Participation of peroxisome proliferator-activated receptors (PPARs) in glucose and lipid metabolism under fish oil diet

2009 ◽  
Vol 160 ◽  
pp. S46-S47
Author(s):  
Masaki Wakutsu ◽  
Nobuyo Tsunoda ◽  
Etsuko Muraki ◽  
Keizou Kasono
Keyword(s):  
Lipid Metabolism ◽  
Fish Oil ◽  
Peroxisome Proliferator ◽  
Glucose And Lipid Metabolism ◽  
Peroxisome Proliferator Activated Receptors ◽  
Fish Oil Diet

scholarly journals Fish oil supplementation attenuates changes in plasma lipids caused by dexamethasone treatment in rats

2016 ◽  
Vol 41 (4) ◽  
pp. 382-390 ◽  
Author(s):  
Amanda Marreiro Barbosa ◽  
Priscila de Cássia Francisco ◽  
Katia Motta ◽  
Thayz Rodrigues Chagas ◽  
Cristiane dos Santos ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
Fish Oil ◽  
Plasma Lipids ◽  
Mineral Oil ◽  
Peroxisome Proliferator ◽  
Dexamethasone Treatment ◽  
Peroxisome Proliferator Activated Receptor ◽  
Hepatic Expression ◽  
Glucose And Lipid Metabolism

Dexamethasone is an anti-inflammatory glucocorticoid that may alter glucose and lipid homeostasis when administered in high doses or for long periods of time. Omega-3 fatty acids, present in fish oil (FO), can be used as potential modulators of intermediary glucose and lipid metabolism. Herein, we evaluate the effects of FO supplementation (1 g·kg–1body weight (BW)) on glucose and lipid metabolism in rats treated with dexamethasone (0.5 mg·kg–1BW) for 15 days. Adult male Wistar rats were distributed among 4 groups: control (saline, 1 mL·kg–1BW and mineral oil, 1 g·kg–1BW), DEX (dexamethasone and mineral oil), FO (fish oil and saline), and DFO (fish oil and dexamethasone). Dexamethasone and saline were administered intraperitoneally, and fish oil and mineral oil were administered by gavage. We evaluated functional and molecular parameters of lipid and glycemic profiles at 8 days and at the end of treatment. FO supplementation increased hepatic docosahexaenoic acid (DEX: 5.6% ± 0.7%; DFO: 10.5% ± 0.8%) and eicosapentaenoic acid (DEX: 0.3% ± 0.0%; DFO: 1.3% ± 0.1%) contents and attenuated the increase of plasma triacylglycerol, total cholesterol, and non–high-density lipoprotein cholesterol concentrations in DFO rats compared with DEX rats. These effects seem not to depend on hepatic expression of insulin receptor substrate 1, protein kinase B, peroxisome proliferator-activated receptor γ coactivator 1-α, and peroxisome proliferator-activated receptor γ. There was no effect of supplementation on body weight loss, fasting glycemia, and glucose tolerance in rats treated with dexamethasone. In conclusion, we show that FO supplementation for 15 days attenuates the dyslipidemia induced by dexamethasone treatment.

scholarly journals Pioglitazone versus Rosiglitazone: Effects on Lipids, Lipoproteins, and Apolipoproteins in Head-to-Head Randomized Clinical Studies

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-6 ◽  
Author(s):  
Mark A. Deeg ◽  
Meng H. Tan
Keyword(s):  
Clinical Trials ◽  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Randomized Clinical Trials ◽  
Peroxisome Proliferator ◽  
Glucose Lowering ◽  
Glucose And Lipid Metabolism ◽  
Ppar Agonists ◽  
Peroxisome Proliferator Activated Receptors ◽  
Regulate Lipid Metabolism

Peroxisome proliferator-activated receptors (PPARs) play an important role in regulating both glucose and lipid metabolism. Agonists for both PPAR and PPAR have been used to treat dyslipidemia and hyperglycemia, respectively. In addition to affecting glucose metabolism, PPAR agonists also regulate lipid metabolism. In this review, we will focus on the randomized clinical trials that directly compared the lipid effects of the thiazolidinedione class of PPAR agonists, pioglitazone and rosiglitazone, head-to-head either as monotherapy or in combination with other lipid-altering or glucose-lowering agents

