Mitochondria: The ketogenic diet—A metabolism-based therapy

Vidali, Silvia; Aminzadeh, Sepideh; Lambert, Bridget; Rutherford, Tricia; Sperl, Wolfgang; Kofler, Barbara; Feichtinger, René G.

doi:10.1016/j.biocel.2015.01.022

Cited by 155 publications

(137 citation statements)

References 38 publications

Supporting

Mentioning

133

Contrasting

Unclassified

Order By: Relevance

“…edu/DominicDAgostino, in order to increase brain endurance for deep see diving, without the onset of seizure activity. The benefits of ketogenic diets are profound and are palliative to the most significant pandemic causes of degenerative diseases today: a. Anti-inflammatory properties [8] b. Protects the Pancreas by sparing the use of Insulin, preventing Diabetes, Hypoglycemia and Metabolic Syndrome [5,6] c. Are neuro-protective and neurotrophic, preventing brain and nervous system degeneration [9][10][11] d. Promotes increased oxygenation, which is protective to all cellular tissues [12] e. Improves ATP production at the mitochondrial level [1,12] f. Aids in the Repair of DNA by preventing cancer [1,8,12] g. Slows aging by promoting elongations of telomeres h. Increases Glutathione production vital for Liver, Brain and Gut protection [1] i. Cardio-protective by increasing HDL, reducing LDL, VLDL [4] The ability to implement a ketogenic lifestyle has become 1000 times easier since this exogenous ketone supplement product has arrived on the scene [13]. It successfully induces nutritional ketosis within 20-40 min of consuming it.…”

Section: What Choice Does One Have?mentioning

confidence: 99%

Obesity is now a Pandemic Worldwide: Is the Lazy, Couch Potato, Over Eating Culture at Fault?

Novick¹

2016

AOWMC

View full text Add to dashboard Cite

Section: What Choice Does One Have?mentioning

confidence: 99%

Obesity is now a Pandemic Worldwide: Is the Lazy, Couch Potato, Over Eating Culture at Fault?

Novick¹

2016

AOWMC

View full text Add to dashboard Cite

“…As the principal site of fatty acid metabolism through β-oxidation, assessment of mitochondrial function through oxidative phosphorylation (OXPHOS) efficiency is a primary measure in KD interventions (Gano et al, 2014; Vidali et al, 2015). However, the literature primarily focuses on the relationship between the KD and brain tissue (Veech, 2004; Masino and Rho, 2012; Milder and Patel, 2012), failing to examine the tissue responsible for ketogenesis—the liver.…”

Section: Introductionmentioning

confidence: 99%

Tissue Specific Impacts of a Ketogenic Diet on Mitochondrial Dynamics in the BTBRT+tf/j Mouse

et al. 2016

View full text Add to dashboard Cite

The ketogenic diet (KD) has been utilized as a dietary therapeutic for nearly a century. One experimental model particularly responsive to the KD is the BTBRT+tf/j (BTBR) mouse, which displays phenotypic characteristics of autism spectrum disorder (ASD) and insulin resistance. Recently, the study of impaired mitochondrial function has become a focal point of research investigating the pathophysiology of ASD. As highly dynamic organelles, mitochondria undergo constant fluctuations in morphology, biogenesis, and quality control in order to maintain cellular homeostasis. An important modifier of mitochondrial dynamics is energy availability. Therefore, the aim of this study was to examine the impact of a KD on mitochondrial dynamics in the liver and brain (prefrontal cortex) of the BTBR mouse model of ASD. Juvenile male C57Bl/6 (B6) and BTBR mice were age-matched to 5 weeks of age before being fed standard chow (CD, 13% kcal fat) or a KD (75% kcal fat) for 10–14 days. Analysis of brain tissue identified differences in mitochondrial gene expression but no correlation with protein levels. Unlike in the brain, KD led to decreased levels of mitochondrial proteins in the liver, despite increased gene expression. Consistent with decreased mitochondrial proteins, we also observed decreased mtDNA for all mice on the KD, demonstrating that the KD reduces the total amount of mitochondria in the liver. In order to explain the discrepancy between protein levels and gene expression, we investigated whether mitochondrial turnover via mitophagy was increased. To this end, we examined expression levels of the mitophagy regulator BNIP3 (BCL2/adenovirus E1B 19 kd-interacting protein 3). BNIP3 gene and protein expression were significantly elevated in liver of KD animals (p < 0.05), indicating the potential activation of mitophagy. Therefore, consumption of a KD exerts highly tissue-specific effects, ultimately increasing mitochondrial turnover in the liver, while gene and protein expression in the brain remaining tightly regulated.

show abstract

“…Kardinal et al 1990 [149] Ib randomised, controlled IG: 295 cancer patients with anorexia and/or cachexia IG: cyproheptadine, 8 mg orally three times a day; CG: placebo effect of cyproheptadine (a serotonin antagonist) on the weight in patients with cancer anorexia/ cachexia patients assigned to cyproheptadine had less nausea (P = 0.02), less emesis (P = 0.11), more sedation (P = 0.07), and more dizziness (P = 0.01) than placebo patients. Patientsʼ appetites, measured by serial patient-completed questionnaires, appeared to be mildly enhanced by cyproheptadine.…”

Section: Leitlinie E19mentioning

confidence: 99%

Untitled

2015

Aktuel Ernahrungsmed

View full text Add to dashboard Cite

Mitochondria: The ketogenic diet—A metabolism-based therapy

Cited by 155 publications

References 38 publications

Obesity is now a Pandemic Worldwide: Is the Lazy, Couch Potato, Over Eating Culture at Fault?

Obesity is now a Pandemic Worldwide: Is the Lazy, Couch Potato, Over Eating Culture at Fault?

Tissue Specific Impacts of a Ketogenic Diet on Mitochondrial Dynamics in the BTBRT+tf/j Mouse

Untitled

Contact Info

Product

Resources

About