bims-kimdis Biomed News
on Ketones, inflammation and mitochondria in disease
Issue of 2023‒02‒26
ten papers selected by
Matías Javier Monsalves Álvarez



  1. bioRxiv. 2023 Feb 19. pii: 2023.02.18.529095. [Epub ahead of print]
      Age-related cognitive decline has been linked to distinct patterns of cellular dysfunction in the prelimbic cortex (PL) and the CA3 subregion of the hippocampus. Because higher cognitive functions require both structures, selectively targeting a neurobiological change in one region, at the expense of the other, is not likely to restore normal behavior in older animals. One change with age that both the PL and CA3 share, however, is a reduced ability to utilize glucose, which can produce aberrant neural activity patterns. The current study used a ketogenic diet (KD) intervention, which reduces the brain’s reliance on glucose, and has been shown to improve cognition, as a metabolic treatment for restoring neural ensemble dynamics in aged rats. Expression of the immediate-early genes Arc and Homer 1a were used to quantify the neural ensembles that were active in the home cage prior to behavior, during a working memory/biconditional association task, and a continuous spatial alternation task. Aged rats on the control diet had increased activity in CA3 and less ensemble overlap in PL between different task conditions than did the young animals. In the PL, the KD was associated with increased activation of neurons in the superficial cortical layers. The KD did not lead to any significant changes in CA3 activity. These observations suggest that the KD does not restore neuron activation patterns in aged animals, but rather the availability of ketone bodies in the frontal cortices may permit the engagement of compensatory mechanisms that produce better cognitive outcomes.Significance Statement: This study extends understanding of how a ketogenic diet (KD) intervention may improve cognitive function in older adults. Young and aged rats were given 3 months of a KD or a calorie-match control diet and then expression of the immediate-early genes Arc and Homer 1a were measured to examine neural ensemble dynamics during cognitive testing. The KD diet was associated with increased activation of neurons in the superficial layers of the PL, but there were no changes in CA3. These observations are significant because they suggest that compensatory mechanisms for improving cognition are engaged in the presence of elevated ketone bodies. This metabolic shift away from glycolysis can meet the energetic needs of the frontal cortices when glucose utilization is compromised.
    DOI:  https://doi.org/10.1101/2023.02.18.529095
  2. J Endocrinol Invest. 2023 Feb 21.
      PURPOSE: Poor response to bariatric surgery, namely insufficient weight loss (IWL) or weight regain (WR), is a critical issue in the treatment of obesity. The purpose of our study was to assess the efficacy, feasibility, and tolerability of very low-calorie ketogenic diet (VLCKD) for the management of this condition.METHODS: A real-life prospective study was conducted on twenty-two patients who experienced poor response after bariatric surgery and followed a structured VLCKD. Anthropometric parameters, body composition, muscular strength, biochemical analyses, and nutritional behavior questionnaires were evaluated.
    RESULTS: A significant weight loss (mean 14.1 ± 4.8%), mostly due to fat mass, was observed during VLCKD with the preservation of muscular strength. The weight loss obtained allowed patients with IWL to reach a body weight significantly lower than that obtained at the post-bariatric surgery nadir and to report the body weight of patients with WR at the nadir observed after surgery. The significantly beneficial changes in nutritional behaviors and metabolic profiles were observed without variations in kidney and liver function, vitamins, and iron status. The nutritional regimen was well tolerated, and no significant side effects were detected.
    CONCLUSION: Our data demonstrate the efficacy, feasibility, and tolerability of VLCKD in patients with poor response after bariatric surgery.
    Keywords:  Bariatric surgery; Insufficient weight loss; Poor response; Very-low-calorie ketogenic diet; Weight regain
    DOI:  https://doi.org/10.1007/s40618-023-02034-2
  3. Front Endocrinol (Lausanne). 2023 ;14 1042744
      Objective: To carry out a systematic review of published studies to evaluate the relationship between different type of ketogenic diet (KD) and bone health as supported by the scientific literature.Methods: The study involved all articles that assessed the relationship between the use of KD for the treatment of overweight or obesity and bone health. The quality assessment was evaluated with using the Cambridge Quality Checklists. The search strategy included the following combination of Medical Subjects Headings terms and keywords: "osteoporosis", "bone health, "bone function", "bone mineral density", and "ketogenic diet".
