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- 2025| Bentham Science Publ...The benefits of physical activity (PA) are well established. However, the majority of children worldwide fail to meet the recommended weekly requirements for PA, which are essential for enhancing cardiorespiratory fitness (CRF) and maintaining a healthy weight for their age. The present review evaluated published work in an effort to study the effects of body composition on aerobic fitness levels and hemodynamic factors in children. Studies were retrieved from the following databases: Cochrane Database of Systematic Reviews, PubMed (2013-June 2024), Google Scholar, Scopus, Science Direct, EBM Reviews, Current Contents, CISTI Source (2011-June 2024), Sports Discuss (2019-June 2024), and international e-catalogues. Search analysis from these periods represents recent developments, ensuring that the review reflects up-to-date understanding in the field. This helps incorporate the latest methodologies, findings, and technological advancements, and strengthens the validity of this review. The population consists of children from both industrialized and developing nations. The selected study designs were cross-sectional, longitudinal, cohort, review, and systematic review. The analysis of research entailed reading titles, abstracts, and complete texts. Following these processes, thirty articles were considered for review. The broad investigation aims to reveal the effects of body composition on aerobic fitness levels and hemodynamic parameters in preventing childhood obesity. The search strategy, as well as Medical Subject Heading (MeSH) phrases and keywords, were used to effectively route significant papers addressing childhood obesity. The relevant terms were “body composition,” “overweight,” “obesity,” “physical activity,” “heart rate,” “blood pressure,” “aerobic fitness”, “nutrition,” “cardiovascular disease,” and “children aged 10-18 years old.”We discovered 12972 publications related to childhood obesity, hemodynamic variables, physical activity (PA), and aerobic fitness; however, 9194 articles were deleted due to duplication. The number of studies left after removing duplicates was 3778. Furthermore, 1657 articles were removed because they were not in English, 1240 articles had no full text available, and 809 articles only included abstracts. Moreover, the full text was reviewed for eligibility, which included 42 reference reviews and 18 titles. Finally, 30 articles were deemed eligible for review.The existing literature suggests that additional investigation is warranted to delineate a precise course of action for mitigating the risks associated with childhood obesity. This entails placing a heightened emphasis on the significance of children engaging in aerobic fitness activities.
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- Traditionally recognised as the energy reservoir and main site of adaptive thermogenesis, white and brown adipose tissues are complex endocrine organs regulating systemic energy metabolism via the secretion of bioactive molecules, termed “adipokines” and “batokines”, respectively. Due to its significant role in regulating whole-body energy metabolism and other physiological processes, adipose tissue has been increasingly explored as a feasible therapeutic target for obesity. Flavonoids are one of the most significant plant polyphenolic compounds holding a great potential as therapeutic agents for combating obesity. However, understanding their mechanisms of action remains largely insufficient to formulate therapeutic theories. This review critically discusses scientific evidence highlighting the role of flavonoids in ameliorating obesity-related metabolic complications, including adipose tissue dysfunction, inflammation, insulin resistance, hepatic steatosis, and cardiovascular comorbidities in part by modulating the release of adipokines and batokines. Further discussion advocates for the use of therapeutics targeting these bioactive molecules as a potential avenue for developing effective treatment for obesity and its adverse metabolic diseases such as type 2 diabetes.
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- We previously demonstrated that an aspalathin-enriched green rooibos extract (GRE) reversed palmitate-induced insulin resistance in C2C12 skeletal muscle and 3T3-L1 fat cells by modulating key effectors of insulin signalling such as phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/AKT) and AMP-activated protein kinase (AMPK). However, the effect of GRE on hepatic insulin resistance is unknown. The effects of GRE on lipid-induced hepatic insulin resistance using palmitate-exposed C3A liver cells and obese insulin resistant (OBIR) rats were explored. GRE attenuated the palmitate-induced impairment of glucose and lipid metabolism in treated C3A cells and improved insulin sensitivity in OBIR rats. Mechanistically, GRE treatment significantly increased PI3K/AKT and AMPK phosphorylation while concurrently enhancing glucose transporter 2 expression. These findings were further supported by marked stimulation of genes involved in glucose metabolism, such as insulin receptor (Insr) and insulin receptor substrate 1 and 2 (Irs1 and Irs2), as well as those involved in lipid metabolism, including Forkhead box protein O1 (FOXO1) and carnitine palmitoyl transferase 1 (CPT1) following GRE treatment. GRE showed a strong potential to ameliorate hepatic insulin resistance by improving insulin sensitivity through the regulation of PI3K/AKT, FOXO1 and AMPK-mediated pathways.
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- Enlargement of adipose tissue through hypertrophy is a key hallmark of obesity. Our previous study demonstrated that chronic obesity induces brown adipose tissue hypertrophy and altered batokine gene expression patterns in vivo. The present study further explored and verified the pathophysiological and molecular changes implicated in brown adipocyte hypertrophy by exposing T37i cells to 0.25, 0.5, 0.75, and 1 mM of palmitic acid for 48 h. The results showed that palmitic acid-induced intracellular lipid accumulation and lipolysis. Gene expression analysis demonstrated that palmitic acid downregulated genes responsible for glucose and lipid metabolism, such as AdipoQ and PIk3r1, while upregulating Cpt1A, a mitochondrial fatty acid transporter, and Tnf-α, a pro-inflammatory cytokine. Moreover, palmitic acid downregulated brown adipocyte transcriptional factors and thermogenic markers, including Prdm16, Pparg, Cidea, Dio2, Sirt1, and Ucp1. Gene expression of batokines involved in regulating substrate metabolism (Fgf21), angiogenesis (Nrg4 and VegfA), and immune cell recruitment (Metrnl, Gdf15, and Cxcl14) were altered by palmitic acid. This data has demonstrated that palmitic acid contributes to the hypertrophy and whitening of brown adipocytes by inhibiting brown adipocyte differentiation and altering batokines expression patterns.
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- It remains essential to decipher some of the pathological mechanisms that link obesity with deterio rating human health. Insulin resistance, due to enhanced free fatty acid substrate delivery, results in disrupted glucose homeostasis and altered mitochondrial oxidative capacity, which is a characteristic feature of an obese state. In fact, as a major site for regulating glucose homeostasis and energy pro duction in response to insulin, the skeletal muscle has become an interesting target tissue to understand the impact of lipid overload on the development of insulin resistance and impaired mitochondrial respiratory function. In addition to systematically retrieving the discussed data, the current review brings an essential perspective in understanding the relevance of experimental models of lipid overload such as high fat diets in understanding the pathological link between insulin resistance and pathological changes in mitochondrial oxidative capacity. Importantly, inclusion of evidence from transgenic model highlights some of the unique molecular targets that are implicated in the development of insulin resistance and inefficient mitochondrial respiration processes within an obese state. Importantly, saturation with lipid products such as ceramides and diacylglycerols, especially within the skeletal muscle, appears to be instrumental in paving the path leading to worsening of metabolic complications. These metabolic consequences mostly interfere with the efficiency of the mitochondrial electron transport chain, leading to overproduction of toxic reactive oxygen species. Therefore, therapeutic agents that reverse the effects of lipid overload by improving insulin sensitivity and mitochondrial oxidative capacity are crucial for the management or even treatment of metabolic diseases.
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