scholarly journals Effect of PPAR-Γ agonist-rosiglitazone-on adiponectin level in the metabolic syndrome

2005 ◽  
Vol 18 (5) ◽  
pp. A204-A204 ◽  
Author(s):  
Y SHARABI ◽  
I AVNI ◽  
Y KAMARI ◽  
M ORONHERMAN ◽  
E PELEG ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adiponectin Level ◽  
Ppar Γ ◽  
The Metabolic Syndrome

Abstract P033: Relationship Between Adiponectin Level and Metabolic Syndrome after Weight Loss in Patients with Abdominal Obesity

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Aelita Berezina ◽  
Olga Belyaeva ◽  
Olga Berkovich ◽  
Elena Baranova ◽  
Tatyina Karonova
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Abdominal Obesity ◽  
Metabolic Disorders ◽  
Intervention Program ◽  
Adiponectin Level ◽  
The Metabolic Syndrome ◽  
Outpatient Intervention ◽  
Before And After ◽  
The Relationship

Objective: to investigate the relationship between adiponectin level and metabolic syndrome (MS) after weight loss in patients with abdominal obesity (AO). Method: A 3-year randomized lifestyle intervention trial performed in 153 patients with AO, age 43,2±0,8 yrs, BMI 32,1±1,9 kg/m 2 . 74 patients keep hypocaloric diet (gr.1), 79 patients keep diet and performed aerobic exercise (gr.2). Adiponectin concentration, body mass (BM), waist circumference (WC), body fat (BF), BMI, the levels of BP, glucose, insulin, HOMA-IR, TC, HDL-C, LDL-C, TG, CRP were measured before and after a 3-years outpatient intervention program. Results. 100% patients with AO had some metabolic disorders and 38% had MS before the treatment. The adiponectin levels and others parameters didn’t differ between the groups before intervention (p>0,05). In 3 years 53 (71,6%) and 58 (73,4%) patients from 1 and 2 groups reduced weight. The rate of improving BM, BMI, BF, WC, HDL-C, TG and insulin was grater in patients gr.2 (p<0,05). The favorable dynamics of MS (MS didn’t appeared at the end of study or didn’t registered in patients who had it before) didn’t differ between the groups 1 and 2 (81,1% and 91,4%, p>0,05). The increasing of adiponectin level occurred more often in patients gr.2, than gr.1 (93,1% and 58,5%, p=0,001, respectively). Adiponectin level increased only in patients gr.2 (18,0±1,1mcg/ml and 23,8±1,3 mcg/ml, p= [[Unable to Display Character: &#1088;]]=0,0001), didn’t changed in gr.1 (p>0,05). It was established that in patients with combination of weight loss and increasing of adiponectin level favorable dynamics of MS occurred more often than in patients who lost weight without increasing of adiponectin level (91,7% and 69,2%, p=0,0001). In patients with favorable dynamics of MS increasing of adiponectin level had met more often, than in patients with unfavorable dynamics of MS (MS continued or appeared) (88,6% and 11,4%, p=0,0001). Increasing of adiponectin level associated with positive dynamics of the MS - OR=9,1 (4,0-20,6). Conclusion. Combination of weight loss and increasing of adiponectin level associated with favorable dynamics of the metabolic syndrome.

Evolution of Peroxisome Proliferator-Activated Receptor Agonists

2007 ◽  
Vol 41 (6) ◽  
pp. 973-983 ◽  
Author(s):  
Feng Chang ◽  
Linda A Jaber ◽  
Helen D Berlie ◽  
Mary Beth O'Connell
Keyword(s):  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Adverse Effects ◽  
Phase Ii ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Metabolism Regulation ◽  
Ppar Γ ◽  
The Metabolic Syndrome ◽  
Phase Ii And Iii