    Results: Seven trials were identified and reviewed. No significant changes in bone mass density (BMD) were observed after KD. The results showed no significant effect on bone resorption by measuring urinary N-telopeptide levels, on bone formation by measuring bone-specific alkaline phosphatase, or alterations in overall bone turnover in patients who followed KD. Only in female subject after a 10% weight loss, bone resorption increases while new bone synthesis decreases, but without increasing the risk of osteoporosis. Finally, patients on KD lost significantly more weight than controls, associated with an increase in serum vitamin D levels and a reduction in plasma parathyroid hormone (PTH) levels.
    Conclusion: No human studies have currently been conducted with adequate and powerful experimental designs to definitively understand the impact of KD therapy on bone health.
    Keywords:  bone health; bone mineral density; ketogenic diet; low-calorie ketogenic diet; osteoporosis; very-low-calorie ketogenic diet
    DOI:  https://doi.org/10.3389/fendo.2023.1042744
  4. Maedica (Bucur). 2022 Dec;17(4): 812-819
      Colon cancer is one of the most common malignancies with significant importance. Recent theories believe that cancers are metabolic diseases. Therefore, the role of metabolism in the prevention and treatment of cancer has been considered and the ketogenic diet is one example. In the present study, we evaluated the effect of the ketogenic diet and a high carbohydrate diet on tumor size and number, histopathology, and insulin level as well as VEGF level in 1, 2 dymethylhydrazine (DMH)-induced colon cancer in rats. Forty adult male Wistar rats were divided into four groups as follows: control, colon cancer, ketogenic diet, and high carbohydrate diet groups. For induction of colon cancer, 30 mg/kg of 1,2 DMH solution was injected subcutaneously twice a week for 24 weeks. The results showed that the ketogenic diet reduced tumor size, number, and histopathological changes as well as VEGF level (P<0.01) compared to the colon cancer group. The ketogenic diet also increased the levels of beta hydroxyl butyrate (P<0.001) and decreased those of glucose, insulin and HbA1c (P<0.001). Furthermore, a high carbohydrate diet did not show any protective effects on colon cancer prevention. In conclusion, the ketogenic diet demonstrated prophylactic effects on colon cancer, and this anti-cancer effect could be partially attributed to the reduction in VEGF and insulin levels.
    DOI:  https://doi.org/10.26574/maedica.2022.17.4.812
  5. bioRxiv. 2023 Feb 18. pii: 2023.02.17.528937. [Epub ahead of print]
      The dependency of cancer cells on glucose can be targeted with high-fat low-carbohydrate ketogenic diet (KD). However, hepatic ketogenesis is suppressed in IL-6 producing cancers, which prevents the utilization of this nutrient source as energy for the organism. In two IL-6 associated murine models of cancer cachexia we describe delayed tumor growth but accelerated onset of cancer cachexia and shortened survival when mice are fed KD. Mechanistically, we find this uncoupling is a consequence of the biochemical interaction of two simultaneously occurring NADPH-dependent pathways. Within the tumor, increased production of lipid peroxidation products (LPPs) and, consequently, saturation of the glutathione (GSH) system leads to ferroptotic death of cancer cells. Systemically, redox imbalance and NADPH depletion impairs the biosynthesis of corticosterone, the main regulator of metabolic stress, in the adrenal glands. Administration of dexamethasone, a potent glucocorticoid, improves food intake, normalizes glucose homeostasis and utilization of nutritional substrates, delays onset of cancer cachexia and extends survival of tumor-bearing mice fed KD, while preserving reduced tumor growth. Our study highlights that the outcome of systemic interventions cannot necessarily be extrapolated from the effect on the tumor alone, but that they have to be investigated for anti-cancer and host effects. These findings may be relevant to clinical research efforts that investigate nutritional interventions such as KD in patients with cancer.
