JOURNAL OF NANOBIOTECHNOLOGY
·
2025
·Vol. 23
·期 1
·1-18
·
IF 12.6
Wang Yingqian,Ma Zeqiang,Jiang Lehua,Bojan Nataraj,Sha Yiwen,Huang Boyu,Ming Lianxi,Shen Junnan,Pang Weijun
Background Skeletal muscle lipid deposition is a key manifestation of obesity, often accompanied by decreased exercise capacity and muscle atrophy. Skeletal muscle as the largest organ in the body, makes it challenges for designing targeted drug delivery systems. Lipid nanoparticles (LNPs) are widely used as a safe and efficient delivery carrier, there is limited research on LNPs that specifically target skeletal muscle. Results A LNP designed with five specific receptor complements on its surface, which specifically targets skeletal muscle in vivo in mice, without off-target effects on other tissues and organs. MiR-130a, a regulator of PPARG, which is a key factor in skeletal muscle lipid deposition, was encapsulated with LNP (LNP@miR-130a). In high-fat diet (HFD) mice, LNP@miR-130a effectively reduced skeletal muscle lipid deposition, increased exercise activity and enhanced muscle mass. Interestingly, the myokines in skeletal muscle have also changed which may leading to reduce the adipose tissue weight and liver lipid deposition in HFD mice. Conclusions These results indicated LNP@miR-130a is a promising inhibitor of skeletal muscle lipid deposition and may help alleviate obesity. This study provides new insights for obesity treatment and lays foundation for the development of targeted skeletal muscle therapeutics. Graphical
研究领域:
生物医学
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分子生物学
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药剂学
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DOI
PubMed
高影响因子
Nutrients
·
2023
·Vol. 15
·期 17
·3736
·
IF 5.9
Changbao Sun,Ang Li,Huan Wang,Jiage Ma,Juncai Hou
Acetate is associated with adipocyte differentiation and lipid deposition. To further develop this scientific point, obese mice on a high-fat diet were given an intragastric administration of acetate for 8 weeks and mouse adipose mesenchymal stem cells (mAMSCs) were treated with acetate for 24 h. The results showed that the body weight, food intake, Lee’s index, adipose tissue coefficient, liver index, blood lipid levels, insulin resistance, pro-inflammatory factors levels and fatty lesions in liver and adipose tissue in obese mice treated with acetate increased markedly, while anti-inflammatory factors levels and liver function decreased significantly (p< 0.05). The mRNA expression levels of PPAR-γ, C/EBP-α, SREBP, AFABP, FAS, ACC-1, SCD-1, LPL, LEPR, GPR41 and GPR43 genes in adipose tissue and mAMSCs were significantly increased, while the mRNA expression levels of HSL, CPT-1, CPT-2, AMPK, AdipoR1 and AdipoR2 genes were significantly reduced (p< 0.05). Except for AMPK-α signaling pathway proteins, the phosphorylation levels of p38 MAPK, ERK1/2, JNK and mTOR were significantly increased (p< 0.05) and these changes were dose-dependent. The findings indicated that acetate played a positive role in regulating adipocyte differentiation and lipid deposition by activating MAPKs and mTOR signaling pathways (the expression up-regulation of genes such as PPAR-γ, C/EBP-α and SREBP-1, etc.) and inhibiting the AMPK signaling pathway (the expression down-regulation of genes such as HSL, CPT-1 and AMPK-α, etc.).Keywords:obesity;lipid metabolism;acetate;adipocyte differentiation;lipid deposition
研究领域:
营养学
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分子生物学
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内分泌学
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产品关联
DOI
PubMed
高影响因子
Comparative Biochemistry and Physiology D-Genomics & Proteomics
·
2025
·
IF 2.4
Changqing He,Youheng Huang,Silvana Rahayu,Hao Liu,Yang Huang,Gang Shi,Huapu Chen,Guangli Li,Chunhua Zhu,Mouyan Jiang
