Butyrate reduction and HDAC4 increase underlie maternal high fructose-induced metabolic dysfunction in hippocampal astrocytes in female rats

Wu, Kay Li Hui; Liu, Wen-Chung; Wu, Chih-Wei; Fu, Mu-Hui; Huang, Hsiu-Mei; Tain, You-Lin; Liang, Chih-Kuang; Hung, Chun-Ying; Chen, I-Chun; Hung, Pi-Lien; Lin, Yu-Ju; Hirase, Hajime

doi:10.1016/j.jnutbio.2024.109571

Cited by 5 publications

(1 citation statement)

References 50 publications

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“…While butyrate itself does not directly bind to AHR, it can induce the nuclear translocation of AHR and activate AHR independently of its HDAC activity and SCFA receptors [167]. Given that perinatal supplementation with butyrate has demonstrated protective effects against offspring hypertension and metabolic dysfunction in various developmental programming models [168][169][170], further investigation is warranted to elucidate the potential role of the AHR signaling pathway in these protective actions.…”

Section: Butyratementioning

confidence: 99%

The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular–Kidney–Metabolic Programming

Tain,

Hsu

2024

IJMS

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Early life exposure lays the groundwork for the risk of developing cardiovascular–kidney–metabolic (CKM) syndrome in adulthood. Various environmental chemicals to which pregnant mothers are commonly exposed can disrupt fetal programming, leading to a wide range of CKM phenotypes. The aryl hydrocarbon receptor (AHR) has a key role as a ligand-activated transcription factor in sensing these environmental chemicals. Activating AHR through exposure to environmental chemicals has been documented for its adverse impacts on cardiovascular diseases, hypertension, diabetes, obesity, kidney disease, and non-alcoholic fatty liver disease, as evidenced by both epidemiological and animal studies. In this review, we compile current human evidence and findings from animal models that support the connection between antenatal chemical exposures and CKM programming, focusing particularly on AHR signaling. Additionally, we explore potential AHR modulators aimed at preventing CKM syndrome. As the pioneering review to present evidence advocating for the avoidance of toxic chemical exposure during pregnancy and deepening our understanding of AHR signaling, this has the potential to mitigate the global burden of CKM syndrome in the future.

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Section: Butyratementioning

confidence: 99%

The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular–Kidney–Metabolic Programming

Tain,

Hsu

2024

IJMS

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SMP30 alleviates cerebral ischemia/reperfusion-induced neuronal injury by inhibiting HDAC4/PSD-95 to preserve mitochondrial function

Chen,

Qian,

Zhang

et al. 2024

Journal of Neuropathology &Amp; Experimental Neurology

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Ischemic stroke is a major cause of global death and permanent disability. Major consequences of ischemic stroke include neuronal mitochondrial dysfunction. We investigated the effects of senescence marker protein 30 (SMP30) on mitochondria-mediated apoptosis and histone deacetylase 4 (HDAC4)/postsynaptic density-95 (PSD-95) signaling in stroke models in vivo and in vitro. Rats with middle cerebral artery occlusion/reperfusion (MCAO/R) were used to simulate cerebral ischemia/reperfusion (I/R) injury. SMP30 was downregulated in the brain tissues of rats after I/R induction. SMP30 overexpression decreased MCAO/R-induced infarct volumes and improved neurologic function and histopathological changes. Increasing SMP30 expression suppressed neuronal apoptosis and reduced mitochondrial dysfunction. SMP30 overexpression in SH-SY5Y and PC12 cells treated with oxygen-glucose deprivation/reoxygenation (OGD/R) decreased HDAC4 and PSD-95 expression; PSD-95 could bind to HDAC4. Furthermore, HDAC4 upregulation abolished the effects of SMP30 overexpression on OGD/R-induced apoptosis and mitochondrial dysfunction in SH-SY5Y cells. Together, these findings indicate that SMP30 alleviates cerebral I/R-induced neuronal injury by inhibiting HDAC4/PSD-95 to preserve mitochondrial function. These interactions might provide new treatment methods for patients with ischemic stroke.

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Navigating the metabolic maze: anomalies in fatty acid and cholesterol processes in Alzheimer’s astrocytes

Zhang,

Chen,

Liu

2024

Alz Res Therapy

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Alzheimer’s disease (AD) is the most common cause of dementia, and its underlying mechanisms have been a subject of great interest. The mainstream theory of AD pathology suggests that the disease is primarily associated with tau protein and amyloid-beta (Aβ). However, an increasing body of research has revealed that abnormalities in lipid metabolism may be an important event throughout the pathophysiology of AD. Astrocytes, as important members of the lipid metabolism network in the brain, play a significant role in this event. The study of abnormal lipid metabolism in astrocytes provides a new perspective for understanding the pathogenesis of AD. This review focuses on the abnormal metabolism of fatty acids (FAs) and cholesterol in astrocytes in AD, and discusses it from three perspectives: lipid uptake, intracellular breakdown or synthesis metabolism, and efflux transport. We found that, despite the accumulation of their own fatty acids, astrocytes cannot efficiently uptake fatty acids from neurons, leading to fatty acid accumulation within neurons and resulting in lipotoxicity. In terms of cholesterol metabolism, astrocytes exhibit a decrease in endogenous synthesis due to the accumulation of exogenous cholesterol. Through a thorough investigation of these metabolic abnormalities, we can provide new insights for future therapeutic strategies by literature review to navigate this complex metabolic maze and bring hope to patients with Alzheimer’s disease.

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Butyrate reduction and HDAC4 increase underlie maternal high fructose-induced metabolic dysfunction in hippocampal astrocytes in female rats

Cited by 5 publications

References 50 publications

The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular–Kidney–Metabolic Programming

The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular–Kidney–Metabolic Programming

SMP30 alleviates cerebral ischemia/reperfusion-induced neuronal injury by inhibiting HDAC4/PSD-95 to preserve mitochondrial function

Navigating the metabolic maze: anomalies in fatty acid and cholesterol processes in Alzheimer’s astrocytes

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