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Updated: Jun 17, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
Published on: January 7, 2018
Atorvastatin improves insulin sensitivity in mice with obesity induced by monosodium glutamate
Ning Zhang1, Yi Huan, Hui Huang
1Institute of Materia Medica, Chinese Academy of Medical Science & Peking Union Medical College, Beijing, China.
Aim:
To examine the mechanisms underlying the effects of atorvastatin on glucose and lipid metabolism.
Methods:
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.
Results:
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.
Conclusion:
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.
Insights
Atorvastatin improved insulin sensitivity and glucose tolerance in obese mice by reducing inflammation. This suggests potential for treating insulin resistance, type 2 diabetes, and cardiovascular disease.
Area of Science:
- Metabolic research
- Pharmacology
- Inflammation studies
Background:
- Insulin resistance and obesity are linked to metabolic dysfunction.
- Chronic inflammation plays a role in insulin resistance.
- Atorvastatin is a statin medication primarily used for lowering cholesterol.
Purpose of the Study:
- To investigate the mechanisms by which atorvastatin affects glucose and lipid metabolism.
- To evaluate the anti-inflammatory effects of atorvastatin in a model of insulin resistance.
Main Methods:
- Utilized monosodium glutamate (MSG)-induced obese and insulin-resistant mice.
- Administered atorvastatin (80 mg.kg(-1).d(-1)) or vehicle control for 30 days.
- Assessed metabolic parameters, inflammatory markers (IL-6, TNF-alpha), and related signaling pathways (NF-kappaB, IkappaB).
Main Results:
- Atorvastatin treatment improved insulin sensitivity and glucose tolerance.
- Reduced plasma levels of total cholesterol, triglycerides, LDL-C, HDL-C, and free fatty acids.
- Decreased expression of IL-6, TNF-alpha, NF-kappaB, and IkappaB kinase-beta, while increasing IkappaB in adipose tissue.
Conclusions:
- Atorvastatin demonstrates potential for preventing and treating insulin resistance-associated diseases like type 2 diabetes and cardiovascular disease.
- Amelioration of chronic inflammation is a likely mechanism for atorvastatin's metabolic benefits.
- Further research supports atorvastatin's role in managing metabolic disorders through anti-inflammatory pathways.
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