The leopard coral grouper ( Plectropomus leopardus ), an increasingly important species in marine aquaculture, has garnered significant research interest due to its high market value. Despite extensive research on ovarian growth and development in fish, the molecular mechanisms governing lipid droplet formation and lipid deposition in P. leopardus remain poorly understood. In this study, we conducted transcriptomic analyses of P. leopardus ovaries at three developmental stages: primary growth (PG), pre-vitellogenesis (PV), and mid-vitellogenesis (MV). A total of 534,847,090 raw reads were obtained from nine cDNA libraries, leading to the identification of 19,155 genes with 13,817 genes expressed at all stages. Differential analysis showed that 1012, 2609, and 4039 genes were up-regulated, while 168, 277, and 577 genes were down-regulated in the three comparisons, respectively. Functional enrichment analyses highlighting the critical roles of differentially expressed genes (DEGs) in lipid transport (such as fatp1 , fatp4 , fatp6 , apoeb , lpl and fabps ), fatty acid metabolism (such as elovl6, acsl1 , dgat2 and gpat4 ) and phospholipid metabolism (such as ept1 , chka and pla2g15 ). These findings underscore their contribution to lipid droplet formation and deposition. Furthermore, key signaling pathways, including Wnt, mTOR, PPAR and PI3K/Akt, were implicated in regulating these processes. The reliability of the RNA-seq data was confirmed through qPCR validation of 10 lipid-related genes. Based on these results, we propose a model for lipid droplet formation and lipid deposition during ovarian development in P. leopardus . This study advances our understanding of ovarian development in P. leopardus and provides a foundation for future research on marine fish reproduction, with potential applications in species conservation and aquaculture management.
研究领域:
水产养殖学
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分子生物学
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生殖生物学
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DOI
PubMed
高影响因子
Frontiers in Veterinary Science
·
2025
·
IF 2.9
Wenhao Tan,Kunyu Jiang,Yuhan Zhang,Hang Gao,Xingyi Tang,Sha Jiang
To investigate the effects of AdipoRon on fatty liver syndrome (FLS) in chicken, we used a corticosterone (CORT)-induced fatty liver model in Cobb broilers in vivo and fat emulsion-induced model in Leghorn male hepatoma cells (LMH) in vitro. In the in vivo study, eighteen 33-day-old male Cobb broilers were randomly assigned to three groups: control group (CONT, vehicle), corticosterone-treated group (CORT, 4 mg/kg), and corticosterone with AdipoRon-treated group (CORT-AR, 4 mg/kg and 0.2 mg/kg, 1 time/1 day) for 5 days. The results showed AdipoRon reduced CORT-induced increase in liver crude fat content (p < 0.05), increased protein expressions of peroxisome proliferator-activated receptor α (PPARα) (p < 0.05) and adiponectin (ADPN) (p < 0.05), and suppressed the protein expressions of Acetyl-CoA carboxylase 1 (ACC) (p < 0.05) and phosphorylated c-Jun N-terminal kinase 1 (p-JNK1) (p < 0.05) in the liver. In the in vitro study, LMH cells were divided into control (CN), fat emulsion (FE, 10%), and FE + AdipoRon (4 μM) group (FE-AR). AdipoRon reduced FE-induced lipid accumulation (p < 0.05), decreased the protein expression of ACC and tumor necrosis factor-alpha (TNF-α), and enhanced PPARα, the phosphorylation of adenosine 5′-monophosphate-activated protein kinase (AMPK), and carnitine palmitoyl transferase 1 (CPT-1) (p < 0.05). In conclusion, AdipoRon effectively reduces hepatic lipid deposition in CORT-induced FLS broilers, likely through PPARα activation and inhibition of lipid synthesis via ACC downregulation.
