Effect of PPAR-δ agonist on the expression of visfatin, adiponectin, and resistin in rat adipose tissue and 3T3-L1 adipocytes

K. C. Choi, S. Y. Lee, Hye-Jin Yoo, O. H. Ryu, K. W. Lee, Seon Mee Kim, Sei-Hyun Baik, Kyung Mook Choi

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Abstract

It has been recently reported that activation of PPAR-δ, by specific agonists or genetic manipulation, alleviates dyslipidemia, hyperglycemia, and insulin resistance in animal models of obesity and type 2 diabetes. The purpose of the present study was to determine whether the PPAR-δ agonist has a direct effect on adipokines in visceral adipose tissue of rats and in cultured adipocytes. We examined the expression of visfatin, adiponectin, and resistin mRNA in visceral adipose tissue of Wistar rats fed a high-fat diet and 3T3-L1 adipocytes treated with PPAR-δ agonist (L-165041). Body weight and biochemical measurements were performed. Rats fed a high-fat diet showed a greater increase in body weight than those fed a standard diet (P < 0.05), and treatment with L-165041 (10 mg/kg/day) significantly decreased weight gain (P < 0.05). The concentration of total cholesterol was lower, and HDL cholesterol was higher in L-165041-treated rats (P < 0.05). In the visceral adipose tissue of L-165041-treated rats, visfatin and adiponectin mRNA levels significantly increased compared to those of the untreated rats (P < 0.05). However, the expression of resistin decreased in the L-165041-treated rats. Furthermore, in cultured 3T3-L1 adipocytes, the level of visfatin and adiponectin mRNA was up-regulated in response to L-165041 treatment for nine days. By contrast, resistin mRNA levels were down-regulated by L-165041 treatment. The present study provides a novel evidence to suggest that the PPAR-δ agonist has regulatory effects on a variety of adipokines, and these effects might explain some of their metabolic function.

Original languageEnglish
Pages (from-to)62-67
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume357
Issue number1
DOIs
Publication statusPublished - 2007 May 25

Fingerprint

4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid
Nicotinamide Phosphoribosyltransferase
Resistin
Peroxisome Proliferator-Activated Receptors
Adiponectin
Adipocytes
Adipose Tissue
Rats
Tissue
Intra-Abdominal Fat
Nutrition
Messenger RNA
Adipokines
High Fat Diet
Fats
Body Weight
Medical problems
Dyslipidemias
rat Retn protein
Hyperglycemia

Keywords

  • Adipokine
  • Adiponectin
  • Metabolic syndrome
  • Peroxisome proliferator-activated receptor delta
  • Resistin
  • Visfatin

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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title = "Effect of PPAR-δ agonist on the expression of visfatin, adiponectin, and resistin in rat adipose tissue and 3T3-L1 adipocytes",
abstract = "It has been recently reported that activation of PPAR-δ, by specific agonists or genetic manipulation, alleviates dyslipidemia, hyperglycemia, and insulin resistance in animal models of obesity and type 2 diabetes. The purpose of the present study was to determine whether the PPAR-δ agonist has a direct effect on adipokines in visceral adipose tissue of rats and in cultured adipocytes. We examined the expression of visfatin, adiponectin, and resistin mRNA in visceral adipose tissue of Wistar rats fed a high-fat diet and 3T3-L1 adipocytes treated with PPAR-δ agonist (L-165041). Body weight and biochemical measurements were performed. Rats fed a high-fat diet showed a greater increase in body weight than those fed a standard diet (P < 0.05), and treatment with L-165041 (10 mg/kg/day) significantly decreased weight gain (P < 0.05). The concentration of total cholesterol was lower, and HDL cholesterol was higher in L-165041-treated rats (P < 0.05). In the visceral adipose tissue of L-165041-treated rats, visfatin and adiponectin mRNA levels significantly increased compared to those of the untreated rats (P < 0.05). However, the expression of resistin decreased in the L-165041-treated rats. Furthermore, in cultured 3T3-L1 adipocytes, the level of visfatin and adiponectin mRNA was up-regulated in response to L-165041 treatment for nine days. By contrast, resistin mRNA levels were down-regulated by L-165041 treatment. The present study provides a novel evidence to suggest that the PPAR-δ agonist has regulatory effects on a variety of adipokines, and these effects might explain some of their metabolic function.",
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author = "Choi, {K. C.} and Lee, {S. Y.} and Hye-Jin Yoo and Ryu, {O. H.} and Lee, {K. W.} and Kim, {Seon Mee} and Sei-Hyun Baik and Choi, {Kyung Mook}",
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T1 - Effect of PPAR-δ agonist on the expression of visfatin, adiponectin, and resistin in rat adipose tissue and 3T3-L1 adipocytes

AU - Choi, K. C.