OBJECTIVE: To discuss the evolution of peroxisome proliferator-activated receptor (PPAR) agonists from single site to multiple subtype or partial agonists for the treatment of type 2 diabetes, dyslipidemia, obesity, and the metabolic syndrome. DATA SOURCES: Information was obtained from MEDLINE (1966-March 2007) using search terms peroxisome proliferator-activated receptor agonist, PPAR dual agonist, PPAR α/γ agonist, PPAR pan agonist, partial PPAR, and the specific compound names. Other sources included pharmaceutical companies, the Internet, and the American Diabetes Association 64th-66th Scientific Sessions abstract books. STUDY SELECTION AND DATA EXTRACTION: Animal data, abstracts, clinical trials, and review articles were reviewed and summarized. DATA SYNTHESIS: PPAR α, γ, and δ receptors play an important role in lipid metabolism, regulation of adipocyte proliferation and differentiation, and insulin sensitivity. The PPAR dual agonists were developed to combine the triglyceride lowering and high-density lipoprotein cholesterol elevation from the PPAR-α agonists (fibrates) with the insulin sensitivity improvement from the PPAR-γ agonists (thiazolidinediones). Although the dual agonists reduced hemoglobin A1C(A1C) and improved the lipid profile, adverse effects led to discontinued development. Currently, PPAR-γ agonists (GW501516 in Phase I trials), partial PPAR-γ agonists (metaglidasen in Phase II and III trials), and pan agonists (α, γ, δ netoglitazone in Phase II and III trials) with improved cell and tissue selectivity are undergoing investigation to address multiple aspects of the metabolic syndrome with a single medication. By decreasing both A1C and triglycerides, metaglidasen did improve multiple aspects of the metabolic syndrome with fewer adverse effects than compared with placebo. Metaglidasen is now being compared with pioglitazone. CONCLUSIONS: Influencing the various PPARs results in improved glucose, lipid, and weight management, with effects dependent on full or partial agonist activity at single or multiple receptors. Although the dual PPAR compounds have been associated with unacceptable toxicities, new PPAR agonist medications continue to be developed and investigated to discover a safe drug with benefits in multiple disease states.

scholarly journals Amelioration of High Fructose Diet-Induced Insulin Resistance, Hyperuricemia, and Liver Oxidative Stress by Combined Use of Selective Agonists of PPAR-α and PPAR-γ in Rats

2020 ◽  
Vol 3 (2) ◽  
pp. 76-86
Author(s):  
Mahmoud M. Farag ◽  
Ehab H. Ashour ◽  
Wessam F. El-Hadidy
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Serum Insulin ◽  
Combined Treatment ◽  
Vehicle Group ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Ppar Γ ◽  
The Metabolic Syndrome ◽  
High Fructose

Background: The use of high-fructose (Fr) corn sweeteners and sucrose in manufactured food has markedly increased recently. This excessive Fr intake has been proposed in the etiology of the metabolic syndrome, which shows an increasing prevalence throughout the world. Objective: In this study, we questioned whether fenofibrate (FF), a peroxisome proliferator-activated receptor (PPAR)-α agonist, and pioglitazone (PG), a PPAR-γ agonist, might be effective in ameliorating the metabolic syndrome in a rat model. Materials and Methods: The metabolic syndrome was induced by feeding rats a high-Fr (60%) diet for 10 weeks. The rats were divided into 5 groups: control group, fed a normal rat chow; Fr + vehicle group; Fr + FF group; Fr + PG group; and Fr + (FF + PG) group (treated with both drugs). Drug or vehicle treatment was given daily for 6 weeks (from weeks 5 to 10). Thereafter, blood and liver samples were obtained for biochemical studies. Results: Rats fed a high-Fr diet developed hyperglycemia, hyperinsulinemia, hyperuricemia, hypertriglyceri­demia, and hypercholesterolemia, and had increased serum alanine aminotransferase, hepatic tumor necrosis factor-α, and malondialdehyde levels but decreases in both glutathione content and superoxide dismutase activity. Rat treatment with FF and/or PG attenuated these alterations. The improvement was greater with the combined treatment than with either drug alone, and normalization of insulin sensitivity was observed only in rats treated with the combination therapy. Conclusion: Acting on the 2 main PPAR subfamilies, the combination of FF and PG provides a more efficacious therapy for modulating the changes in serum insulin, uric acid, and lipids, as well as the accompanying hepatic inflammation and oxidative stress that characterize the Fr-induced metabolic syndrome.

scholarly journals Effect of PPAR-γ Agonist on Adiponectin Levels in the Metabolic Syndrome: Lessons From the High Fructose Fed Rat Model

