• Animal Bioscience
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• v.34 no.4
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• pp.662-669
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• 2021

Objective: Effects of linseed oil (LO) supplementation on the fat content and fatty acid profile of breast meat, and the expression of three genes in the liver, breast muscle and fat tissues of commercial 154-day-old hybrid male turkeys were investigated. Methods: The animals in the control group were fed a commercially available feed and received no LO supplementation (n = 70), whereas animals in the LO group (n = 70) were fed the same basic diet supplemented with LO (day 15 to 21, 0.5%; day 22 to 112, 1%). The effect of dietary LO supplementation on fatty acid composition of breast muscle was examined by gas chromatography, and the expression of fatty acid desaturase 2 (FADS2), peroxisome proliferator activated receptor gamma (PPARγ), and insulin-like growth factor 1 (IGF1) genes was analysed by means of quantitative reverse transcription polymerase chain reaction. Results: The LO supplementation affected the fatty acid composition of breast muscle. Hepatic FADS2 levels were considerably lower (p<0.001), while adipose tissue expression was higher (p<0.05) in the control compared to the LO group. The PPARγ expression was lower (p<0.05), whereas IGF1 was higher (p<0.05) in the fat of control animals. There were no significant (p>0.05) differences in FADS2, PPARγ, and IGF1 gene expressions of breast muscle; however, omega-6/omega-3 ratio of breast muscle substantially decreased (p<0.001) in the LO group compared to control. Conclusion: Fatty acid composition of breast meat was positively influenced by LO supplementation without deterioration of fattening parameters. Remarkably, increased FADS2 expression in the liver of LO supplemented animals was associated with a significantly decreased omega-6/omega-3 ratio, providing a potentially healthier meat product for human consumption. Increased PPARγ expression in fat tissue of the LO group was not associated with fat content of muscle, whereas a decreased IGF1 expression in fat tissue was associated with a trend of decreasing fat content in muscle of the experimental LO group.

• Journal of Nutrition and Health
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• v.57 no.2
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• pp.171-184
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• 2024

Purpose: Although activating thermogenic adipocytes is a promising strategy to reduce the risk of obesity and related metabolic disorders, emerging evidence suggests that it is difficult to induce adipocyte thermogenesis in obesity. Therefore, this study aimed to investigate the regulation of adipocyte thermogenesis in diet-induced obesity. Methods: Adipose progenitor cells were isolated from the white and brown adipose tissues of control diet (CD) or high-fat diet (HFD) fed mice, and fully differentiated white and brown adipocytes were treated with β-agonists or 18-carbon fatty acids for β-adrenergic activation or peroxisome proliferator-activated receptor (PPAR) activation. Results: Compared to the CD-fed mice, the expression of uncoupling protein 1 (Ucp1) was lower in the white adipose tissue of the HFD-fed mice; however, this was not observed in the brown adipose tissue. The expression of peroxisome proliferator-activated receptor gamma (Pparg) was lower in the brown adipose progenitor cells isolated from HFD-fed mice than in those isolated from the CD-fed mice. Norepinephrine (NE) treatment exerted lesser effect on peroxisome proliferator-activated receptor-γ coactivator (Pgc1a) upregulation in white adipocytes derived from HFD-fed mice than those derived from CD-fed mice. Regardless which 18-carbon fatty acids were treated, the expression levels of thermogenic genes including Ucp1, Pgc1a, and positive regulatory domain zinc finger region protein 16 (Prdm16) were higher in the white adipocytes derived from HFD-fed mice. Oleic acid (OLA) and γ-linolenic acid (GLA) upregulated Pgc1a expression in white adipocytes derived from HFD-fed mice. Brown adipocytes derived from HFD-fed mice had higher expression levels of Pgc1a and Prdm16 compared to their counterparts. Conclusion: These results indicate that diet-induced obesity may downregulate brown adipogenesis and NE-induced thermogenesis in white adipocytes. Also, HFD feeding may induce thermogenic gene expression in white and brown primary adipocytes, and OLA and GLA could augment the expression levels.

• Archives of Pharmacal Research
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• v.27 no.11
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• pp.1099-1105
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• 2004

The peroxisome proliferator-activated receptors (PPARs) are a primary regulator of lipid metabolism. Potency for activation of PPAR$\gamma$, one of a subfamily of PPARs, particularly mirrors glucose lowering activity. We prepared thiazolidinediones featuring benzoxazole moiety for subtype selective PPAR$\gamma$ activators. 5-[4-[2-(Benzoxazol-2-yl-alkylamino)ethoxy]benzyl]thiazolidine-2,4-diones have been prepared by Mitsunobu reaction of benzoxazolylalkylaminoethanol 8 and hydroxybenzylthiazolidinedione 6 and their activities were evaluated. Most compounds tested were identified as potent PPAR$\gamma$ agonists.

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.162.3-163
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• 2001

• 대한생식의학회:학술대회논문집
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• 2005.11a
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• pp.114-114
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• 2005

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.118-118
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• 2003

The use of PPARν (peroxisome proliferator activated receptor ν) activators in the treatment of type 2 diabetes is well established due to their ability to lower blood glucose and insulin levels and omprove insulin sensitivity. Thiazolidinedione analog is one of the potential antidiabetic drug that binds and activates PPARν selectively. In an effort to develop novel and effective antidiabetic thiazolidindione analogs, synthesis of tetrahydroquinoline and para-substituted benzene-linked thiazolidinedione analogs were carried out via coupling reaction of the hydrophobic segments with hydroxybenzylthiazolidinedione.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.149.2-150
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• 2002

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.180-180
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• 2003

Peroxisome proliferator-activated receptor gamma (PPAR-gamma), a member of the nuclear hormone receptor superfamily, is involved in the suppression of growth of several types of tumors such as liposarcoma, cancers of breast, prostate, and colon, possibly through induction of cell cycle arrest and/or apoptosis.(omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.247.1-247.1
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• 2003

PPAR-$\gamma$(Peroxisome Proliferator-Activated Receptor $\gamma$) 리간드들은 논문 조사를 통해 이루어졌다. PPAR-$\gamma$의 45개 알려진 화합물들을 찾았고, 12 생물활성 화합물을 선택했다. 리간드(rosiglitazone)과 단백질의 결합된 구조는 (1fm6)는 PDB로부터 획득했고, 단백질 coordinate를 가져와 PPAR의 활성 영역 잔기들은 확인했다. (2TYR, 1SER, 1HIS). CoMFA와 Flexi Dock을 통해 단백질과 리간드 사이의 상호작용과 결합에너지에 대한 상호 관계를 밝혔다.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.177.2-177.2
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• 2003

Thiazolidinediones (TZDs) are a new class of compound that increase insulin sensitivity in type 2 diabetic patients. Thiazolidinediones (TZDs) act as ligands for a member of the nuclear hormone receptor superfamily, peroxisome proliferator-activated receptor-$\gamma$ (PPAR-$\gamma$), which is highly expressed in fatty tissue and, moreover, has been shown to play an important role in fat cell differentiation. The strong interaction between the antidiabetic activity ofTZDs and their ability to activate PPAR-$\gamma$ suggests that PPAR-$\gamma$, through downstream-regulated genes, mediates the effects of TZDs. (omitted)