Adipocyte最新文献

Considering the adverse effects of marketed drugs, we isolated and analysed topse fish oil (FO) in this study for the first time and examined its effect on obesity. Topse, scientifically known as Polynemus paradiseus, is a common fish species found in the maritime environment of the West Bengal region. To explore the role of marine P. paradiseus FO in alleviating obesity-related metabolic disorders in vivo model. Twenty-four male BALB/c mice with a standard body weight of 18.2 ± 2.1 g were taken and randomly divided into four groups: control group (C), normal chow feeding; obese control (OC), high fat diet (HFD) feeding; Treatment I (T-I) and Treatment II (T-II) group received 200 mg and 400 mg crude oil/kg body weight/day by gavage along with HFD. Here, we examined the effects of P. paradiseus oil on white adipose tissue (WAT) weight, lipid profiles, blood glucose, and adipokine expression levels in the OC group compared to the treated groups to evaluate the anti-obesity effects of FO. Compared to the HFD-induced OC group, the treated obese mice group (T-I and T-II) showed a significant reduction in body weight, Body Mass Index (BMI), and serum lipid profiles following the application of FO. The FO-treated HFD-induced obese mice group showed a moderate reduction in obesity and inflammatory-related adipocytokines compared to the OC group. Topse FO was enhanced with a large amount of essential fatty acids (FAs) and it might be administered as a dietary supplement to prevent obesity.

Obesity is associated with chronic inflammation and disruptions in cellular homeostasis, including impaired autophagy in adipose tissue. This study aimed to investigate the key mitophagy markers in the adipose tissue of individuals with obesity, compared to healthy controls. A total of 60 participants were enrolled, comprising 30 individuals with obesity and 30 healthy controls. Adipose tissue and peripheral blood samples were collected from all participants. Biochemical analyses included measurement of tumor necrosis factor-alpha (TNF-α), leptin, succinate dehydrogenase (SDH), and oxidative stress markers. Gene expression levels of mitophagy-related genes, PARK2, PINK1, and BNIP3L were assessed using quantitative real-time PCR. Additionally, immunohistochemistry was performed to evaluate BNIP3L protein levels in adipose tissue. Compared to the control group, individuals with obesity showed significantly elevated levels of TNF-α and SDH, along with evidence of oxidative stress. Moreover, the expression of PARK2, PINK1, and BNIP3L was significantly upregulated in the obesity group, suggesting increased mitophagy activity in adipose tissue. These findings indicate heightened inflammation and upregulation of mitophagy pathways in the adipose tissue of individuals with obesity. The upregulation of mitophagy-related genes seems to indicate a possible activation of mitophagy-associated pathways in the altered metabolic and inflammatory environment of obesity.

White and brown adipocytes differ markedly in lipid composition and metabolic function. White adipocytes primarily serve as energy storage depots, whereas brown adipocytes are mitochondria-rich and specialized for thermogenesis. However, the lipidomic profiles of white-like (WLAs) and brown-like adipocytes (BLAs) differentiated from human mesenchymal stem cells (MSCs) remain incompletely characterized. Human adipose-derived MSCs were differentiated into WLAs and BLAs. Lipid fractions were isolated and analysed by gas-liquid chromatography. Fatty acid composition data were used to calculate indices of stearoyl-CoA desaturase-1 (SCD1) activity, elongation, and ω6 synthesis. Compared to MSCs, BLAs showed consistently elevated oleate (≥4.2-fold) and stearate (≥2.3-fold), along with reduced palmitate (≤-20%) and linoleate (≤-28%) across phospholipid, triglyceride, and free fatty acid fractions. WLAs versus MSCs showed similar trends, with oleate increasing up to 15-fold and palmitate decreasing by 67-82% depending on the lipid class. SCD1 activity and elongation indices were elevated in WLAs (SCD1: up to 4.7-fold; elongation: up to 28-fold). The ω6 synthesis index was also increased in triglyceride and free fatty acid fractions of WLAs (≥3.3-fold), but markedly suppressed in BLAs (≤-88.7%). WLAs and BLAs differentiated from MSCs exhibit distinct lipid profiles and inferred enzymatic activity patterns, reflecting their respective capacities for lipid storage and metabolic flexibility. These findings provide a foundation for future translational research aimed at targeting adipose tissue in obesity and metabolic diseases.

Stem cell-based bone tissue engineering offers a promising approach for treating oral and cranio-maxillofacial bone defects. This study investigated the role of Atoh8, a key regulator in various cells, in the osteogenic potential of adipose-derived stem cells (ADSCs). ADSCs transfected with small interfering RNA (siRNA) targeting Atoh8 were evaluated for proliferation, migration, adhesion, and osteogenic capacity. In vivo, 20 SD rats were used to assess bone regeneration using Atoh8-knockdown ADSC sheets, with new bone formation quantified via micro-CT and histological analysis. Atoh8 knockdown in vitro reduced ADSC proliferation and migration but enhanced osteogenic differentiation and upregulation of osteogenic-related factors. This approach improved bone healing in rat defect models, accelerating repair both in vitro and in vivo. The findings underscore the clinical potential of ADSCs in bone tissue engineering and elucidate Atoh8's regulatory role in ADSC osteogenesis, providing a novel therapeutic strategy for enhancing bone regeneration through targeted modulation of stem cell differentiation pathways.

Obesity remains a global health challenge, underscoring the need for more effective therapeutic strategies. Recent evidence highlights the central role of adipose tissue autophagy in metabolic homoeostasis, with its dysregulation contributing to obesity-related pathophysiology. MicroRNAs (miRNAs) have emerged as critical regulators of autophagy in adipocytes, influencing differentiation, lipid metabolism, and systemic energy balance. This review synthesizes current knowledge on how specific miRNAs modulate autophagic activity in adipose tissue and discusses their functional impact on adipocyte biology. Based on the accumulated evidence, we conclude that targeting miRNA-mediated autophagy pathways holds significant therapeutic potential for obesity and related metabolic disorders. Future research should focus on translating these mechanistic insights into targeted interventions, overcoming delivery challenges, and advancing miRNA-based therapeutics towards clinical application.