2007 ◽  
Vol 20 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Y SHARABI ◽  
M ORONHERMAN ◽  
Y KAMARI ◽  
I AVNI ◽  
E PELEG ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
Ppar Γ ◽  
The Metabolic Syndrome ◽  
High Fructose

Mouse models of PPAR-γ deficiency: dissecting PPAR-γ's role in metabolic homoeostasis

2005 ◽  
Vol 33 (5) ◽  
pp. 1053-1058 ◽  
Author(s):  
S.L. Gray ◽  
E. Dalla Nora ◽  
A.J. Vidal-Puig
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Mouse Models ◽  
Murine Models ◽  
Metabolic Processes ◽  
Glucose Homoeostasis ◽  
Ppar Γ ◽  
The Metabolic Syndrome

The identification of humans with mutations in PPAR-γ (peroxisome-proliferator-activated receptor-γ) has underlined its importance in the pathogenesis of the metabolic syndrome. Genetically modified mice provide powerful tools to dissect the mechanisms by which PPAR-γ regulates metabolic processes. Ablation of PPAR-γ in vivo is lethal and thus dissection of PPAR-γ function using mouse models has relied on the development of tissue and isoform-specific ablation and mouse models of human mutations. These models exhibit phenotypes of partial PPAR-γ impairment and are useful to elucidate how PPAR-γ regulates specific metabolic processes. These murine models have confirmed the involvement of PPAR-γ in adipose tissue development, maintenance and distribution. The mechanism involved in PPAR-γ regulation of glucose homoeostasis is obscure as both agonism and partial impairment of PPAR-γ increase insulin sensitivity. While adipose tissue is likely to be the primary target for the insulin-sensitizing effects of PPAR-γ, some murine models suggest PPAR-γ expressed outside adipose tissue may also contribute actively to maintain glucose homoeostasis. Interestingly, mutations in PPAR-γ that cause severe insulin resistance in humans when expressed in mice do not result in insulin insensitivity. However, these murine models can recapitulate the effects in fuel partitioning, post-prandial lipid handling and vasculature dysfunction observed in humans. In summary, these murine models of PPAR-γ have provided useful in vivo systems to dissect the function of PPAR-γ, but additionally have revealed a picture of complexity. These models have confirmed a key role for PPAR-γ in the metabolic syndrome; however, they challenge the concept that insulin resistance is the main factor linking the clinical manifestations of the metabolic syndrome.

scholarly journals Low plasma adiponectin concentration is an indicator of the metabolic syndrome

2006 ◽  
Vol 155 (5) ◽  
pp. 745-750 ◽  
Author(s):  
Merja Santaniemi ◽  
Y Antero Kesäniemi ◽  
Olavi Ukkola
Keyword(s):  
Metabolic Syndrome ◽  
Acid Metabolism ◽  
Adiponectin Level ◽  
International Diabetes Federation ◽  
Adiponectin Concentration ◽  
Plasma Adiponectin ◽  
The Metabolic Syndrome ◽  
Novel Method ◽  
New Criteria

Objective: Adiponectin is an adipocytokine known to be decreased in obesity. It functions in glucose and fatty acid metabolism and also has an anti-inflammatory role in microvasculature. We wanted to investigate the role of adiponectin as a biomarker of metabolic syndrome (MS) and see how the plasma adiponectin levels relate to new criteria of MS proposed by the International Diabetes Federation. Methods: Plasma adiponectin concentrations were measured from total of 1041 Finnish subjects with an ELISA – a novel method planned in our laboratory. Results: In both the sexes, the plasma adiponectin levels were lower in subjects with MS when compared with subjects with no diagnosis of MS (P< 0.001). Plasma adiponectin levels did not differ between subjects with National Cholesterol Education Program (ATPIII) and International Diabetes Federation-defined MS. Lower adiponectin levels were associated with different components of the MS and there was a trend towards decreasing adiponectin levels with an increasing number of components of MS in both the sexes. Subjects in the lowest adiponectin quartile had a significantly higher probability of having MS (P< 0.001), 4.4-fold in males and 7.5-fold in females, when compared with the corresponding individuals in the highest quartile. The probability increased in every lowering quartile of adiponectin level and was independent of body mass index. Conclusion: We conclude that adiponectin levels correlate with most of the components of the MS and the metabolic cluster per se.

