Epigenetic Mechanisms of Obesity: Insights from Transgenic Animal Models DOI Creative Commons
Elisa S. Na

Life, Journal Year: 2025, Volume and Issue: 15(4), P. 653 - 653

Published: April 16, 2025

Obesity is a chronic disease with prevalence rates that have risen dramatically over the past four decades. This increase not due to changes in human genome but rather environmental factors promote maladaptive physiological responses. Emerging evidence suggests external influences, such as high-fat diets, modify epigenome—the interface between genes and environment—leading persistent alterations energy homeostasis. review explores role of epigenetic mechanisms obesity, emphasizing insights from transgenic animal models clinical studies. Additionally, we discuss evolution obesity research homeostatic allostatic frameworks, highlighting key neuroendocrine regulators balance.

Language: Английский

The impact of cortical and subcortical volumes on major depression risk: A genetic study DOI
Lingyi Shi, Xiangjun Zhou,

Yucai Qu

et al.

Journal of Affective Disorders, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0
Epigenetic and metabolic regulation of developmental timing in neocortex evolution DOI Creative Commons

Matilde Aquilino,

Nora Ditzer, Takashi Namba

et al.

Trends in Neurosciences, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

The human brain is characterized by impressive cognitive abilities. neocortex the seat of higher cognition, and expansion a hallmark evolution. While developmental programs are similar in different species, timing transitions capacity neural progenitor cells (NPCs) to proliferate differ, contributing increased production neurons during cortical development. Here, we review epigenetic regulation corticogenesis, focusing mostly on humans while building knowledge from studies mice. We discuss metabolic-epigenetic interplay as potential mechanism integrate extracellular signals into chromatin. Moreover, synthesize current understanding how metabolic deregulation can cause neurodevelopmental disorders. Finally, outline be investigated using organoid models.

Language: Английский

Citations

0
Mechanisms for Regulatory Effects of Exercise on Metabolic Diseases from the Lactate–Lactylation Perspective DOI Open Access

G Chen,

Jinchao Liu,

Yongbin Guo

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(8), P. 3469 - 3469

Published: April 8, 2025

Metabolic diseases, including cardiovascular type 2 diabetes mellitus (T2DM), osteoporosis, and non-alcoholic fatty liver disease (NAFLD), constitute a major global health burden associated with chronic morbidity mortality. Lactate, once considered as metabolic byproduct, has emerged key regulator of cellular reprogramming through lactylation, novel post-translational modification (PTM) that dynamically couples flux to chromatin remodeling. Lactylation exerts dual regulatory roles signaling molecule via GPR81/GPR4-mediated pathways substrate for the covalent histones enzymes. Pathologically, hyperlactatemia suppresses mitochondrial biogenesis, driving cardiomyopathy epigenetic silencing oxidative metabolism genes. Conversely, exercise-induced lactate surges transiently enhance insulin sensitivity AMPK/PGC-1α/GLUT4 signaling, resolve inflammation GPR81-mediated M2 macrophage polarization, restore function lactylation-dependent pathways. This review delineates lactylation spatiotemporal rheostat: dysregulation perpetuates disorders, whereas acute exercise-mediated remodels transcriptional networks homeostasis. Future research should integrate multiomics clarify lactylation’s dynamics, tissue-specific thresholds, metabolism–immunity interactions, metabolic–epigenetic crosstalk precision management diseases.

Language: Английский

Citations

0
Epigenetic Mechanisms of Obesity: Insights from Transgenic Animal Models DOI Creative Commons
Elisa S. Na

Life, Journal Year: 2025, Volume and Issue: 15(4), P. 653 - 653

Published: April 16, 2025

Obesity is a chronic disease with prevalence rates that have risen dramatically over the past four decades. This increase not due to changes in human genome but rather environmental factors promote maladaptive physiological responses. Emerging evidence suggests external influences, such as high-fat diets, modify epigenome—the interface between genes and environment—leading persistent alterations energy homeostasis. review explores role of epigenetic mechanisms obesity, emphasizing insights from transgenic animal models clinical studies. Additionally, we discuss evolution obesity research homeostatic allostatic frameworks, highlighting key neuroendocrine regulators balance.

Language: Английский

Citations

0