AU - Lee, S. Y.

AU - Yoo, Hye-Jin

AU - Ryu, O. H.

AU - Lee, K. W.

AU - Kim, Seon Mee

AU - Baik, Sei-Hyun

AU - Choi, Kyung Mook

PY - 2007/5/25

Y1 - 2007/5/25

N2 - It has been recently reported that activation of PPAR-δ, by specific agonists or genetic manipulation, alleviates dyslipidemia, hyperglycemia, and insulin resistance in animal models of obesity and type 2 diabetes. The purpose of the present study was to determine whether the PPAR-δ agonist has a direct effect on adipokines in visceral adipose tissue of rats and in cultured adipocytes. We examined the expression of visfatin, adiponectin, and resistin mRNA in visceral adipose tissue of Wistar rats fed a high-fat diet and 3T3-L1 adipocytes treated with PPAR-δ agonist (L-165041). Body weight and biochemical measurements were performed. Rats fed a high-fat diet showed a greater increase in body weight than those fed a standard diet (P < 0.05), and treatment with L-165041 (10 mg/kg/day) significantly decreased weight gain (P < 0.05). The concentration of total cholesterol was lower, and HDL cholesterol was higher in L-165041-treated rats (P < 0.05). In the visceral adipose tissue of L-165041-treated rats, visfatin and adiponectin mRNA levels significantly increased compared to those of the untreated rats (P < 0.05). However, the expression of resistin decreased in the L-165041-treated rats. Furthermore, in cultured 3T3-L1 adipocytes, the level of visfatin and adiponectin mRNA was up-regulated in response to L-165041 treatment for nine days. By contrast, resistin mRNA levels were down-regulated by L-165041 treatment. The present study provides a novel evidence to suggest that the PPAR-δ agonist has regulatory effects on a variety of adipokines, and these effects might explain some of their metabolic function.

AB - It has been recently reported that activation of PPAR-δ, by specific agonists or genetic manipulation, alleviates dyslipidemia, hyperglycemia, and insulin resistance in animal models of obesity and type 2 diabetes. The purpose of the present study was to determine whether the PPAR-δ agonist has a direct effect on adipokines in visceral adipose tissue of rats and in cultured adipocytes. We examined the expression of visfatin, adiponectin, and resistin mRNA in visceral adipose tissue of Wistar rats fed a high-fat diet and 3T3-L1 adipocytes treated with PPAR-δ agonist (L-165041). Body weight and biochemical measurements were performed. Rats fed a high-fat diet showed a greater increase in body weight than those fed a standard diet (P < 0.05), and treatment with L-165041 (10 mg/kg/day) significantly decreased weight gain (P < 0.05). The concentration of total cholesterol was lower, and HDL cholesterol was higher in L-165041-treated rats (P < 0.05). In the visceral adipose tissue of L-165041-treated rats, visfatin and adiponectin mRNA levels significantly increased compared to those of the untreated rats (P < 0.05). However, the expression of resistin decreased in the L-165041-treated rats. Furthermore, in cultured 3T3-L1 adipocytes, the level of visfatin and adiponectin mRNA was up-regulated in response to L-165041 treatment for nine days. By contrast, resistin mRNA levels were down-regulated by L-165041 treatment. The present study provides a novel evidence to suggest that the PPAR-δ agonist has regulatory effects on a variety of adipokines, and these effects might explain some of their metabolic function.

KW - Adipokine

KW - Adiponectin

KW - Metabolic syndrome

KW - Peroxisome proliferator-activated receptor delta

KW - Resistin

KW - Visfatin

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