CTSK inhibitor exert its anti-obesity effects through regulating adipocyte differentiation in high-fat diet induced obese mice

Han, Junfeng; Li, Wei; Xu, Weibin; Lu, Junxi; Wang, Chen; Bao, Yuqian; Jia, Weiping

doi:10.1507/endocrj.ej14-0336

Cited by 15 publications

(12 citation statements)

References 15 publications

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“…Cathepsin K is not only involved in enhancing bone resorption, but also implicated in adipogenesis and glucose metabolism [47]. Inhibition of cathepsin K reduces body weight gain and glycaemia in HFD insulted rats [44, 47]. In the current study, we found that diabetes may potentiate cathepsin K expression.…”

Section: Discussionsupporting

confidence: 56%

“…The PPARγ agonists, rosiglitazone and GW1929, could increase osteoclastogenesis through enhancement of cathepsin K and tartrate-resistant acid phosphatase expressions in bone marrow-derived macrophages [43]. Conversely, inhibition of cathepsin K also down-regulates PPARγ expression in HFD-induced mice [44]. In addition, β-catenin activation enhances osteoblastogenesis and suppresses adipogenesis by inhibiting PPARγ expression [45].…”

Section: Discussionmentioning

confidence: 99%

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Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/β-Catenin in Rats

Wang

Zhao

et al. 2017

Cell Physiol Biochem

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Purpose: Increasing evidence supported that semaphorin 3A (Sema3A), insulin-like growth factor (IGF)-1 and β-catenin were involved in the development of osteoporosis and diabetes. This study is aimed to evaluate whether Sema3A/IGF-1/β-catenin is directly involved in the alterations of bone microarchitecture and bone strength of diabetic rats. Methods: Diabetic rats were induced by streptozotocin and high fat diet exposure. Bone microarchitecture and strength in the femurs were evaluated by micro-CT scanning, three-point bending examination and the stainings of HE, alizarin red S and safranin O/fast green, respectively. The alterations of lumbar spines microarchitecture were also determined by micro-CT scanning. Western blot and immunohistochemical analyses were used to examine the expression of Sema3A, β-catenin, IGF-1, peroxisome proliferator-activated receptor γ (PPARγ) and cathepsin K in rat tibias. Results: Diabetic rats exhibited decreased trabecular numbers and bone formation, but an increased trabecular separation in the femurs and lumbar spines. Moreover, the increased bone fragility and decreased bone stiffness were evident in the femurs of diabetic rats. Diabetic rats also exhibited a pronounced bone phenotype which manifested by decreased expression of Sema3A, IGF-1 and β-catenin, as well as increased expression of cathepsin K and PPARγ. Conclusions: This study suggests that diabetes could perturb bone loss through the Sema3A/IGF-1/β-catenin pathway. Sema3A deficiency in bone may contribute to upregulation of PPARγ and cathepsin K expression, which further disrupts bone remodeling in diabetic rats.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/β-Catenin in Rats

Wang

Zhao

et al. 2017

Cell Physiol Biochem

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“…[678] (2) enhancing lipid metabolism,[910] (3) enhancing thermogenesis,[1112] (4) inhibiting pancreatic lipase,[13141516] (5) inhibiting α-amylase activity,[171819] and (6) preventing adipocyte differentiation. [2021] In this review, we addressed the most recent studies about the antiobesity property of capsaicin and its possible mechanisms of action is also discussed.…”

Section: Trend Of Overweightmentioning

confidence: 99%

Current understanding of antiobesity property of capsaicin

Narang¹,

Jiraungkoorskul²,

Jamrus³

2017

Phcog Rev

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The capsaicin is an ingredient that we normally mix in food in many cultural cuisines even in fresh and dried production. Because of its anticancer, anticholesterolemic, antidiabetic, antihypertensive, anti-inflammatory, antimicrobial, and antioxidant properties, capsaicin is used worldwide. Moreover, capsaicin is also used for the protection of cardiovascular and hepatic diseases. The electronic databases PubMed, Scopus, Web of Science, Google Scholar, and ScienceDirect were searched since 2000 to present for antiobesity term. This review article is provided the update information about the antiobesity property and mechanism of capsaicin for further researches.

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“…At the cellular level, obesity is de ned as accelerated AT expansion and remodeling that induces either AT hypertrophy (i.e., adipocyte expansion due to excessive fat storage) or hyperplasia (i.e., increased adipogenesis from preadipocytes) through ECM remodeling and angiogenesis [7,8]. Various ECM proteins, including MMP2, ADAM, TIMP, CTSK, and CTSS, are altered in obese AT [9][10][11][12]. Angiogenic genes such as VEGF and ANGPT2 are upregulated in response to activated HIF1A (i.e., hypoxia-related transcription factor) [13,14].…”

Section: Introductionmentioning

confidence: 99%

Putative positive role of inflammatory genes in fat deposition supported by altered gene expression in purified human adipocytes and preadipocytes from lean and obese adipose tissues

Lee

Choi

Koh

et al. 2020

Preprint

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BackgroundObesity is a chronic low-grade inflammatory disease that is generally characterized by enhanced inflammation in obese adipose tissue (AT). Here, we investigated alterations in gene expression between lean and obese conditions using mRNA-Seq data derived from human purified adipocytes (ACs) and preadipocytes (preACs). ResultsWe defined four classes of differentially expressed genes (DEGs) by comparing gene expression between 1) lean and obese ACs, 2) lean and obese preACs, 3) lean ACs and lean preACs, and 4) obese ACs and obese preACs. Based on an analysis of comparison 1, numerous canonical obesity-related genes, particularly inflammatory genes including IL6, TNF- and IL-1, i.e., the genes that are expected to be upregulated in obesity conditions, were found to be expressed at significantly lower levels in obese ACs than in lean ACs. In contrast, some inflammatory genes were found to be expressed at higher levels in obese preACs than lean preACs in the analysis of comparison 2. These two results indicate that (1) up-/downregulation of genes in ACs and preACs is inversely controlled during the fat deposition process and (2) preACs rather than ACs have increased inflammatory response genes in comparisons of lean and obese conditions for each of these cell types. Analysis of comparisons 3 and 4 showed that inflammatory gene classes were expressed at higher levels in differentiated ACs than undifferentiated preACs under both lean and obese conditions; however, the degree of upregulation was greater for lean than for obese conditions.ConclusionsTaken together, our analyses may suggest that lean fat differentiation involves even greater enhancement of inflammatory responses than does obese fat differentiation.

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CTSK inhibitor exert its anti-obesity effects through regulating adipocyte differentiation in high-fat diet induced obese mice

Cited by 15 publications

References 15 publications

Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/β-Catenin in Rats

Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/β-Catenin in Rats

Current understanding of antiobesity property of capsaicin

Putative positive role of inflammatory genes in fat deposition supported by altered gene expression in purified human adipocytes and preadipocytes from lean and obese adipose tissues

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