Peroxisome Proliferator-Activated Receptors and Lipid Metabolism

1993 ◽  
Vol 684 (1 Zinc-Finger P) ◽  
pp. 157-173 ◽  
Author(s):  
HANSJÖRG KELLER ◽  
ABDERRAHIM MAHFOUDI ◽  
CHRISTINE DREYER ◽  
ABDELMADJID K. HIHI ◽  
JEFFREY MEDIN ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors

GLP-1-mediated delivery of the PPAR𝛼/𝛾 dual-agonist Tesaglitazar improves obesity and glucose metabolism in mice

2021 ◽  
Author(s):  
Carmelo Quarta ◽  
Kerstin Stemmer ◽  
Aaron Novikoff ◽  
Bin Yang ◽  
Felix Klingelhuber ◽  
...  
Keyword(s):  
Body Weight ◽  
Glucose Metabolism ◽  
Peroxisome Proliferator ◽  
Protein Targets ◽  
Beneficial Effects ◽  
Glucose And Lipid Metabolism ◽  
Therapeutic Value ◽  
Affect Body Weight ◽  
Peroxisome Proliferator Activated Receptors ◽  
Dual Agonist

Abstract Dual-agonists activating the peroxisome proliferator-activated receptors alpha and gamma (PPAR𝛼/𝛾) have shown beneficial effects on glucose and lipid metabolism in patients with type 2 diabetes, but their development was discontinued due to unfavorable cardiovascular and/or renal effects. Here we report the design and preclinical evaluation of a molecule that covalently links the PPAR𝛼/𝛾 dual-agonist Tesaglitazar to GLP-1 to allow for the GLP-1 receptor-dependent delivery of Tesaglitazar. GLP-1/Tesaglitazar does not differ from matched GLP-1 in GLP-1R signaling, but shows GLP-1R-dependent PPAR𝛾-RXR heterodimerization with enhanced efficacy to improve body weight, food intake, and glucose metabolism relative to GLP-1 or Tesaglitazar in mice with diet- and genetically-induced obesity. The conjugate fails to affect body weight and glucose metabolism in GLP-1R knockout (ko) mice and shows preserved effects in DIO mice at doses subthreshold for GLP-1 and Tesaglitazar to improve metabolism. Consistent with the GLP-1R expression pattern, LC/MS-based proteomics identified a series of novel PPAR protein targets in the hypothalamus that are acutely upregulated by Tesaglitazar and by GLP-1/Tesaglitazar, but not by treatment with GLP-1. Collectively, our data show that GLP-1/Tesaglitazar improves energy and glucose metabolism with superior efficacy to GLP-1 or Tesaglitazar alone and suggest that this conjugate holds therapeutic value to treat hyperglycemia and insulin resistance.

scholarly journals The Roots ofAtractylodes macrocephalaKoidzumi Enhanced Glucose and Lipid Metabolism in C2C12 Myotubes via Mitochondrial Regulation

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Mi Young Song ◽  
Seok Yong Kang ◽  
Tae Woo Oh ◽  
Rethineswaran Vinoth Kumar ◽  
Hyo Won Jung ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Mitochondrial Function ◽  
Weight Control ◽  
Glucose Consumption ◽  
C2c12 Myotubes ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nuclear Respiratory Factor ◽  
Glucose And Lipid Metabolism

The root ofAtractylodes macrocephalaKoidzumi (Atractylodis Rhizoma Alba, ARA) is a Traditional Korean Medicine and has been commonly used for weight control. Mitochondrial dysfunction appears to be a key contributor to insulin resistance, and therefore mitochondrial targeting drugs represent an important potential strategy for the treatment of insulin resistance and obesity. In this study, the authors investigated the regulatory effects of ARA on mitochondrial function with respect to the stimulation of glucose and lipid metabolism in C2C12 myotubes. After differentiating C2C12 myotubes, cells were treated with or without different concentrations (0.2, 0.5, and 1.0 mg/mL) of ARA extract. ARA extract significantly increased the expression of peroxisome proliferator-activated receptor coactivator 1 alpha (PGC1α) and the downregulations of its targets, nuclear respiratory factor-1 (NRF-1), transcription factor A (TFAM), and total ATP content in C2C12 myotubes. ARA extract also increased the expressions of PGC1αactivator and of the metabolic sensors, AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase and sirtuin (SIRT) 1. Furthermore, it significantly increased glucose uptake by enhancing glucose consumption and subsequently decreased FFA contents and increased carnitine palmitoyltransferase (CPT) 1b expression. Our study indicates that ARA has a potential for stimulating mitochondrial function and energy metabolism in muscle.

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