Contribution of PGC-1α to Obesity- and Caloric Restriction-Related Physiological Changes in White Adipose Tissue

Kobayashi, Masaki; Deguchi, Yusuke; Nozaki, Yuka; Higami, Yoshikazu

doi:10.3390/ijms22116025

Cited by 34 publications

(39 citation statements)

References 139 publications

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“…Phosphorylated AMP-activated protein kinase alpha (pAMPKα), which is a crucial factor for energy homeostasis in adipose tissue [ 46 ] inhibits adipocyte differentiation [ 47 ] and adipogenesis [ 48 , 49 ]. Moreover, pAMPKα interacts with PPAR-γ coactivator 1 alpha (PGC-1α), which suppresses adipogenesis via morphological changes in white adipose tissue [ 50 ]. In the present study, both WP supplementation itself demonstrated by PGC-1α and WP supplementation with RE represented by pAMPK/AMPK improved energy metabolism homeostasis in sarcopenic obesity [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, both WP supplementation itself demonstrated by PGC-1α and WP supplementation with RE represented by pAMPK/AMPK improved energy metabolism homeostasis in sarcopenic obesity [ 51 ]. It is expected that WP supplementation regardless of RE significantly reduced fat mass and fat (epididymal) weight by inhibiting adipocyte differentiation demonstrated by PPAR-γ and C/EBPα under the activation of PGC-1α and AMPK in sarcopenic obese condition [ 50 ]. Adipose tissue maintains energy homeostasis itself and that of other organs by secretion and communication [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

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Effects of Whey Peptide Supplementation on Sarcopenic Obesity in High-Fat Diet-Fed Mice

Lim

2022

Nutrients

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The incidence of sarcopenic obesity gradually increased in parallel with the aged population. This research examined the effects of whey peptide (WP) supplementation with/without resistant exercise (RE) on sarcopenic obesity. Male 8-month-old C57BL/6J mice were fed a control diet (10 kcal% fat) or a high-fat diet (60 kcal% fat) for 8 weeks. High-fat diet-fed mice were randomly divided into four groups: obesity control group (OB), RE (RE only), WP (WP only), and WPE (RE and WP). WP supplementation (1500 mg/day/kg B.W.) gavage and RE (ladder climbing, five times weekly, 8–10 repetitions, 10–20% B.W. load) were conducted for an additional 8 weeks. Protein and mRNA levels of markers related to energy, protein, and lipid metabolism were analyzed in skeletal muscle and adipose tissue by one-way analysis of variance (ANOVA). WP supplementation regardless of RE significantly suppressed the increasing fat mass (p = 0.016) and decreasing lean mass (p = 0.014) and alleviated abnormal morphological changes in skeletal muscle and adipose tissue (p < 0.001). In adipose tissue, WP supplementation regardless of RE ameliorated dysregulated energy metabolism and contributed to the reduction in adipocyte differentiation (PPAR-γ (p = 0.017), C/EBPα (p = 0.034)). In skeletal muscle, WP supplementation regardless of RE alleviated energy metabolism dysregulation and resulted in down-regulated protein degradation (Atrogin-1 (p = 0.003), MuRF1 (p = 0.006)) and apoptosis (Bax) (p = 0.004). Taken together, the current study elucidated that WP supplementation regardless of RE has potential anti-obesity and anti-sarcopenic effects in sarcopenic obesity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Whey Peptide Supplementation on Sarcopenic Obesity in High-Fat Diet-Fed Mice

Lim

2022

Nutrients

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“…We selected two hub genes (PPARGC1a and COQ3) that were downregulated in all datasets and were closely related to mitochondrial function. Downregulation of PPARGC1a impairs mitochondrial biogenesis and oxidative metabolism in obesity (46). PPARGC1a expression has been reported to be altered in neurodegenerative disorders, leading to mitochondrial defects and increased ROS levels; increasing its levels results in reductions in Alzheimer's disease pathology and improvements in behavior (47).…”

Section: Discussionmentioning

confidence: 99%

Exploring the common gene signatures and pathogeneses of obesity with Alzheimer’s disease via transcriptome data

et al. 2022

Front. Endocrinol.