研究领域:
兽医学
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动物营养学
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分子生物学
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代谢病学
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药理学
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产品关联
DOI
PubMed
高影响因子
ATHEROSCLEROSIS
·
2024
·
IF 4.9
Yanhua Zhen,Jiaqi Yang,Ji Song,Zeyu Xing,Jiahe Zheng
Background and aims Atherosclerosis (AS), an arterial vasculature disease, is characterized by abnormal lipid accumulation and inflammatory response. ADP ribosylation factor like GTPase 11 (ARL11) is linked to multifarious processes in cells. This study aims to clarify the underlying mechanism of ARL11 in AS. Methods ApoE -/- mice fed with high-fat diet were used as the mouse models of AS. Gene expression in AS was determined by mRNA-sequencing. The ARL11 expression was detected by real-time PCR, western blot and immunofluorescence. The M1 polarization of macrophages was indicated by TNF-α and IL-6 levels detected by ELISA and iNOS expression determined by real-time PCR and western blot. The role of ARL11 during AS was explored through loss-of-function. Results There were 1301 upregulated and 1110 downregulated genes during AS. These differently expressed genes (DEGs) were mainly enriched in pathways and terms which are involved in inflammation. Moreover, Arl11 was highly expressed in AS models. Downregulation of Arl11 decreased the lipid deposition and atherosclerotic plaques in the aortas of AS mice, and declined inflammatory cytokines and M1 polarization of macrophages induced by IFN-γ. Furthermore, ARL11 interacted with JAK2 and p-JAK2 and modulated their degradation, thus inhibiting the activation of JAK2/STAT1 pathway. Conclusions : ARL11 promoted the development of AS via interacting with JAK2 and activating JAK2/STAT1 pathway. Thus, silencing ARL11 may prevent the process of AS and be a novel way to treat AS.
研究领域:
心血管疾病
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分子生物学
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免疫学
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DOI
PubMed
高影响因子
AQUACULTURE
·
2023
·
IF 4.5
Wei Zhao,Rong Yao,Han-Lin Wei,Yu-Cai Guo,An-Qi Chen,Bao-Yang Chen,Jin-Niu
This study aimed to examine the effects of high-fat diets supplemented with astaxanthin , chlorogenic acid, and bile acid on the growth, lipid accumulation, oxidation resistance, inflammatory response, and liver morphology in Oncorhynchus mykiss cultured in the convection-water cages. Fish were fed five isonitrogenous diets (D1: 20% lipid; D2: 30% lipid; D3: 30% lipid +0.1% BASF astaxanthin; D4: 30% + 0.06% chlorogenic acid; and D5: 30% lipid +0.1% bile acid) for 6 weeks. The results found that fish fed the D2 diet achieved a lower growth, while the optimal growth was identified in D4 diet. The higher crude lipid contents in the whole body were identified in fish fed the D3-D5 diets. Fish fed the high-fat diet showed liver vacuolization and lower superoxide dismutase (SOD) activity and transcriptional levels of NF-E2-related nuclear factor 2 ( Nrf2 ), catalase ( CAT ) , and SOD , as well as higher malondialdehyde content. Supplementing above three additives can reverse above results and enhance the total antioxidant capacity. Besides, the three additives alleviated the inflammatory responses caused by the high-fat diet via inhibiting proinflammatory cytokines. Moreover, high-fat diet reduced the endogenous lipid production and promoted the lipoprotein hydrolysis by increasing the lipoprotein lipase and inhibiting the fatty acid synthesis . The above results showed that three additives could mitigate the negative effects caused by the high-fat diet. Among them, astaxanthin showed the best antioxidant and anti-inflammatory properties and chlorogenic acid could elevate the growth greatest.
研究领域:
营养学
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水产养殖学
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生物化学
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产品关联
DOI
高影响因子
Food Bioscience
·
2023
·
IF 5.2
Hengju Ge,Jiaxin Li,Yang Xu,Jiahong Xie,Naymul Karim,Fujie Yan,Jianling Mo,Wei Chen
Curcumin (CUR), the main compound extracted from Curcuma longa , has various biological actions, including hepatoprotective, anti-infective, anti-inflammatory, antioxidant, and neurotrophic properties. But it has not yet been clarified how CUR affects the accumulation of fatty in hepatic cells. Our study uncovered that CUR decreased the lipid deposition in free fat acids (FFAs)-treated hepatocytes, which could be blocked by Compound C (an AMPK inhibitor). This result suggests that protective effect was associated with the AMPK pathway activation. MiR-3666 directly targets the AMPK gene, and overexpression of miR-3666 greatly weakens the hypolipidemic effect of CUR. Our results showed that CUR reduced FFAs-induced lipid deposition by targeting miR-3666. This boosted AMPK phosphorylation and inhibited its downstream targets, including ACC and SREBP1 . These findings together confirm that CUR-mediated inhibition of miR-3666 to activate the AMPK pathway is a potential alternative for alleviation of hepatic lipid deposition.
