• Asian-Australasian Journal of Animal Sciences
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• v.28 no.5
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• pp.697-702
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• 2015

While athletic abilities such as speed, endurance and recovery are important in the horse, genes related to these abilities have not been extensively investigated. Here, we characterized the horse peroxisome proliferator-activated receptor delta ($PPAR{\delta}$) gene and analyzed the expression of $PPAR{\delta}$ during exercise. $PPAR{\delta}$ is a known regulator of ${\beta}$-oxidation, muscle fiber transformation, and running endurance. Through evolutionary analysis using the synonymous and non-synonymous mutation ratio, it was revealed that positive selection occurred in the horse $PPAR{\delta}$ gene. Two important domains related to nuclear hormone receptors, C4 zinc finger and ligand binding domain, were also found to be conserved well in horse $PPAR{\delta}$. Horse $PPAR{\delta}$ was expressed ubiquitously in many tissues, but the expression level was various depending on the tissues. In the skeletal muscle, $PPAR{\delta}$ increased about 2.5 folds after 30 min of exercise. Unlike in muscle, the increase of $PPAR{\delta}$ expression was observed at 60 min but not 30 min of exercise in leukocytes. This finding might be useful for testing the endurance of horse using blood samples. Conclusively, the horse $PPAR{\delta}$ gene is evolutionarily conserved well and can be used as a biomarker of endurance in horse.

• Molecules and Cells
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• v.40 no.6
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• pp.393-400
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• 2017

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by lack of insulin and high glucose levels. T2DM can cause bone loss and fracture, thus leading to diabetic osteoporosis. Promoting osteogenic differentiation of osteoblasts may effectively treat diabetic osteoporosis. We previously reported that Sirtuin 1 (Sirt1), a $NAD^+$-dependent deacetylase, promotes osteogenic differentiation through downregulation of peroxisome proliferator-activated receptor (PPAR) ${\gamma}$. We also found that miR-132 regulates osteogenic differentiation by downregulating Sirt1 in a $PPAR{\beta}/{\delta}$-dependent manner. The ligand-activated transcription factor, $PPAR{\alpha}$, is another isotype of the peroxisome proliferator-activated receptor family that helps maintain bone homeostasis and promot bone formation. Whether the regulatory role of $PPAR{\alpha}$ in osteogenic differentiation is mediated via Sirt1 remains unclear. In the present study, we aimed to determine this role and the underlying mechanism by using high glucose (HG) and free fatty acids (FFA) to mimic T2DM in MC3T3-E1 cells. The results showed that HG-FFA significantly inhibited expression of $PPAR{\alpha}$, Sirt1 and osteogenic differentiation, but these effects were markedly reversed by $PPAR{\alpha}$ overexpression. Moreover, siSirt1 attenuated the positive effects of $PPAR{\alpha}$ on osteogenic differentiation, suggesting that $PPAR{\alpha}$ promotes osteogenic differentiation in a Sirt1-dependent manner. Luciferase activity assay confirmed interactions between $PPAR{\alpha}$ and Sirt1. These findings indicate that $PPAR{\alpha}$ promotes osteogenic differentiation via the Sirt1-dependent signaling pathway.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.167-167
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• 2001

Peroxisome proliferator-activated receptors(PPARs) are member of the neuclear hormone receptor superfamiliy of ligand-dependent transcription factors that heterodimerizes with the retinoid X receptor to function as a transcriptional regulator. They are divided into three subtypes(PPAR-$\alpha$, $\beta$ and ${\gamma}$).(omitted)

• 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)

• Journal of Life Science
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• v.24 no.1
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• pp.67-73
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• 2014

This study was conducted to investigate the effects of supplementation with Opuntia humifusa on the expression of peroxisome proliferator-activated receptor-delta (PPAR-${\delta}$), peroxisome proliferator-activated receptor-gamma (PPAR-${\gamma}$) and peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-$1{\alpha}$) in the skeletal muscle of rats fed a high-fat diet. Sixteen Sprague-Dawley male rats at 6 weeks of age were randomly divided into 2 groups: a control diet group (CG, n=8) and an experimental diet group (EG, n=8). The rats were fed a high-fat diet (CG) or a high-fat diet supplemented with 5% O. humifusa (EG) for 8 weeks. The results showed that the abdominal fat pad and epididymal fat pad weights were significantly lower in the EG than in the CG (p<0.01). In the blood, serum glucose, triglycerides, and total cholesterol in the EG group were lower than in the CG (p<0.01). The expression of PPAR-${\gamma}$ and PGC-$1{\alpha}$ protein in the skeletal muscle of the EG was increased compared with that of the CG (p<0.05). These results indicate that 8 weeks of O. humifusa supplementation lowers serum glucose and triglyceride levels and suppresses weight gain by reducing fat weight through an increase in the expression of PPAR-${\gamma}$ and PGC-$1{\alpha}$ in the muscle tissue of rats.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.3
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• pp.340-350
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• 2007

