Atorvastatin improves insulin sensitivity in mice with obesity induced by monosodium glutamate
| Autor: | Guang-ming Song, Zhufang Shen, Sujuan Sun, Ning Zhang, Yi Huan, Hui Huang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Blood Glucose
medicine.medical_specialty medicine.medical_treatment Atorvastatin Blotting Western Adipose tissue Administration Oral chemistry.chemical_compound Mice High-density lipoprotein Insulin resistance Internal medicine Sodium Glutamate medicine Animals Insulin Pharmacology (medical) Pyrroles Obesity Pharmacology Mice Inbred ICR biology Cholesterol Reverse Transcriptase Polymerase Chain Reaction General Medicine medicine.disease Lipid Metabolism Disease Models Animal Endocrinology chemistry Adipose Tissue Heptanoic Acids Low-density lipoprotein HMG-CoA reductase biology.protein lipids (amino acids peptides and proteins) Original Article Female Hydroxymethylglutaryl-CoA Reductase Inhibitors Insulin Resistance medicine.drug Signal Transduction |
| Popis: | To examine the mechanisms underlying the effects of atorvastatin on glucose and lipid metabolism.Mice with insulin resistance and obesity induced by monosodium glutamate (MSG) were used. Atorvastatin (80 mg.kg(-1).d(-1)) or vehicle control treatment was given orally once a day for 30 days. Plasma levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and free fatty acids were monitored. Serum insulin and glucose concentrations were used to calculate the insulin resistance index and insulin sensitivity index using a homeostasis model. Body length, waistline circumference, intraperitoneal adipose tissue mass, and total body mass were measured. Semi-quantitative RT-PCR and Western analysis were used to determine the expression of inflammatory factors and proteins involved in inflammation signaling pathways.Atorvastatin improved insulin sensitivity, ameliorated glucose tolerance, and decreased plasma levels of total cholesterol, triglycerides, LDL-C, HDL-C and free fatty acids. Semi-quantitative RT-PCR and Western analysis revealed increased expression of interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) in serum and adipose tissue in MSG obese mice. Atorvastatin treatment decreased expression of IL-6, TNF-alpha, nuclear factor kappaB (NF-kappaB) and I-kappa-B (IkappaB) kinase-beta, but increased the expression of IkappaB, in adipose tissue.Atorvastatin is a potential candidate for the prevention and therapy of diseases associated with insulin resistance such as type 2 diabetes mellitus and cardiovascular disease. One possible mechanism underlying the effects of atorvastatin on glucose and lipid metabolism may be to ameliorate a state of chronic inflammation. |
| Databáze: | OpenAIRE |
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