    DOI:  https://doi.org/10.1101/2023.02.17.528937
  6. J Physiol. 2023 Feb 22.
      Exercise-induced perturbation of skeletal muscle metabolites is a likely mediator of long-term health benefits in older adults. While specific metabolites have been identified to be impacted by age, physical activity, and exercise, the depth of coverage of the muscle metabolome is still limited. Here, we investigated resting and exercise-induced metabolite distribution in muscle from well-phenotyped older adults that were active or sedentary, and a group of active young adults. Percutaneous biopsies of the vastus lateralis were obtained before, immediately after, and 3-hours following a bout of endurance cycling. Metabolite profile in muscle biopsies was determined by tandem mass spectrometry. Mitochondrial energetics in permeabilized fiber bundles was assessed by high resolution respirometry and fiber type proportion was assessed by immunohistology. We found that metabolites of the kynurenine/tryptophan pathway were impacted by age and activity. Specifically, kynurenine was elevated in muscle from older adults, while downstream metabolites of kynurenine (kynurenic acid and nicotinamide adenine dinucleotide (NAD+ )) were elevated in muscle from active adults and associated with cardiorespiratory fitness and muscle oxidative capacity. Acylcarnitines, a potential marker of impaired metabolic health, were elevated in muscle from physically active participants. Surprisingly, despite baseline group difference, acute exercise-induced alterations in whole-body substrate utilization and muscle acylcarnitines and ketone bodies were remarkably similar between groups. Our data identified novel muscle metabolite signatures that associate with the healthy aging phenotype provoked by physical activity and reveal the metabolic responsiveness of muscle to acute endurance exercise is retained with age regardless of activity levels. KEY POINTS: Kynurenine/tryptophan pathway metabolites were impacted by age and physical activity in human muscle, with kynurenine elevated in older muscle, while downstream products kynurenic acid and NAD+ were elevated in exercise-trained muscle regardless of age. Acylcarnitines, a marker of impaired metabolic health when heightened in circulation, was elevated in exercise-trained muscle of young and older adults, suggesting muscle act as a metabolic sink to reduce circulating acylcarnitines observed with unhealthy aging. Despite the phenotypic differences, the exercise-induced response of various muscle metabolite pools, including acylcarnitine and ketone bodies, was similar amongst the groups, suggesting older adults can achieve the metabolic benefits of exercise seen in young counterparts. Abstract figure legend Muscle metabolite profiles at baseline and in response to an acute bout of endurance exercise were examined in three groups: Young Active, Older Active, Older Sedentary. Baseline profiles revealed distinct age- and activity-related metabolite profiles in muscle that associated with clinical and biochemical characteristics of the oxidative phenotype (cardiorespiratory fitness (VO2peak), muscle mitochondrial energetics, and type I fiber type proportion). Specifically, kynurenine-related metabolites (kynurenine, kynurenic acid, and quinolinate) were impacted by age, while nicotinamide adenine dinucleotide (NAD+ ) and acylcarnitines levels were impacted by activity/exercise training. Despite baseline differences, the whole-body and muscle-specific metabolic responses were similarly amongst young and older adults regardless of training status. This article is protected by copyright. All rights reserved.
    Keywords:  NAD+; aging; ketones; kynurenic acid
    DOI:  https://doi.org/10.1113/JP284142
  7. Nat Commun. 2023 Feb 21. 14(1): 949
      Obesity caused by genetic and environmental factors can lead to compromised skeletal muscle function. Time-restricted feeding (TRF) has been shown to prevent muscle function decline from obesogenic challenges; however, its mechanism remains unclear. Here we demonstrate that TRF upregulates genes involved in glycine production (Sardh and CG5955) and utilization (Gnmt), while Dgat2, involved in triglyceride synthesis is downregulated in Drosophila models of diet- and genetic-induced obesity. Muscle-specific knockdown of Gnmt, Sardh, and CG5955 lead to muscle dysfunction, ectopic lipid accumulation, and loss of TRF-mediated benefits, while knockdown of Dgat2 retains muscle function during aging and reduces ectopic lipid accumulation. Further analyses demonstrate that TRF upregulates the purine cycle in a diet-induced obesity model and AMPK signaling-associated pathways in a genetic-induced obesity model. Overall, our data suggest that TRF improves muscle function through modulations of common and distinct pathways under different obesogenic challenges and provides potential targets for obesity treatments.
    DOI:  https://doi.org/10.1038/s41467-023-36474-4
  8. Int Immunopharmacol. 2023 Feb 22. pii: S1567-5769(23)00236-9. [Epub ahead of print]117 109916
      The present article provides a detailed concept of the role of NLRP3 inflammasome in the pathophysiology of depression-like chronic diseases where inflammation and release of various cytokines plays a pivotal role in exaggerating the condition. The various pathways involved in NLRP3 activation are the main target of NLRP3 inhibitors for the therapeutic management of depression as per the recent clinical and research studies conducted so far. Further various drug inhibitors for NLRP3 available in preclinical and clinical trials have been discussed in detail. Hence, blockage of the action of NLRP3 inflammasome is crucial to anticipate the inflammatory cytokine release from the mediators that contributes to cause depression.
    Keywords:  Caspase; Cytokine; Depression; Inflammation; NLRP3; Pathways
    DOI:  https://doi.org/10.1016/j.intimp.2023.109916
  9. J Clin Endocrinol Metab. 2023 Feb 24. pii: dgad106. [Epub ahead of print]
      
    Keywords:  aldosterone; ketogenic; mineralocorticoid; zona glomerulosa
    DOI:  https://doi.org/10.1210/clinem/dgad106