研究领域:
药理学
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分子生物学
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肝病学
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产品关联
DOI
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
·
2023
·
IF 13.6
Rui Zhang,Jingyao Guo,Yupeng Wang,Rundong Sun,Guangzhu Dong,Xinru Wang,Guizhen Du
The increased usage of bisphenol S (BPS) results in wide distribution in pregnant women. In this study, pregnant mice were given multiple-dose BPS during gestation. Results showed that prenatal BPS exposure (50 μg/kg/day) induced increased weight gain, dyslipidemia, higher liver triglyceride (TG), adipocyte hypertrophy, and hepatic lipid deposition in male offspring . Exosomes play important roles in regulating lipid metabolism . Here, serum exosomes and adipose miRNA sequencing of male offspring indicated a remarkable decrease in miR-29a-3p expression. To clarify whether adipocyte-derived exosomes mediate hepatic lipid deposition, exosomes were extracted from BPS-treated adipocytes and co-cultured with hepatocytes. These exosomes could be taken up by hepatocytes and promoted lipid deposition, and notably, exosomal miR-29a-3p was downregulated. Furthermore, miR-29a-3p knockdown in adipocyte-derived exosomes promoted hepatocyte lipid deposition, whereas overexpression led to the opposite effect. Also, the role of miR-29a-3p was demonstrated in hepatocytes by overexpressing or knocking it down. Subsequent studies have shown that miR-29a-3p can promote lipid deposition by directly targeting Col4a1 . Taken together, prenatal BPS exposure could lead to lower miR-29a-3p yield in adipocyte-derived exosomes and decrease miR-29a-3p content transported to hepatocytes, which further negatively regulate Col4a1 and promote hepatic lipid deposition. Our findings provided clues to maternal environmental exposure-induced liver metabolic diseases.
研究领域:
毒理学
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分子生物学
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内分泌学
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发育生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2025
·
IF 11.5
Anning Yang,Hongwen Zhang,Huiping Zhang,Nan Li,Cong Chen,Xiaoling Yang,Jue Tian,Jianmin Sun,Guizhong Li,Yue Sun,Bin Liu,Yideng Jiang
Atherosclerosis (AS) therapy has been commonly based on lipid-lowering agents ( e.g. , statins), supplemented by other therapies, such as anti-inflammatory agents and antioxidants, through traditional Chinese herbs. Ferroptosis, a form of regulated cell death characterized by iron-dependent lipid peroxidation, has been implicated in the progression of AS, particularly in macrophages. In the study, we constructed a macrophage targeted hybridization nanodrug of HMLRPP NPs, which used Pit-loaded Poly(lactic- co -glycolic) acid (PLGA) nanoparticles and Res-loaded liposomes (Lipo) as nano-core, then, coated with a macrophage membrane hybridized by hyaluronic acid (HA). The nanodrug prolonged blood circulation time and achieved optimal Res and Pit accumulation in the atherosclerotic plaques by effectively evading immune system clearance. In vivo studies demonstrated that HMLRPP NPs significantly attenuated plaque progression, characterized by decreased plaque area, less lipid deposition, and increased collagen. Meanwhile, HMLRPP NPs inhibited macrophage ferroptosis by decreasing the expression of β-Hydroxybutyrate dehydrogenase 1 (BDH1), Orosomucoid 1 (ORM1) and enhancing the expression of Ribosomal protein S27-like (RPS27L), which resulted in the alleviation of lipid accumulation and inflammation. Our data suggest that the HMLRPP nanodrug delivery system with ferroptosis-regulating capability provides a feasible therapeutic strategy for atherosclerosis.
