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  1. Article ; Online: Hepatic safety profile of pancreatic cancer‑bearing mice fed a ketogenic diet in combination with gemcitabine.

    Cortez, Natalia E / Lanzi, Cecilia Rodriguez / Vahmani, Payam / Matsukuma, Karen / Mackenzie, Gerardo G

    Oncology letters

    2023  Volume 26, Issue 5, Page(s) 479

    Abstract: Ketogenic diets (KDs) are actively being evaluated for their potential anticancer effects. Although KDs are generally considered safe, their safety profile when combined with chemotherapy remains unknown. It is known that a KD enhances the anticancer ... ...

    Abstract Ketogenic diets (KDs) are actively being evaluated for their potential anticancer effects. Although KDs are generally considered safe, their safety profile when combined with chemotherapy remains unknown. It is known that a KD enhances the anticancer effect of gemcitabine (2',2'-difluoro-2'-deoxycytidine) in
    Language English
    Publishing date 2023-09-22
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2573196-8
    ISSN 1792-1082 ; 1792-1074
    ISSN (online) 1792-1082
    ISSN 1792-1074
    DOI 10.3892/ol.2023.14067
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Anthocyanins and their metabolites promote white adipose tissue beiging by regulating mitochondria thermogenesis and dynamics.

    Cremonini, Eleonora / Da Silva, Leane M E / Lanzi, Cecilia Rodriguez / Marino, Mirko / Iglesias, Dario E / Oteiza, Patricia I

    Biochemical pharmacology

    2024  Volume 222, Page(s) 116069

    Abstract: High-fat diet (HFD) consumption and excess nutrient availability can cause alterations in mitochondrial function and dynamics. We previously showed that anthocyanins (AC) decreased HFD-induced body weight gain and fat deposition. This study investigated: ...

    Abstract High-fat diet (HFD) consumption and excess nutrient availability can cause alterations in mitochondrial function and dynamics. We previously showed that anthocyanins (AC) decreased HFD-induced body weight gain and fat deposition. This study investigated: i) the capacity of AC to mitigate HFD-induced alterations in mitochondrial dynamics, biogenesis, and thermogenesis in mouse subcutaneous white adipose tissue (sWAT), and ii) the underlying mechanisms of action of cyanidin-3-O-glucoside (C3G), delphinidin-3-O-glucoside (D3G), and their gut metabolites on mitochondria function/dynamics in 3T3-L1 adipocytes treated with palmitate. Mice were fed control or HFD diets, added or not with 40 mg AC/kg body weight (BW). Compared to control and AC-supplemented mice, HFD-fed mice had fewer sWAT mitochondria that presented alterations of their architecture. AC supplementation prevented HFD-induced decrease of proteins involved in mitochondria biogenesis (PPARγ, PRDM16 and PGC-1α), and thermogenesis (UCP-1), and decreased AMPK phosphorylation. AC supplementation also restored the alterations in sWAT mitochondrial dynamics (Drp-1, OPA1, MNF-2, and Fis-1) and mitophagy (BNIP3L/NIX) caused by HFD consumption. In mature 3T3-L1, C3G, D3G, and their metabolites protocatechuic acid (PCA), 4-hydroxybenzaldehyde (HB), and gallic acid (GA) differentially affected palmitate-mediated decreased cAMP, PKA, AMPK, and SIRT-1 signaling pathways. C3G, D3G, and metabolites also prevented palmitate-mediated decreased expression of PPARγ, PRDM16, PGC-1α, and UCP1. Results suggest that consumption of select AC, i.e. cyanidin and delphinidin, could promote sWAT mitochondriogenesis and improve mitochondria dynamics in the context of HFD/obesity-induced dysmetabolism in part by regulating PKA, AMPK, and SIRT-1 signaling pathways.
    MeSH term(s) Mice ; Animals ; Anthocyanins/pharmacology ; Adipose Tissue, Brown/metabolism ; PPAR gamma/metabolism ; AMP-Activated Protein Kinases/metabolism ; Adipose Tissue, White/metabolism ; Obesity/metabolism ; Diet, High-Fat/adverse effects ; Transcription Factors/metabolism ; Thermogenesis ; Mitochondria/metabolism ; Glucosides/metabolism ; Palmitates/metabolism ; Mice, Inbred C57BL
    Chemical Substances Anthocyanins ; PPAR gamma ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Transcription Factors ; Glucosides ; Palmitates
    Language English
    Publishing date 2024-02-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2024.116069
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Correction: A Ketogenic Diet in Combination with Gemcitabine Increases Survival in Pancreatic Cancer KPC Mice.

