peoniflorin and Obesity

Our aim was to confirm earlier studies showing tcPO. Subjects were randomized to don either PET shirts first (PETF n=73) or CEL first (CELF n=80), switching garments after 90 minutes. Skin temperature (ST), arterial oxygen saturation (O. The ability of ceramic-embedded fabric to induce higher tcPO

Topics: Adult; Anabolic Agents; Androgens; Animals; Anthraquinones; Birth Weight; Body Mass Index; Carbon Isotopes; Cardiac Output; Case-Control Studies; Chromatography, High Pressure Liquid; Doping in Sports; Drugs, Chinese Herbal; Echocardiography; Emodin; Estranes; Exercise; Female; Gas Chromatography-Mass Spectrometry; Glucosides; Glycolysis; Hemodynamics; Hemoglobins; Herb-Drug Interactions; Humans; Hypothermia, Induced; Lactic Acid; Linear Models; Male; Monoterpenes; Muscle, Skeletal; Myoglobin; Nandrolone; Obesity; Oxygen Consumption; Predictive Value of Tests; Pregnancy; Pregnancy Complications, Cardiovascular; Pregnancy Outcome; Pregnant Women; Prospective Studies; Pulmonary Gas Exchange; Rats; Rats, Sprague-Dawley; Reference Values; Reproducibility of Results; Sensitivity and Specificity; Steroids; Substance Abuse Detection; Sulfates; Tandem Mass Spectrometry; Testosterone

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. Paeoniflorin, a natural product and active ingredient of Paeonia lactiflora, has been demonstrated to have many pharmacological effects including antiinflammatory and antihyperglycemic activity. We investigated the effects of paeoniflorin on NAFLD in mice and its underlying mechanisms. We examined this hypothesis using a well-established animal model of NAFLD. The effects of paeoniflorin on inflammation and glucolipid metabolism disorder were evaluated. The corresponding signaling pathways were measured using real-time polymerase chain reaction (PCR). We demonstrated that the mice developed obesity, dyslipidemia, and fatty liver, which formed the NAFLD model. Paeoniflorin attenuated NAFLD and exhibited potential cardiovascular protective effects in vivo by lowering body weight, hyperlipidemia, and insulin resistance; blocking inflammation; and inhibiting lipid ectopic deposition. Further investigation revealed that the antagonistic effect on hyperlipidemia and lipid ectopic deposition was related to lowering the lipid synthesis pathway (de novo pathway, 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMG-CoAR)), promoting fatty acid oxidation [peroxisome proliferator-activated receptor-alpha (PPARα), carnitine palmitoyltransferase-1, etc.] and increasing cholesterol output (PPARγ-liver X receptor-α-ATP-binding cassette transporter-1); the inhibitory effects on inflammation and hyperglycemia were mediated by blocking inflammatory genes activation and reducing gluconeogenic genes expression (phosphoenolpyruvate carboxykinase and G6Pase). These results suggest that paeoniflorin prevents the development of NAFLD and reduces the risks of atherosclerosis through multiple intracellular signaling pathways. It may therefore be a potential therapeutic compound for NAFLD.

Topics: Animals; Blood Glucose; Body Weight; Diet, High-Fat; Glucosides; Lipid Metabolism; Liver; Male; Mice, Inbred C57BL; Monoterpenes; Non-alcoholic Fatty Liver Disease; Obesity; Organ Size; Protective Agents; Transcriptome

TNFα plays an important role in the adipocyte dysfunction, including lipolysis acceleration, insulin resistance and changes of adipokines. Recently, we showed that paeoniflorin attenuates adipocyte lipolysis and inhibits the phosphorylation of ERK, JNK, IKK stimulated by TNFα. However, the effects of paeoniflorin on adipocytes insulin resistance and changes of adipokines remain unknown. The aim of the current study was to investigate the role of paeoniflorin in preventing insulin resistance or inflammation in 3T3-L1 adipocytes treated with TNFα. Our results showed that paeoniflorin restored insulin-stimulated [(3)H]2-DOG uptake, which was reduced by TNFα, with concomitant restoration in serine phosphorylation of IRS-1 and insulin-stimulated phosphorylation of AKT in adipocytes. Paeoniflorin attenuated TNFα-mediated suppression of the expressions of PPARγ and PPARγ target genes, and the improvement of paeoniflorin on TNFα-induced insulin resistance was attenuated by GW9662, an antagonist of PPARγ activity. Moreover, paeoniflorin could inhibit the expressions and secretions of IL-6 and MCP-1 from adipocytes induced by TNFα. These results, together with our previous data, indicate that paeoniflorin exerts a beneficial effect on adipocytes to prevent TNFα-induced insulin resistance and inflammatory adipokine release. Our studies provide important evidence for an ability of paeoniflorin in amelioration of TNFα-induced adipocyte dysfunction, which would be helpful to clarify its potential role in the treatment of obesity.

Topics: 3T3-L1 Cells; Adipocytes; Adipokines; Anilides; Animals; Benzoates; Bridged-Ring Compounds; Chemokine CCL2; Drugs, Chinese Herbal; Gene Expression; Glucose; Glucosides; Inflammation; Insulin; Insulin Receptor Substrate Proteins; Insulin Resistance; Interleukin-6; Mice; Monoterpenes; Obesity; Paeonia; Phosphorylation; PPAR gamma; Proto-Oncogene Proteins c-akt; Tumor Necrosis Factor-alpha