scholarly journals Association of Serum Adiponectin Levels with Metabolic Syndrome Risk Factors in Malay Adults

2017 ◽  
Vol 1 (1) ◽  
pp. 17
Author(s):  
Nur Firdaus Isa ◽  
Laila Ruwaida Mohd Zainuddin ◽  
Wan Manan Wan Muda ◽  
Hamid Jan B. Jan Mohamed
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Adiponectin Level ◽  
Hdl Cholesterol ◽  
Serum Adiponectin ◽  
Biochemical Tests ◽  
The Metabolic Syndrome ◽  
Overnight Fasting ◽  
Serum Adiponectin Concentration ◽  
The Relationship

Introduction: This study aimed to investigate the relationship between serum adiponectin and metabolic syndrome in adults living in rural Malaysia.Methods: A total of 299 Malay adults (men=124; women = 175) with a mean age 48.8 (11.7) years were recruited. Measurements for waist circumference and blood pressure were taken before drawing an overnight fasting blood samples. Biochemical tests for triglycerides, HDL cholesterol, glucose and serum adiponectin concentration were measured.Results: Our results show that the adiponectin level in the subjects with metabolic syndrome was significantly lower than those without metabolic syndrome (p < 0.05). Among the metabolic syndrome risk factors, adiponectin level was significantly associated with hypertriglyceridemia and reduced HDL cholesterol (p < 0.001).Conclusion: The outcome from this study which highlights the association of hypoadiponectinemia with risk factors of metabolic syndrome in Malay adults, suggests that the reduced level of adiponectin may play a pivotal role in the development of metabolic syndrome in this ethnic group.

scholarly journals Flax oil-mediated activation of PPAR-γ correlates with reduction of hepatic lipid accumulation in obese spontaneously hypertensive/NDmcr-cp rats, a model of the metabolic syndrome

2010 ◽  
Vol 104 (9) ◽  
pp. 1313-1321 ◽  
Author(s):  
Kanta Chechi ◽  
Naomi Yasui ◽  
Katsumi Ikeda ◽  
Yukio Yamori ◽  
Sukhinder K. Cheema
Keyword(s):  
Metabolic Syndrome ◽  
Genetic Model ◽  
Serum Insulin ◽  
Fatty Acid Content ◽  
Spontaneously Hypertensive ◽  
Hepatic Lipid ◽  
Flax Oil ◽  
Ppar Γ ◽  
The Metabolic Syndrome ◽  
Obese Rats

Flax oil feeding has been proposed to have beneficial effects on the outcome of the metabolic syndrome due to the high n-3 fatty acid content of flax oil; however, the mechanisms of its action remain largely unknown. We investigated the effects of flax oil feeding on hyperlipidaemia, hyperglycaemia, hepatic steatosis and oxidative stress in the spontaneously hypertensive (SHR)/NDmcr-cp rats, a genetic model of the metabolic syndrome. Hepatic gene expression of PPAR-α, PPAR-γ and sterol-regulatory element-binding protein-1c was also assessed in order to investigate the possible underlying mechanisms. Obese and lean SHR/NDmcr-cp rats were fed high-fat diets enriched with either lard or flax oil for a period of 4 weeks. Obese rats exhibited higher body weight, liver weight and mesenteric fat-, epididymal fat- and renal fat-pad weights, and also TAG and cholesterol concentrations in serum and VLDL, LDL and HDL fractions, when compared with the lean rats (P < 0·001), irrespective of the diets. Concentrations of fasting serum insulin and urinary thiobarbituric acid reactive substances were lower in flax oil-fed obese (FO) rats compared with the lard-fed obese (LO) rats (P < 0·01). Flax oil feeding also revealed a significant reduction in hepatic TAG and cholesterol concentrations in obese rats compared with the LO rats (P < 0·05). In addition, FO rats exhibited significantly higher hepatic mRNA expression of PPAR-γ, which negatively correlated (r − 0·98, P < 0·05) with their hepatic lipid levels. These findings suggest that flax oil feeding may activate PPAR-γ-dependent pathways to alter the hepatic lipid metabolism and to increase insulin sensitivity in the obese SHR/NDmcr-cp rats.

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