    Cortez, Natalia E / Lanzi, Cecilia Rodriguez / Hong, Brian V / Xu, Jihao / Wang, Fangyi / Chen, Shuai / Ramsey, Jon J / Pontifex, Matthew G / Müller, Michael / Vauzour, David / Vahmani, Payam / Hwang, Chang-Il / Matsukuma, Karen / Mackenzie, Gerardo G

    Cancer research communications

    2022  Volume 2, Issue 12, Page(s) 1668

    Abstract: This corrects the article DOI: 10.1158/2767-9764.CRC-22-0256.][This corrects the article DOI: 10.1158/2767-9764.CRC-22-0256.]. ...

    Abstract [This corrects the article DOI: 10.1158/2767-9764.CRC-22-0256.][This corrects the article DOI: 10.1158/2767-9764.CRC-22-0256.].
    Language English
    Publishing date 2022-12-19
    Publishing country United States
    Document type Published Erratum
    ISSN 2767-9764
    ISSN (online) 2767-9764
    DOI 10.1158/2767-9764.CRC-22-0510
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Dietary (-)-epicatechin mitigates oxidative stress, NO metabolism alterations, and inflammation in renal cortex from fructose-fed rats.

    Prince, Paula D / Lanzi, Cecilia Rodríguez / Toblli, Jorge E / Elesgaray, Rosana / Oteiza, Patricia I / Fraga, César G / Galleano, Monica

    Free radical biology & medicine

    2016  Volume 90, Page(s) 35–46

    Abstract: High fructose consumption has been associated to deleterious metabolic conditions. In the kidney, high fructose causes renal alterations that contribute to the development of chronic kidney disease. Evidence suggests that dietary flavonoids have the ... ...

    Abstract High fructose consumption has been associated to deleterious metabolic conditions. In the kidney, high fructose causes renal alterations that contribute to the development of chronic kidney disease. Evidence suggests that dietary flavonoids have the ability to prevent/attenuate risk factors of chronic diseases. This work investigated the capacity of (-)-epicatechin to prevent the renal damage induced by high fructose consumption in rats. Male Sprague Dawley rats received 10% (w/v) fructose in the drinking water for 8 weeks, with or without supplementation with (-)-epicatechin (20mg/kg body weight/d) in the rat chow diet. Results showed that, in the presence of mild proteinuria, the renal cortex from fructose-fed rats exhibited fibrosis and decreases in nephrin, synaptopodin, and WT1, all indicators of podocyte function in association with: (i) increased markers of oxidative stress; (ii) modifications in the determinants of NO bioavailability, i.e., NO synthase (NOS) activity and expression; and (iii) development of a pro-inflammatory condition, manifested as NF-κB activation, and associated with high expression of TNFα, iNOS, and IL-6. Dietary supplementation with (-)-epicatechin prevented or ameliorated the adverse effects of high fructose consumption. These results suggest that (-)-epicatechin ingestion would benefit when renal alterations occur associated with inflammation or metabolic diseases.
    MeSH term(s) Animals ; Catechin/pharmacology ; Dietary Supplements ; Fructose/administration & dosage ; Glutathione Peroxidase/metabolism ; Inflammation/prevention & control ; Kidney Cortex/metabolism ; Male ; NF-kappa B/physiology ; Nitric Oxide/metabolism ; Oxidative Stress/drug effects ; Rats ; Rats, Sprague-Dawley
    Chemical Substances NF-kappa B ; Fructose (30237-26-4) ; Nitric Oxide (31C4KY9ESH) ; Catechin (8R1V1STN48) ; Glutathione Peroxidase (EC 1.11.1.9)
    Language English
    Publishing date 2016-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2015.11.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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