A Ketogenic Formula Prevents Tumor Progression and Cancer Cachexia by Attenuating Systemic Inflammation in Colon 26 Tumor-Bearing Mice

Nakamura, Kentaro; Tonouchi, Hidekazu; Sasayama, Akina; Ashida, Kouzou

doi:10.3390/nu10020206

Cited by 75 publications

(55 citation statements)

References 33 publications

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“…The pathogenesis of this syndrome has not been fully elucidated but involves several metabolic and immune-mediated mechanisms, recently reviewed in [ 86 ]. In animal models, a ketogenic diet was proven effective in mitigating cancer cachexia, acting both on nutrient availability and by reducing systemic inflammation [ 87 ]. A ketogenic diet has also been administered to cachectic cancer patients showing a reduction in gluconeogenesis and circulating lactate, but there was no effect on protein turnover [ 88 ].…”

Section: Relevance Of Immunometabolism In Cancer Immunotherapymentioning

confidence: 99%

Manipulation of Glucose Availability to Boost Cancer Immunotherapies

Marchesi

Vignali

Manini

et al. 2020

Cancers

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The orchestration of T cell responses is intimately linked to the execution of metabolic processes, both in homeostasis and disease. In cancer tissues, metabolic alterations that characterize malignant transformation profoundly affect the composition of the immune microenvironment and the accomplishment of an effective anti-tumor response. The growing understanding of the metabolic regulation of immune cell function has shed light on the possibility to manipulate metabolic pathways as a strategy to improve T cell function in cancer. Among others, glucose metabolism through the glycolytic pathway is central in shaping T cell responses and emerges as an ideal target to improve cancer immunotherapy. However, metabolic manipulation requires a deep level of control over side-effects and development of biomarkers of response. Here, we summarize the metabolic control of T cell function and focus on the implications of metabolic manipulation for the design of immunotherapeutic strategies. Integrating our understanding of T cell function and metabolism will hopefully foster the forthcoming development of more effective immunotherapeutic strategies.

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Section: Relevance Of Immunometabolism In Cancer Immunotherapymentioning

confidence: 99%

Manipulation of Glucose Availability to Boost Cancer Immunotherapies

Marchesi

Vignali

Manini

et al. 2020

Cancers

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“…In recent years, the link between dietary factors and different cancers has been extensively studied [ 13 , 14 , 15 , 16 ]. Among these cancers, colorectal cancer has been reported as the third most common cancer worldwide, with nearly 1.4 million new cases diagnosed in 2012 according to the World Cancer Report 2014 [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Food Additive Sodium Benzoate (NaB) Activates NFκB and Induces Apoptosis in HCT116 Cells

Yılmaz

Karabay

2018

Molecules

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NaB, the metabolite of cinnamon and sodium salt of benzoic acid is a commonly used food and beverage preservative. Various studies have investigated NaB for its effects on different cellular models. However, the effects of NaB on cancer cell viability signaling is substantially unknown. In this study, the effects of NaB on viability parameters and NFκB, one of the most important regulators in apoptosis, were examined in HCT116 colon cancer cells. Cell culture, light microscopy, spectrophotometry, flow cytometry, and western blot were used as methods to determine cell viability, caspase-3 activity, NFκB, Bcl-xl, Bim, and PARP proteins, respectively. NaB (6.25 mM–50 mM) treatment inhibited cell viability by inducing apoptosis, which was evident with increased Annexin V-PE staining and caspase-3 activity. NFκB activation accompanied the induction of apoptosis in NaB treated cells. Inhibition of NFκB with BAY 11-7082 did not show a pronounced effect on cell viability but induced a more apoptotic profile, which was confirmed by increased PARP fragmentation and caspase-3 activity. This effect was mostly evident at 50 mM concentration of NaB. Bcl-xl levels were not affected by NaB or BAY 11-7082/NaB treatment; whereas, total Bim increased with NaB treatment. Inhibition of NFκB activity further increased Bim levels. Overall, these results suggest that NaB induces apoptosis and activates NFκB in HCT116 colon cancer cells. Activation of NFκB emerges as target in an attempt to protect cells against apoptosis.

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“…An IL-6-induced proteasomal degradation and decreased generation of skeletal muscle, via muscle-specific E3 ligase, atrogin-1, and muscle RING finger protein 1, associated with cancer cachexia that involved muscle weight and fat depletion (Recinella et al, 2017;Tisdale, 2009). The anti-inflammatory role of KD, particularly β-hydroxybutyrate, prevented the muscle cell proteolysis and degeneration in that situation (Nakamura, Tonouchi, Sasayama, & Ashida, 2018). In fact, KD has been demonstrated to cause a 45% increase in the muscle mass in pancreatic tumor (Shukla et al, 2014).…”

Section: Kd and Muscle In Diabetes Cancer And Neurodegenerationmentioning

confidence: 98%

Ketogenic diets and protective mechanisms in epilepsy, metabolic disorders, cancer, neuronal loss, and muscle and nerve degeneration

Liu

et al. 2020

J Food Biochem

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Ketogenic diet (KD), the “High‐fat, low‐carbohydrate, adequate‐protein” diet strategy, replacing glucose with ketone bodies, is effective against several diseases, from intractable epileptic seizures, metabolic disorders, tumors, autosomal dominant polycystic kidney disease, and neurodegeneration to skeletal muscle atrophy and peripheral neuropathy. Key mechanisms include augmented mitochondrial efficiency, reduced oxidative stress, and regulated phospho‐AMP‐activated protein kinase, gamma‐aminobutyric acid‐glutamate, Na+/K+ pump, leptin and adiponectin levels, ghrelin levels, lipogenesis, ketogenesis, lipolysis, and gluconeogenesis. In cancer cells, KD targets glucose metabolism, suppresses insulin‐like growth factor‐1 and PI3K/AKT/mTOR pathways, and reduces cancer cachexia and muscle waste and fatigue. An associated increased skeletal proliferator‐activated receptor‐γ coactivator‐1α activity alters systemic ketone body homeostasis, contributing toward attenuated diabetic hyperketonemia. Antioxidative and anti‐inflammatory properties enable KD enhance endurance and sports performances while preventing exercise‐induced muscle and organ debility. KD reduces metabolic syndromes‐associated allodynia and promotes peripheral axonal and sensory regeneration. This review enlightens effects of KD on various disease conditions. Practical applications It is increasingly being realized that diet plays a very important role in our fight against several diseases. This can range from neurological disorders to diabetes and cancer. In this context, the potential of KD, the “High‐fat, low‐carbohydrate, adequate‐protein” diet strategy, is increasingly being realized. In this article, we provide a comprehensive analysis of the benefits of KD against many diseases and discuss the underlying biochemical mechanisms. We hope that our write‐up will stimulate further research on KD and help generate an interest for the populations to adopt this healthy diet. It can help overcome the problems associated with weight and dysregulated metabolism.

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A Ketogenic Formula Prevents Tumor Progression and Cancer Cachexia by Attenuating Systemic Inflammation in Colon 26 Tumor-Bearing Mice

Cited by 75 publications

References 33 publications

Manipulation of Glucose Availability to Boost Cancer Immunotherapies

Manipulation of Glucose Availability to Boost Cancer Immunotherapies

Food Additive Sodium Benzoate (NaB) Activates NFκB and Induces Apoptosis in HCT116 Cells

Ketogenic diets and protective mechanisms in epilepsy, metabolic disorders, cancer, neuronal loss, and muscle and nerve degeneration

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