Intermittent fasting interventions to leverage metabolic and circadian mechanisms for cancer treatment and supportive care outcomes

JNCI Monographs, Journal Year: 2023, Volume and Issue: 2023(61), P. 84 - 103

Published: May 4, 2023

Abstract Intermittent fasting entails restricting food intake during specific times of day, days the week, religious practice, or surrounding clinically important events. Herein, metabolic and circadian rhythm mechanisms underlying proposed benefits intermittent for cancer population are described. We summarize epidemiological, preclinical, clinical studies in published between January 2020 August 2022 propose avenues future research. An outstanding concern regarding use among patients is that often results caloric restriction, which can put already prone to malnutrition, cachexia, sarcopenia at risk. Although trials do not yet provide sufficient data support general this summary may be useful patients, caregivers, clinicians who exploring as part their journey outcomes symptom management.

Language: Английский

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Amino acids and KLHL22 do not activate mTORC1 via DEPDC5 degradation

Nature, Journal Year: 2025, Volume and Issue: 637(8045), P. E11 - E14

Published: Jan. 8, 2025

Language: Английский

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Metabolic Homeostasis of Amino Acids and Diabetic Kidney Disease

Nutrients, Journal Year: 2022, Volume and Issue: 15(1), P. 184 - 184

Published: Dec. 30, 2022

Diabetic kidney disease (DKD) occurs in 25–40% of patients with diabetes. Individuals DKD are at a significant risk progression to end-stage morbidity and mortality. At present, although renal function-decline can be retarded by intensive glucose lowering strict blood pressure control, these current treatments have shown no beneficial impact on preventing failure. Recently, addition control sugar pressure, dietary approach has been recommended for management DKD. Amino acids (AAs) both biomarkers causal factors progression. AA homeostasis contributes hemodynamic response glomerular hyperfiltration alteration diabetic patients. This review discusses the links between progressive dysfunction metabolic histidine, tryptophan, methionine, glutamine, tyrosine, branched-chain AAs. In addition, we emphasize regulation effects special metabolites progression, focus causality potential mechanisms. paper may offer an optimized protein diet strategy concomitant reduce risks setting hyperglycemia.

Language: Английский

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The Effects of Dietary Interventions on Brain Aging and Neurological Diseases

Nutrients, Journal Year: 2022, Volume and Issue: 14(23), P. 5086 - 5086

Published: Nov. 30, 2022

Dietary interventions can ameliorate age-related neurological decline. Decades of research in vitro studies, animal models, and clinical trials support their ability efficacy to improve behavioral outcomes by inducing biochemical physiological changes that lead a more resilient brain. including calorie restriction, alternate day fasting, time restricted feeding, fasting mimicking diets not only normal brain aging but also slow down, or even reverse, the progression diseases. In this review, we focus on effects intermittent periodic improving phenotypic outcomes, such as cognitive motor-coordination decline, through an increase neurogenesis synaptic plasticity, decrease neuroinflammation, mitochondrial dysfunction, oxidative stress. We summarize results various dietary models diseases Alzheimer's disease, Parkinson's epilepsy, Multiple Sclerosis discuss explore feasibility prevention treatment these

Language: Английский

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Treatment-Resistant Epilepsy and Tuberous Sclerosis Complex: Treatment, Maintenance, and Future Directions

Neuropsychiatric Disease and Treatment, Journal Year: 2023, Volume and Issue: Volume 19, P. 733 - 748

Published: April 1, 2023

Abstract: Tuberous sclerosis complex (TSC) is a neurogenetic disorder that affects multiple organ systems, including the heart, kidneys, eyes, skin, and central nervous system. The neurologic manifestations have highest morbidity mortality, in particular children. Clinically, patients with TSC often present new-onset seizures within first year of life. TSC-associated epilepsy difficult to treat refractory antiseizure medications. Refractory associated increased risk neurodevelopmental comorbidities, developmental delay, intellectual disability, autism spectrum disorder, attention hyperactivity disorder. An increasing body research suggests early, effective treatment during critical periods can potentially improve cognitive outcomes. Therefore, it important aggressively, whether be pharmacological therapy, surgical intervention, and/or neuromodulation. This review discusses current future treatments for epilepsy, as well importance early evaluation children consideration neuromodulatory interventions young adults. Keywords: neurodevelopment, infantile spasms, vigabatrin, surgery

