The scientific innovations have emphasized the importance of diet for one's health and wellbeing. The genetic revolution has enhanced our understanding about the effect of nutrients on genomic and transcriptomic profiles and gene-nutrition interactions (nutritional genomics). Furthermore, the contribution of micronutrient insufficiencies and macronutrient excess is evident in the development and progression of many diseases, especially cancer. It is speculated that nutrients have capacity to implicitly affect the physiological and pathophysiological processes via gene expression various regulatory processes. Moreover, the nutrients are known to affect the cellular networks involved in cancer progression and cancer inhibitory mechanisms targeting apoptosis or impaired angiogenesis. The interplay of regulatory processes in physiological systems and nutrients provides basis for the nutrigenomics. The functional genomics data further argue that cellular and molecular processes involved in the cancer progression are possibly programed genes during early development which may persist into adulthood and become detrimental. The incorporation of the functional interactions between nutrients and the genome has revolutionized the field of personalized medicine and provided the foundation for targeted cancer therapy through nutrients. There is growing evidence on the beneficial impacts of eating habits on lowering the risk of cancer, even if it can be difficult to pinpoint the precise role of nutrients. The nutrigenomic information may provide bases to develop disease prevention and treatment via nutrition, at the molecular level.
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http://dx.doi.org/10.1007/978-3-031-55622-7_9 | DOI Listing |
AACE Clin Case Rep
July 2024
Division of Endocrinology, Metabolism, and Molecular Medicine, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Background/objective: Fanconi-Bickel Syndrome (FBS) is an inherited disorder of glucose metabolism resulting from functional loss of glucose transporter 2 characterized by fasting hypoglycemia oscillating with postprandial hyperglycemia. Dysglycemia treatment strategies during FBS pregnancy have not been reported, and insulin therapy carries significant risk due to fasting hypoglycemia in FBS. We report for the first time: (1) glycemic profiles obtained via continuous glucose monitoring (CGM), (2) CGM-guided strategies for cornstarch and nutritional therapy for fasting hypoglycemia and postprandial hyperglycemia, respectively, and (3) placental glucose transporter 2 isoform expression in a pregnant individual with FBS.
View Article and Find Full Text PDFJ Cardiovasc Dev Dis
December 2024
Independent Researcher, 4 Evkariou Street, 17122 Athens, Greece.
The intention of this study was to profile the cohort from the Greek Registry for the prevalence of Familial Hypercholesterolemia (GRegistry-FH) by estimating the prevalence of coronary artery disease (CAD), myocardial infarction (MI), stroke, dyslipidemia, arterial hypertension, diabetes mellitus (DM), pre-DM, smoking, abnormal thyroid function (ATF), and lipid values. The GRegistry-FH is a prospective study involving door-to-door interviews conducted by trained interviewers. Overall, 7704 individuals aged ≥18 years, randomly selected from all the regions of Greece, participated.
View Article and Find Full Text PDFJ Pers Med
November 2024
Coriell Life Sciences, Philadelphia, PA 19112, USA.
Pharmacogenomics (PGx) has revolutionized personalized medicine by empowering the tailoring of drug treatments based on individual genetic profiles. However, the complexity of drug response mechanisms necessitates the integration of additional biological and environmental factors. This article explores integrating epigenetics, nutrigenomics, microbiomes, protein interactions, exosomes, and metabolomics with PGx to enhance personalized medicine.
View Article and Find Full Text PDFJ Inherit Metab Dis
January 2025
Department of Biochemistry and Chemistry and La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Victoria, Australia.
Short-chain enoyl-CoA hydratase 1 deficiency (ECHS1D) is a rare genetic disorder caused by biallelic pathogenic variants in the ECHS1 gene. ECHS1D is characterised by severe neurological and physical impairment that often leads to childhood mortality. Therapies such as protein and single nutrient-restricted diets show poor efficacy, whereas the development of new treatments is hindered by the low prevalence of the disorder and a lack of model systems for treatment testing.
View Article and Find Full Text PDFJ Nutr Biochem
December 2024
Research Group Nutrigenomics of Obesity and Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany; German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany; Research Group Molecular and Clinical Life Science of Metabolic Diseases, Faculty of Health Sciences Brandenburg, University of Potsdam, Brandenburg, Germany. Electronic address:
Alternative splicing contributes to diversify the cellular protein landscape, but aberrant splicing is implicated in many diseases. To which extent mis-splicing contributes to insulin resistance as the causal defect of type 2 diabetes and whether this can be reversed by lifestyle interventions is largely unknown. Therefore, RNA sequencing data from skeletal muscle and adipose tissue of diabetes-susceptible NZO mice treated with or without intermittent fasting and of healthy C57BL/6J mice subjected to exercise were analyzed for alternative splicing differences using Whippet and rMATS.
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