研究领域:
药理学
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心血管疾病
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纳米医学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
KOREAN JOURNAL OF INTERNAL MEDICINE
·
2025
·Vol. 40
·期 1
·92
·
IF 2.4
Mingli Su,Ying Wang,Zheng Yan,Jia Luo,Jie Yang,Hua Ye,Aiming Liu,Julin Yang
Background/Aims Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood. Methods In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches. Results DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease. Conclusions DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.
研究领域:
药理学
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内分泌学
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营养学
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代谢学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Molecular Therapy-Nucleic Acids
·
2020
·
IF 7.032
Yihao Liu,Jie Wang,Xiaomin Zhou,Haigang Cao,Xiaoyu Zhang,Kuilong Huang,Xiao Li,Gongshe Yang,Xin’e Shi
Skeletal muscle is an important metabolic organ of the body, and impaired skeletal muscle differentiation can result in a wide range of metabolic diseases. It has been shown that microRNAs (miRNAs) play an important role in skeletal muscle differentiation. The aim of this study was to investigate the role of mmu-miR-324-5p in the differentiation of C2C12 myoblasts and lipid droplet deposition in myotubes for future targeted therapies. We found that mmu-miR-324-5p was highly expressed in mouse skeletal muscle. Overexpression of miR-324-5p significantly inhibited C2C12 myoblast differentiation while promoting oleate-induced lipid accumulation and β-oxidation in C2C12 myoblasts. Conversely, inhibition of mmu-miR-324-5p promoted C2C12 myoblast differentiation and inhibited lipid deposition in myotubes. Mechanistically, mmu-miR-324-5p negatively regulated the expression of long non-coding Dum (lncDum) and peptidase M20 domain containing 1 (Pm20d1) in C2C12 myoblasts. Reduced lncDum expression was associated with a significant decrease in the expression of myogenesis-related genes. Knockdown of mmu-miR-324-5p increased the levels of lncDum and myogenesis-related gene expression. Following oleate-induced lipid deposition in C2C12 myoblasts, overexpression of mmu-miR-324-5p decreased the expression of Pm20d1 while increasing the expression of mitochondrial β-oxidation and long-chain fatty acid synthesis-related genes. In conclusion, we provide evidence that miR-324-5p inhibits C2C12 myoblast differentiation and promotes intramuscular lipid deposition by targeting lncDum and Pm20d1, respectively.
研究领域:
分子生物学
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细胞生物学
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肌肉生理学
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代谢
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产品关联
DOI
PubMed
高影响因子
CELLULAR AND MOLECULAR LIFE SCIENCES
·
2022
·Vol. 79
·期 7
·1-22
·
IF 9.207
Song Chang-Chun,Pantopoulos Kostas,Chen Guang-Hui,Zhong Chong-Chao,Zhao Tao,Zhang Dian-Guang,Luo Zhi
Iron is an essential micro-element, involved in multiple biological activities in vertebrates. Excess iron accumulation has been identified as an important mediator of lipid deposition. However, the underlying mechanisms remain unknown. In the present study, we found that a high-iron diet significantly increased intestinal iron content and upregulated the mRNA expression of two iron transporters ( zip14 and fpn 1). Intestinal iron overload increased lipogenesis, reduced lipolysis and promoted oxidative stress and mitochondrial dysfunction. Iron-induced lipid accumulation was mediated by hypoxia-inducible factor-1 α (HIF1α), which was induced in response to mitochondrial oxidative stress following inhibition of prolyl hydroxylase 2 (PHD2). Mechanistically, iron promoted lipid deposition by enhancing the DNA binding capacity of HIF1α to the pparγ and fas promoters. Our results provide experimental evidence that oxidative stress, mitochondrial dysfunction and the HIF1α-PPARγ pathway are critical mediators of iron-induced lipid deposition.
研究领域:
营养学
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生物化学
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分子生物学
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细胞生理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）