Objective: Brown adipose tissue activation is a potential anti-obesity strategy. N⁷-methylguanosine (m⁷G) modification is a novel RNA epigenetic modification, but its role in adipose metabolism remains unexplored.

Methods: Male mice were fed a high-fat diet (HFD), followed by PCR array screening. Gain-of-function experiments and TRAC-seq were employed to explore WDR4 function.

Result: A Mouse Epigenetic Modification Enzymes PCR Array revealed that WDR4 expression showed the most pronounced downregulation in HFD mice. Overexpression of WDR4 in 3T3-L1 cells and primary adipocytes significantly increased UCP1 expression and suppressed lipid droplet formation, and enhanced mitophagy as evidenced by mitochondrial ultrastructure, autophagic vesicles, and LC3 expression. Suppression of mitophagy using 3-MA and bafilomycin A1 attenuated WDR4-induced adipocyte browning. WDR4 overexpression enhanced translational activity and reshaped the tRNA m⁷G methylome in 3T3-L1 adipocytes, specifically induced 38 unique tRNA m⁷G modification sites, and increasing cleavage scores of multiple tRNAs. GSE229240 dataset revealed that WDR4 mutation significantly reduced translation efficiency of 195 genes enriched in the TGF-β signalling , including BMP8B. Knockdown of BMP8B partially counteracted WDR4-mediated mitophagy.

Conclusion: WDR4 promotes adipocyte browning by enhancing BMP8B translation through tRNA m⁷G modification, revealing a novel m⁷G epitranscriptomic mechanism with therapeutic potential for obesity.

Adipocyte hypertrophy is a critical contributor to obesity-induced inflammation and insulin resistance. This study employed a human adipocyte hypertrophy model to investigate the adipokine release, inflammatory responses, and the intracellular singling pathways. Hypertrophic adipocytes exhibited increased lipid content and lipolysis, a decline of anti-inflammatory adipokine adiponectin release and an increase of pro-inflammatory adipokine leptin release compared to mature adipocytes. Moreover, TNFα and LPS exacerbated the decrease in adiponectin secretion by hypertrophic adipocytes while promoting the secretion of leptin, MCP-1 and IL-6, which is associated with impaired activation of p38 and JNK MAPK and persistent activation of ERK and IκBα in hypertrophic adipocytes. These altered adipokine secretions and inflammatory responses within hypertrophic adipocytes may contribute to adipocyte dysfunction in human obesity.

A subpopulation of adipocytes in mice and humans is produced from haematopoietic stem cells rather than mesenchymal progenitors; the source of conventional white and brown/beige adipocytes. The abundance of these haematopoietic stem cell-derived adipocytes (HSCDAs) is elevated in female mice by ovariectomy (OVX) or oestrogen receptor alpha (ERα) knockdown, suggesting that they may be involved in the metabolic and inflammatory pathology that accompany the loss of oestrogen signalling. However, we previously demonstrated that ablation of HSCDAs elevated circulating leptin levels while suppressing physical activity and insulin sensitivity. Here, we tested the combined impact of OVX with and without HSCDA ablation. We discovered that HSCDA depletion plus OVX raised circulating leptin levels more than HSCDA depletion alone. Likewise, while HSCDA depletion or OVX alone inhibited physical activity and insulin responsiveness, their combination further suppressed these endpoints. Other physiologic endpoints were regulated by OVX alone. We conclude that HSCDAs play a role inthe maintenance of a subset of metabolic endpoints related to normal adipose tissue function, and their elevated production in models of female sex hormone suppression occurs to normalize these endpoints. The results highlight the ability of HSCDAs to target physical activity and insulin responsiveness, possibly by normalizing leptin production.

Skin contracts during wound healing to facilitate wound closure. In some patients, skin contraction can lead to the formation of skin contractures that limit movement, impair function, and significantly impact well-being. Current treatment options for skin contractures are burdensome for patients, and there is a high risk of recurrence. Autologous fat grafting can improve the structure and function of scarred skin; however, relatively little is known about the effect of fat on skin contraction. In this study, an in vitro tissue-engineered model of human skin was used to test the effects of adipose tissue and adipose-derived stromal cells on skin contraction. Untreated tissue-engineered skin contracted to approximately 60% of the original area over 14 days in culture. The addition of adipose tissue reduced this contraction by 50%. Adipose tissue, which was emulsified or concentrated and high doses of adipose-derived stromal cells (ADSC) were able to inhibit contraction to a similar degree; however, lower doses of ADSC did not show the same effect. In conclusion, the subcutaneous application of adipose tissue has the potential to inhibit skin contraction. This study provides in vitro evidence to support the use of autologous fat grafting to prevent skin contraction in patients most at risk.

Adipose tissue (AT), one of the largest endocrine tissues in the human body, is an important site for the storage and production of steroid hormones. In particular, AT's capacity to produce androgens could enable it to have a regulatory role in local or general hormone homoeostasis. The links between obesity, polycystic ovary syndrome (PCOS), metabolic disorders, and hormonal balance emphasise the importance of understanding the intricate relationships between AT and androgen dynamics within AT. This review, focusing on androgen metabolism, summarises the androgen profile in white adipose tissue (WAT) and brown adipose tissue (BAT) of humans and animal models, along with the androgen-metabolising enzymes present in WAT, and explores the role of androgens on AT physiology.