The objective of this study was to determine whether peroxisome proliferator-activated receptor ${\gamma}$(PPAR${\gamma}$ is involved in the regulation of weaning to estrus of primiparous sows. Twelve sows composed of 6 groups of 2 full-sibs in a similar age (325.2 d), body weight (BW; 152.4 kg) and backfat thickness (BFT; 27.0 mm) at start of lactation, were allocated to accept 31 MJ (restricted group, R-group) or 53 MJ (control group, C-group) DE/d treatment, respectively. The experimental results indicated that the low energy intake resulted in excessive losses of BW and BFT during lactation in R-group sows, which may be related to decrease of serum 15-deoxy-${\Delta}^{12,14}$-prostaglandin $J_2$ (15d-$PGJ_2$), a ligand of PPAR${\gamma}$ The obvious peak and the frequency of LH, FSH and estradiol ($E_2$) were only observed in C-group sows. Except for $E_2$ at d 1 and 2, serum FSH, LH and $E_2$ concentrations in R-group were lower than those in C-group sows after weaning. However, the serum progesterone ($P_4$) level in R-group sows was always more than that in C-group. The expression abundances of PPAR${\gamma}$and GnRH receptor (GnRH-R) in pituitary, FSH receptor (FSH-R), LH receptor (LH-R), estrogen receptor (ES-R) and aromatase in ovary of anestrous sows were lower than those of estrous sows. Neither the BFT nor the BW was associated with the mRNA abundance of PPAR${\gamma}$in hypothalamus during lactation. Expressions of PPAR${\gamma}$in pituitary and ovary were affected evidently by the BFT changes and only by the loss of BW of sows during and after lactation. Furthermore, PPAR${\gamma}$mRNA level in ovary was significantly related to the expression abundances of GnRH-R, FSH-R, ES-R and aromatase, and GnRH-R was obviously associated with PPAR${\gamma}$expression in pituitary. However, PPAR${\gamma}$expression in hypothalamus likely has no effects on these genes expression and no obvious difference for all sows. Not serum $E_2$ or $P_4$ alone but the ratios of $E_2$ to $P_4$ and 15d-$PGJ_2$ to $P_4$, and serum FSH and LH were evidently related to PPAR${\gamma}$expression in pituitary and ovary. It is concluded that PPAR${\gamma}$is associated with body conditions, reproduction hormones and their receptor expression, which affected the functions of pituitary and ovary and ultimately the estrus after weaning of primiparous sows.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.3
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• pp.293-300
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• 2017

Prostaglandin $D_2$ ($PGD_2$) may act against myocardial ischemia-reperfusion (I/R) injury and play an anti-inflammatory role in the heart. Although the effect of $PGD_2$ in regulation of ANP secretion of the atrium was reported, the mechanisms involved are not clearly identified. The aim of the present study was to investigate whether $PGD_2$ can regulate ANP secretion in the isolated perfused beating rat atrium, and its underlying mechanisms. $PGD_2$ (0.1 to $10{\mu}M$) significantly increased atrial ANP secretion concomitantly with positive inotropy in a dose-dependent manner. Effects of $PGD_2$ on atrial ANP secretion and mechanical dynamics were abolished by AH-6809 ($1.0{\mu}M$) and AL-8810 ($1.0{\mu}M$), $PGD_2$ and prostaglandin $F2{\alpha}$ ($PGF2{\alpha}$) receptor antagonists, respectively. Moreover, $PGD_2$ clearly upregulated atrial peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) and the $PGD_2$ metabolite 15-deoxy-${\Delta}12$, 14-$PGJ_2$ (15d-$PGJ_2$, $0.1{\mu}M$) dramatically increased atrial ANP secretion. Increased ANP secretions induced by $PGD_2$ and 15d-$PGJ_2$ were completely blocked by the $PPAR{\gamma}$ antagonist GW9662 ($0.1{\mu}M$). PD98059 ($10.0{\mu}M$) and LY294002 ($1.0{\mu}M$), antagonists of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling, respectively, significantly attenuated the increase of atrial ANP secretion by $PGD_2$. These results indicated that $PGD_2$ stimulated atrial ANP secretion and promoted positive inotropy by activating $PPAR{\gamma}$ in beating rat atria. MAPK/ERK and PI3K/Akt signaling pathways were each partially involved in regulating $PGD_2$-induced atrial ANP secretion.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.110-110
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• 2002