Language: Английский

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DEPDC5 plays a vital role in epilepsy: Genotypic and phenotypic features in cohort and literature

Epileptic Disorders, Journal Year: 2024, Volume and Issue: 26(3), P. 341 - 349

Published: May 16, 2024

DEPDC5 emerges to play a vital role in focal epilepsy. However, genotype-phenotype correlation DEPDC5-related epilepsies is challenging and controversial. In this study, we aim investigate the genotypic phenotypic features DEPDC5-affected patients.

Language: Английский

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Ancient genomic linkage of α-globin and Nprl3 couples metabolism with erythropoiesis

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: March 24, 2025

Red blood cell development from erythroid progenitors requires profound reshaping of metabolism and gene expression. How these transcriptional metabolic alterations are coupled is unclear. Nprl3 (an inhibitor mTORC1) has remained in synteny with the α-globin genes for >500 million years, harbours most a-globin enhancers. However, whether serves an role unknown. We found that while haematopoietic require basal expression, expression further boosted by This lineage-specific upregulation required sufficient erythropoiesis. Loss affects erythroblast via elevating mTORC1 signalling, suppressing autophagy disrupting glycolysis. Broadly consistent murine findings, human NPRL3-knockout produce fewer enucleated cells demonstrate dysregulated signalling response to nutrient availability erythropoietin. Therefore, we propose anciently conserved linkage NprI3, their associated enhancers developmental control

Language: Английский

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The effects of ketone bodies and ketogenesis on the PI3K/AKT/mTOR signaling pathway, a systematic review

Nutrition Research, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

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Tetrastigma hemsleyanum suppresses neuroinflammation in febrile seizures rats via regulating PKC-δ/caspase-1 signaling pathway

Journal of Ethnopharmacology, Journal Year: 2023, Volume and Issue: 318, P. 116912 - 116912

Published: July 13, 2023

Language: Английский

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Disruption of lysosomal nutrient sensing scaffold contributes to pathogenesis of a fatal neurodegenerative lysosomal storage disease

Journal of Biological Chemistry, Journal Year: 2024, Volume and Issue: 300(2), P. 105641 - 105641

Published: Jan. 9, 2024

The ceroid lipofuscinosis neuronal 1 (CLN1) disease, formerly called infantile lipofuscinosis, is a fatal hereditary neurodegenerative lysosomal storage disorder. This disease caused by loss-of-function mutations in the CLN1 gene, encoding palmitoyl-protein thioesterase-1 (PPT1). PPT1 catalyzes depalmitoylation of S-palmitoylated proteins for degradation and clearance hydrolases. Numerous proteins, especially brain, require dynamic S-palmitoylation (palmitoylation-depalmitoylation cycles) endosomal trafficking to their destination. While 23 palmitoyl-acyl transferases mammalian genome catalyze S-palmitoylation, catalyzed thioesterases such as PPT1. Despite these discoveries, pathogenic mechanism has remained elusive. Here, we report that brain Cln1-/- mice, which mimic mechanistic target rapamycin complex-1 (mTORC1) kinase hyperactivated. activation mTORC1 nutrients requires its anchorage limiting membrane Rag GTPases Ragulator complex. These form nutrient sensing scaffold must attach activate. We found two constituent complex (vacuolar (H+)-ATPase Lamtor1) membrane. Intriguingly, Ppt1 deficiency mice misrouted plasma disrupting scaffold. this defect, was hyperactivated via IGF1/PI3K/Akt-signaling pathway, suppressed autophagy contributing neuropathology. Importantly, pharmacological inhibition PI3K/Akt activation, restored autophagy, ameliorated neurodegeneration mice. Our findings reveal previously unrecognized role Cln1/Ppt1 regulating suggest IGF1/PI3K/Akt may be targetable pathway disease.

Language: Английский

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