The Link Between Nutrition, Developmental Plasticity and Human Health

A special issue of Foods (ISSN 2304-8158). This special issue belongs to the section "Food Nutrition".

Deadline for manuscript submissions: 25 February 2025 | Viewed by 751

Special Issue Editor


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Guest Editor
Studies in Nutrition and Phenotypic Plasticity Unit, Federal University of Pernambuco, Recife 50670-901, PE, Brazil
Interests: nutrition; phenotypic plasticity; skeletal muscle; locomotor behavior; cerebral palsy; neuropharmacology
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Special Issue Information

Dear Colleagues,

Nutrition is one of the factors that can influence the plasticity of organisms. Developmental plasticity is one of the branches of phenotypic plasticity, which specifically works on the trajectory of growth and development of individuals from the pre-gestational period to adulthood. Environmental stimuli such as malnutrition models due to a low-protein diet or obesity due to a high-fat diet can promote permanent or non-permanent morphological, physiological, or behavioral changes throughout an individual's life, which are explained by the change in phenotype through adaptations provided by plasticity. Nutritional interventions, such as vitamins, polyphenols, and functional foods, among others, can be used as strategies to improve human health. These interventions can promote cognitive (central nervous system), behavioral, muscular, cardiovascular, and intestinal (microbiota) changes or reduce inflammatory conditions related to diet throughout life.

This Special Issue aims to bring together leading scientific researchers to provide highly qualified manuscripts on nutrition and malnutrition (undernutrition or obesity) in light of developmental plasticity and associations with human health in situations of early brain injury or not. We aim to understand this association of nutrition with human health, whether through immediate or permanent adaptive responses throughout life.

You may choose our Joint Special Issue in Nutrients.

Dr. Ana Elisa Toscano
Guest Editor

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • malnutrition
  • cerebral palsy
  • phenotypic plasticity
  • polyphenols
  • early brain injury
  • vitamins
  • cognition
  • skeletal muscle
  • brain
  • inflammation

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Published Papers (1 paper)

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Research

13 pages, 3252 KiB  
Article
Protective Effects of Food-Derived Kaempferol on Pancreatic β-Cells in Type 1 Diabetes Mellitus
by Chenmeng Song, Wei Zheng, Chengyi Song, Houfeng Zhou and Jengyuan Yao
Foods 2024, 13(23), 3797; https://doi.org/10.3390/foods13233797 - 26 Nov 2024
Viewed by 564
Abstract
Background: Kaempferol (KPF), a flavonoid abundant in edible plants, possesses potent anti-inflammatory and antioxidant properties beneficial with notable health benefits. Objective: To evaluate the protective effects of KPF on metabolic disturbances and pancreatic damage in a Type 1 diabetes mellitus (T1DM) mouse model. [...] Read more.
Background: Kaempferol (KPF), a flavonoid abundant in edible plants, possesses potent anti-inflammatory and antioxidant properties beneficial with notable health benefits. Objective: To evaluate the protective effects of KPF on metabolic disturbances and pancreatic damage in a Type 1 diabetes mellitus (T1DM) mouse model. Methods: Male C57BL/6 mice were divided into normal, T1DM, T1DM + KPF 25 mg/kg, and T1DM + KPF 50 mg/kg groups. T1DM was induced by streptozotocin (STZ). KPF was administered via intraperitoneal injection for 2 weeks. After 4 weeks from the start, metabolic parameters, pancreatic histology, and plasma metabolites were analyzed. Network pharmacology and molecular docking identified key targets and pathways. In vitro, INS-1 cells were used to assess reactive oxygen species (ROS) production and apoptosis. Results: KPF significantly reduced blood glucose (GLU) and triglyceride (TG) levels, increased high-density lipoprotein (HDL) levels, and preserved pancreatic β-cell structure. Metabolomics revealed changes in energy metabolism and oxidative stress-related metabolites. Network analysis highlighted the PI3K/AKT/mTOR pathway, with strong binding affinities to targets such as AKT1. In vitro, KPF decreased ROS production in INS-1 cells; this effect was reversed by a PI3K/AKT inhibitor. KPF also reduced apoptosis in INS-1 cells. Conclusions: KPF ameliorates metabolic disturbances and pancreatic damage in T1DM mice, suggesting potential as a functional food ingredient for diabetes management. Full article
(This article belongs to the Special Issue The Link Between Nutrition, Developmental Plasticity and Human Health)
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