracellular, tissue, and whole-body level, with special emphasis on different metabolic links to BCAA intermediates and the role of insulin in substrate handling.
    Trvalý link: http://hdl.handle.net/11104/0328171

     
     
Počet záznamů: 1