metabolic programming
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Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 114
Author(s):  
Catalina Picó ◽  
Mariona Palou

This Special Issue of Nutrients “Leptin and Metabolic Programming” includes one review article regarding the function of leptin throughout the entire life on cardiometabolic fates and four original articles related to the new function of leptin present in milk and liquid amniotic, its possible relation with other components of breast milk, and how environmental conditions may impact on leptin action and metabolic programming [...]


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Liana Carla Albuquerque Peres Martinho

Obesity is a multifactorial health problem characterized by the excessive accumulation of fat in the body and affects approximately 338 million children and adolescents worldwide. For this reason, this study consisted of a literature review to investigate how the causes and treatments of pediatric obesity are being addressed in light of epigenetic modulation as a factor in metabolic programming. For this, preferentially original articles published in English between the years 2017 to 2021 in the PubMed and Scholar Google databases were searched using the epigenetics descriptors; epigenetic modulation; child obesity; metabolic syndrome, combined with each other. A total of 54,000 articles were returned to searches in PubMed and 16,107,000 in Scholar Google. Fewer than 500 studies jointly addressed epigenetics and aspects of obesity or metabolic syndromes in childhood. Only 14 works matched the search criteria. The most discussed epigenetic mechanism in the literature is DNA methylation, whose rates observed mainly in CpG islands of promoter regions in several genes contribute to the prevention and early diagnosis of obesity and other pediatric comorbidities even before birth, based on the correlation between the epigenetic marks, maternal and paternal health and anthropometric indices. Although experimental studies on infant metabolic programming are scarce, existing knowledge suggests that environmental, nutritional, and energy expenditure changes are capable of modulating the epigenome and reversing marks that induce susceptibility to metabolic comorbidities.


Author(s):  
Hassan A. Ali ◽  
Andrew Metcalfe ◽  
James T. Topham ◽  
Cassia S. Warren ◽  
Joanna M. Karasinska ◽  
...  

Nutrire ◽  
2021 ◽  
Vol 46 (2) ◽  
Author(s):  
Ana Claudia Losinskas Hachul ◽  
Danielle Araujo de Miranda ◽  
Fernanda Cristina Alves Nakakura ◽  
Valter Tadeu Boldarine ◽  
Lila Missae Oyama

Author(s):  
Sofie Hedlund Møller ◽  
Limei Wang ◽  
Ping-Chih Ho

AbstractIt is being increasingly acknowledged that immune cells depend on certain metabolic traits to perform their functions and that the extracellular environment can influence cell metabolism and vice versa. Dendritic cell (DC) subsets traffic through highly diverse environments from the bone marrow, where they develop, to the various peripheral tissues, where they differentiate and capture antigens, before they migrate to the lymph node to present antigens and prime T cells. It is plausible that DC subsets modulate their stimulatory abilities in response to unique metabolic programming. The metabolic requirements of DCs are just recently being discovered, and subset- and context-specific metabolic phenotypes in DCs are highly intertwined with DC functions. In this review, we present the current knowledge on the intrinsic and extrinsic determinants of DC metabolism, how they regulate DC function with examples from tumor biology and in interaction with the microbiota, and discuss how this can be applied therapeutically.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Gizem Inak ◽  
Agnieszka Rybak-Wolf ◽  
Pawel Lisowski ◽  
Tancredi M. Pentimalli ◽  
René Jüttner ◽  
...  

AbstractLeigh syndrome (LS) is a severe manifestation of mitochondrial disease in children and is currently incurable. The lack of effective models hampers our understanding of the mechanisms underlying the neuronal pathology of LS. Using patient-derived induced pluripotent stem cells and CRISPR/Cas9 engineering, we developed a human model of LS caused by mutations in the complex IV assembly gene SURF1. Single-cell RNA-sequencing and multi-omics analysis revealed compromised neuronal morphogenesis in mutant neural cultures and brain organoids. The defects emerged at the level of neural progenitor cells (NPCs), which retained a glycolytic proliferative state that failed to instruct neuronal morphogenesis. LS NPCs carrying mutations in the complex I gene NDUFS4 recapitulated morphogenesis defects. SURF1 gene augmentation and PGC1A induction via bezafibrate treatment supported the metabolic programming of LS NPCs, leading to restored neuronal morphogenesis. Our findings provide mechanistic insights and suggest potential interventional strategies for a rare mitochondrial disease.


2021 ◽  
Vol 12 ◽  
Author(s):  
Lauren H. Fairley ◽  
Jia Hui Wong ◽  
Anna M. Barron

Alzheimer’s disease (AD) is an age-associated terminal neurodegenerative disease with no effective treatments. Dysfunction of innate immunity is implicated in the pathogenesis of AD, with genetic studies supporting a causative role in the disease. Microglia, the effector cells of innate immunity in the brain, are highly plastic and perform a diverse range of specialist functions in AD, including phagocytosing and removing toxic aggregates of beta amyloid and tau that drive neurodegeneration. These immune functions require high energy demand, which is regulated by mitochondria. Reflecting this, microglia have been shown to be highly metabolically flexible, reprogramming their mitochondrial function upon inflammatory activation to meet their energy demands. However, AD-associated genetic risk factors and pathology impair microglial metabolic programming, and metabolic derailment has been shown to cause innate immune dysfunction in AD. These findings suggest that immunity and metabolic function are intricately linked processes, and targeting microglial metabolism offers a window of opportunity for therapeutic treatment of AD. Here, we review evidence for the role of metabolic programming in inflammatory functions in AD, and discuss mitochondrial-targeted immunotherapeutics for treatment of the disease.


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