Heliyon, Год журнала: 2024, Номер 10(16), С. e35498 - e35498
Опубликована: Авг. 1, 2024
The increasing scientific interest in antioxidants and naturally derived compounds as potential remedies for obesity non-alcoholic fatty liver disease (NAFLD) has led to extensive research. objective of this bibliometric analysis is present an updated perspective on the topic antioxidants, herbs, phytochemicals, natural compounds, control NAFLD, identify new areas future Publications from years 2012-2022 were retrieved using Scopus database. research trends analyzed Biblioshiny VOSviewer tools. field seen a significant increase activity, indicated by annual growth rate 10 % number published manuscripts. China, Korea, USA emerged most prominent contributors specific field, supported their notable volumes publications citations. density revealed that frequently occurring authors' keywords related herbal species are, rank order
Язык: Английский
Процитировано
2Clinical and Translational Discovery, Год журнала: 2024, Номер 4(4)
Опубликована: Авг. 1, 2024
Recent research has highlighted the significant effects of high-fat diets (HFDs) on brain health, particularly focusing mitochondrial complex I activity and protein lipoxidation. Mitochondrial I, first enzyme electron transport chain, is crucial for oxidative phosphorylation adenosine triphosphate (ATP) production. In individuals consuming an HFD, notably increases, initially appearing beneficial due to enhanced energy However, this upregulation linked elevated reactive oxygen species (ROS) production, leading stress dysfunction. Over past 5 years, studies have associated imbalance with neurodegenerative conditions cognitive decline in obese individuals.1 The brain's demands are met primarily through phosphorylation, playing a pivotal role. context upregulated, ostensibly meet increased requirements. heightened downside. Increased closely ROS chemically molecules containing oxygen. While normal byproducts cellular metabolism, excessive production can overwhelm cell's antioxidant defences, (Figure 1).2, 3 Oxidative critical factor pathogenesis diseases. It damages components, including lipids, proteins DNA, disrupting functions cell death. brain, which high metabolic rate limited regenerative capacity, detrimental. Studies shown that individuals, exhibits higher levels damage, correlated impairments risk disorders such as Alzheimer's disease. Lipoxidation, modification by lipid peroxidation products, another consequence HFD. Lipid process where attack polyunsaturated fatty acids membranes, resulting formation aldehydes. These aldehydes covalently modify proteins, forming advanced lipoxidation end-products (ALEs). ALEs accumulate neural tissues alter structure function, impaired processes neuronal damage.4, synaptic function vulnerable Synaptic essential neurotransmission, their disrupt signal transduction, dysfunction, deficits changes. provided evidence accelerates peroxidation, thereby enhancing resultant damage exacerbates neuroinflammation promotes progression relationship between dietary fats health multifaceted, involving both proteomic HFDs been dynamics, biogenesis, fusion fission, maintaining health. biogenesis new mitochondria formed, while fission regulate morphology function. Disruptions these lead contributing damage.6 Proteomic analyses revealed differential expression involved defences inflammatory responses brain. changes indicate attempt adapt imposed adaptations often insufficient counteract detrimental altered metabolism suggests shift pathways, potentially neurons.7 Similarly, defence reflect efforts combat stress, though overwhelmed Understanding underscores importance patterns neurological well-being. This knowledge clinical translational medicine, it informs development targeted interventions mitigate adverse Interventions could focus modulating reducing protect dietary-induced obesity. By integrating recommendations, lifestyle modifications therapies, clinicians better support well-being prevent face challenges.8 Vetriselvan Subramaniyan Ainil Hawa Jansi: Conceptualization; Methodology; Supervision; Writing review editing. Harshini Muruganantham: Resources final proofreading. authors thankful Monash Sunway University Library. declare no conflicts interest. Data sharing does not apply article datasets were generated or analysed during current study.
Язык: Английский
Процитировано
1International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(17), С. 9573 - 9573
Опубликована: Сен. 4, 2024
Alzheimer’s disease (AD) represents a significant global health challenge and affects approximately 50 million people worldwide. This overview of published reviews provides comprehensive understanding the intricate correlations between AD body composition, focusing particularly on obesity. We used systematic approach to collect analyze relevant topic obesity disease. A search electronic databases, including PubMed, MEDLINE, Google Scholar, was conducted. searched keywords such as “Alzheimer’s disease”, “body composition”, “lean mass”, “bone “fat mass”. considered only written within past 5 years in English. Fifty-six were identified that shed light multiple connections composition. The review involves several aspects, impact lean mass, bone endocrinological factors related obesity, well inflammation, neuroinflammation, molecular/genetic factors. findings highlight complex interplay these elements development AD, underscoring need for holistic approaches reduce risk explore innovative strategies diagnosis, prevention, treatment.
Язык: Английский
Процитировано
1International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(23), С. 12637 - 12637
Опубликована: Ноя. 25, 2024
Neurodegeneration is preeminent in many neurological diseases, and still a major burden we fail to manage patient's care. Its pathogenesis complicated, intricate, far from being completely understood. Taking multiple sclerosis as an example, propose that neurodegeneration neither cause nor consequence by itself. Mitochondrial dysfunction, leading energy deficiency ion imbalance, plays key role neurodegeneration, partly caused the oxidative stress generated microglia astrocytes. Nodal paranodal disruption, with or without myelin alteration, further involved. Myelin loss exposes axons directly inflammatory environment. Moreover, oligodendrocytes provide singular metabolic trophic support axons, but do not emerge unscathed pathological events, primary defects cell apoptosis secondary neuroinflammation axonal damage. Hereby, failure might be overlooked contributor neurodegeneration. Thus, complex interplay between neuroinflammation, demyelination, wherein each primarily secondarily involved, offer more comprehensive understanding of help establishing novel therapeutic strategies for diseases beyond.
Язык: Английский
Процитировано
1Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Авг. 7, 2024
Язык: Английский
Процитировано
0Опубликована: Янв. 1, 2024
Процитировано
0