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BackgroundObesity is a complex condition that influences several organ systems and physiologic systems. Obesity (OB) is closely linked to Alzheimer’s disease (AD). However, the interrelationship between them remains unclear. The purpose of this study is to explore the key genes and potential molecular mechanisms in obesity and AD.MethodsThe microarray data for OB and AD were downloaded from the Gene Expression Omnibus (GEO) database. Weighted gene correlation network analysis (WGCNA) was used to delineate the co-expression modules related to OB and AD. The shared genes existing in obesity and AD were identified through biological process analyses using the DAVID website, which then constructed the Protein–Protein Interaction (PPI) Network and selected the hub genes by Cytoscape. The results were validated in other microarray data by differential gene analysis. Moreover, the hub gene expressions were further determined in mice by qPCR.ResultsThe WGCNA identifies five modules and four modules as significant modules with OB and AD, respectively. Functional analysis of shared genes emphasized that inflammation response and mitochondrial functionality were common features in the pathophysiology of OB and AD. The results of differential gene analysis in other microarray data were extremely similar to them. Then six important hub genes were selected and identified using cytoHubba, including MMP9, PECAM1, C3AR1, IL1R1, PPARGC1α, and COQ3. Finally, we validated the hub gene expressions via qPCR.ConclusionsOur work revealed the high inflammation/immune response and mitochondrial impairment in OB patients, which might be a crucial susceptibility factor for AD. Meanwhile, we identified novel gene candidates such as MMP9, PECAM1, C3AR1, IL1R1, PPARGC1α, and COQ3 that could be used as biomarkers or potential therapeutic targets for OB with AD.

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“…Caloric restriction and exercise contribute to PGC1α activation and associated health outcomes [ 343 , 344 , 345 , 346 , 347 , 348 ]. Aligning meal times with the circadian rhythms by time-restricted feeding in animal models can also modulate PGC1α activity and mitochondrial biogenesis.…”

Section: Mechanisms Of Chrononutrition In Energy Homeostasis and Obesitymentioning

confidence: 99%

Chrononutrition—When We Eat Is of the Essence in Tackling Obesity

Ahluwalia

2022

Nutrients

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Obesity is a chronic and relapsing public health problem with an extensive list of associated comorbidities. The worldwide prevalence of obesity has nearly tripled over the last five decades and continues to pose a serious threat to wider society and the wellbeing of future generations. The pathogenesis of obesity is complex but diet plays a key role in the onset and progression of the disease. The human diet has changed drastically across the globe, with an estimate that approximately 72% of the calories consumed today come from foods that were not part of our ancestral diets and are not compatible with our metabolism. Additionally, multiple nutrient-independent factors, e.g., cost, accessibility, behaviours, culture, education, work commitments, knowledge and societal set-up, influence our food choices and eating patterns. Much research has been focused on ‘what to eat’ or ‘how much to eat’ to reduce the obesity burden, but increasingly evidence indicates that ‘when to eat’ is fundamental to human metabolism. Aligning feeding patterns to the 24-h circadian clock that regulates a wide range of physiological and behavioural processes has multiple health-promoting effects with anti-obesity being a major part. This article explores the current understanding of the interactions between the body clocks, bioactive dietary components and the less appreciated role of meal timings in energy homeostasis and obesity.

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Contribution of PGC-1α to Obesity- and Caloric Restriction-Related Physiological Changes in White Adipose Tissue

Cited by 34 publications

References 139 publications

Effects of Whey Peptide Supplementation on Sarcopenic Obesity in High-Fat Diet-Fed Mice

Effects of Whey Peptide Supplementation on Sarcopenic Obesity in High-Fat Diet-Fed Mice

Exploring the common gene signatures and pathogeneses of obesity with Alzheimer’s disease via transcriptome data

Chrononutrition—When We Eat Is of the Essence in Tackling Obesity

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