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Middle-aged obesity, characterized by excessive fat accumulation and systemic energy imbalance, often precedes various health complications. Recent research has unveiled a surprising link between DNA damage response and energy metabolism. Here, we explore the role of Eepd1, a DNA repair enzyme, in regulating adipose tissue function and obesity onset.

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Zearalenone exacerbates lipid metabolism disorders by promoting liver lipid droplet formation and disrupting gut microbiota.

Ecotoxicol Environ Saf

January 2025

Key Laboratory of Precision Nutrition and Food Quality, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China; Key Laboratory of Safety Assessment of Genetically Modified Organism (Food Safety),Ministry of Agriculture and Rural Affairs of the P.R. China, Beijing 100083, China. Electronic address:

Zearalenone (ZEA), produced by Fusarium, is a fungal toxin commonly found in maize, wheat, and other cereals. ZEA has the ability to bind to estrogen receptors of humans and animals and is an environmental endocrine disruptor that may interfere with glucose homeostasis and lipid metabolism. In this study, we first investigated the effects of chronic exposure to low doses of ZEA with a high-fat-diet (HFD) in obese C57BL/6 J mice.

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Pectin is an acidic heteropolysaccharide with natural, green, and inexpensive characteristics. Compared to polysaccharides, oligosaccharides are more easily utilized by the body, and the physiological function of hawthorn pectin oligosaccharides (POS) may vary depending on their degree of polymerization (DP). Therefore, we mainly studied the effects of hawthorn pectin (HP) and POS with different DP on gut microbiota disorders induced by high-fat diet (HFD).

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The cardioprotective effects of histone deacetylase (HDAC) inhibitors (HDIs) are at odds with the deleterious effects of HDAC depletion. Here, we use HDAC3 as a prototype HDAC to address this contradiction. We show that adult-onset cardiac-specific depletion of HDAC3 in mice causes cardiac hypertrophy and contractile dysfunction on a high-fat diet (HFD), excluding developmental disruption as a major reason for the contradiction.

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Background & Aims: The role of infiltrating neutrophils in hepatocellular carcinoma (HCC) is modulated by cellular metabolism, specifically lipid homeostasis. Throughout the progression of HCC, alterations in lipid metabolism are intricately linked with regulation of neutrophil function and the release of neutrophil extracellular traps (NETs). However, how much the protumor effect of a high-fat diet (HFD) depends on NETs and the potential interplay between NETs and other leukocytes in HCC remains uncertain.

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