15-Deoxy-$\Delta$12, 14-prostaglandin J2 (15-deoxy-PGJ2), a naturally occurring ligand activates the peroxisome proliferator-activated receptor-$\gamma$(PPAR-$\gamma$). It was known to have promoting ability of nerve growth factor(NGF)-induced neurite extension. However, it is not clear yet as to what signaling pathway is involved in its promoting ability of neurite extension.(omitted)

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.2
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• pp.383-387
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• 2006

To investigate the effect of GyeongshinhaeGihwan 1(GGT1) frequently used as an anti-obesity herbal medicine in oriental medicine on the expression of obesity-related genes, we measured the changes in mRNA levels of these genes by GGT1 in human growth hormone transgenic (hGHTg) obese female rats, and these effects by GGT1 were compared with those of reductil (RD), an anti-obesity drug approved by FDA. Rats received once daily oral administrations of autoclaved water, RD, or GGT1 for 8 weeks. At the end of study, rats were sacrificed and tissues were harvested. Total RNA from adipose tissue, liver and kidney was prepared and the mRNA levels for LPL (lipoprotein lipase), $PPAR{\gamma}$ (peroxisome proliferator activated receptor-gamma), $PPAR{\delta}$ (peroxisome proliferator activated receptor-delta), leptin, $TNF{\alpha}$ (tumor necrosis factor-alpha), and internal standard G3PDH (glyceraldehyde-3-phosphate dehydrogenase) were analyzed by RT-PCR. Compared with control group, $PPAR{\gamma}$ mRNA levels of liver and kidney were decreased in both RD and GGT1 groups, and the effects were more prominent in GGT1 group than in RD group, suggesting that GGT1 is effective in the inhibition of lipid storage by decreasing the $PPAR{\gamma}$ expression. $PPAR{\delta}$ mRNA levels of adipose tissue were increased by RD and GGT1 compared with DW, and the magnitude of increase were higher in GGT1 group than in RD group, indicating that GGT1 stimulates fatty acid oxidation and energy metabolism by activating $PPAR{\delta}$ expression. GGT1 group had higher concentrations of serum leptin, a well-known inhibitor of appetite, than control and RD groups. However, The mRNA levels of leptin, LPL, and $TNF{\alpha}$ were not changed by GGT1. These results indicate that GGT1 can prevent obesity in hGHTg obese female rats by down-regulating and up-regulating the mRNA expression of $PPAR{\gamma}$ and $PPAR{\delta}$, respectively, and that this anti-obesity effects were more pronounced in GGT1 group compared with RD group. In addition, GGT1 seems to inhibit obesity by increasing the circulating leptin levels.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.1
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• pp.93-97
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• 2006

To investigate whether GyeongshinhaeGihwan 1(GGT1), an anti-obesity herbal medicine widely used in oriental medicine, regulates the expression of obesity-related genes, we measured the changes in mRNA levels of these genes by GGT1 in human growth hormone transgenic (hGHTg) obese male rats, and these effects by GGT1 were compared with those of reductil (RD), an anti-obesity drug approved by FDA. Rats received once daily oral administrations of autoclaved water, RD, or GGT1 for 8 weeks. At the end of study, rats were sacrificed and tissues were harvested. Total RNA from adipose tissue, liver and kidney was prepared and the mRNA levels for LPL (lipoprotein lipase), PPAR $\gamma$ (peroxisome proliferator activated receptor-gamma), PPAR$\delta$ (peroxisome proliferator activated receptor-delta), leptin, TNF$\alpha$ (tumor necrosis factor-alpha), and internal standard G3PDH (glyceraldehyde-3- phosphate dehydrogenase) were analyzed by RT-PCR. PPAR$\gamma$ mRNA levels of liver and kidney were decreased in drug-treated groups compared with control group and the decrease of PPAR$\gamma$ expression was more prominent in GGT1 group than in RD group, suggesting that GGT1 is effective in the inhibition of adipogenesis and lipid storage by decreasing the PPAR$\gamma$ expression. In contrast, PPAR$\delta$ mRNA levels of adipose tissue and kidney were increased by RD and GGT1 , and the magnitudes of increase were higher in GGT1 group than in RD group, indicating that GGT1 stimulates fatty acid oxidation and energy metabolism by activating PPAR$\delta$ expression, Compared with control and RD groups, GGT1 group had higher concentrations of serum leptin, a well-known inhibitor of appetite. However, The mRNA levels of leptin, LPL, and TNF$\alpha$ were not changed by GGT1 and RD, compared with DW. These results demonstrate that GGT1 not only decreases PPAR$\gamma$ expression of liver and kidney, but also increases PPAR$\delta$ expression of adipose tissue and kidney, leading to the regulation of obesity and that these effects were more pronounced in GGT1 group compared with RD group. In addition, GGT1 seems to prevent obesity by increasing the serum leptin levels.