Related Experiment Video
Updated: Mar 29, 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
Different effects of statins on induction of diabetes mellitus: an experimental study
1Department of Cardiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.
Background:
To determine the effect of different statins on the induction of diabetes mellitus.
Materials And Methods:
Four statins (atorvastatin, pravastatin, rosuvastatin, and pitavastatin) were used. Cytotoxicity, insulin secretion, glucose-stimulated insulin secretion, and G0/G1 phase cell cycle arrest were investigated in human pancreas islet β cells, and glucose uptake and signaling were studied in human skeletal muscle cells (HSkMCs).
Results:
Human pancreas islet β cells treated with 100 nM atorvastatin, pravastatin, rosuvastatin, and pitavastatin had reduced cell viability (32.12%, 41.09%, 33.96%, and 29.19%, respectively) compared to controls. Such cytotoxic effect was significantly attenuated by decreasing the dose to 10 and 1 nM, ranged from 1.46% to 17.28%. Cells treated with 100 nM atorvastatin, pravastatin, rosuvastatin, and pitavastatin had a reduction in the rate of insulin secretion rate by 34.07%, 30.06%, 26.78%, and 19.22%, respectively. The inhibitory effect was slightly attenuated by decreasing the dose to 10 and 1 nM, ranging from 10.84% to 29.60%. Insulin secretion stimulated by a high concentration of glucose (28 mmol/L) was significantly higher than a physiologic concentration of glucose (5.6 mmol/L) in all treatment groups. The glucose uptake rates at a concentration of 100 nM were as follows: atorvastatin (58.76%) < pravastatin (60.21%) < rosuvastatin (72.54%) < pitavastatin (89.96%). We also found that atorvastatin and pravastatin decreased glucose transporter (GLUT)-2 expression and induced p-p38 MAPK levels in human pancreas islet β cells. Atorvastatin, pravastatin, and rosuvastatin inhibited GLUT-4, p-AKT, p-GSK-3β, and p-p38 MAPK levels in HSkMCs.
Conclusion:
Statins similar but different degree of effects on pancreas islet β cells damage and induce insulin resistance in HSkMC.
Insights
Different statins impact pancreas islet beta cells and induce insulin resistance, with varying effects on cell viability and insulin secretion. These findings highlight potential risks associated with statin use.
Area of Science:
- Pharmacology
- Endocrinology
- Cell Biology
Background:
- Statins are widely prescribed for cholesterol management.
- A potential side effect of statin use is the induction of new-onset diabetes mellitus.
- The precise mechanisms underlying statin-induced diabetes remain incompletely understood.
Purpose of the Study:
- To investigate the differential effects of four common statins (atorvastatin, pravastatin, rosuvastatin, pitavastatin) on pancreatic islet beta cells and skeletal muscle cells.
- To elucidate the impact of these statins on cellular viability, insulin secretion, and glucose metabolism.
Main Methods:
- Human pancreas islet beta cells and human skeletal muscle cells (HSkMCs) were utilized.
- Assays included cytotoxicity, insulin secretion, glucose-stimulated insulin secretion, cell cycle analysis, glucose uptake, and Western blotting for key signaling proteins.
- Cells were treated with varying concentrations of atorvastatin, pravastatin, rosuvastatin, and pitavastatin.
Main Results:
- All tested statins at 100 nM reduced human pancreas islet beta cell viability and insulin secretion, with atorvastatin and pitavastatin showing the most pronounced cytotoxic effects.
- Glucose uptake in HSkMCs varied, with pitavastatin exhibiting the highest rate.
- Specific statins differentially affected glucose transporter (GLUT) expression and key signaling pathways (MAPK, AKT, GSK-3β) in both cell types, indicating varied mechanisms of insulin resistance induction.
Conclusions:
- Statins exhibit similar but quantitatively different effects on pancreatic islet beta cell damage and insulin resistance induction in HSkMCs.
- These findings suggest that the choice of statin may influence the risk of developing diabetes mellitus.
- Further research is warranted to explore personalized statin therapy to mitigate metabolic side effects.
Related Concept Videos
01:20Lipid-Lowering Drugs: Statins and Miscellaneous Agents
01:26Oral Hypoglycemic Agents: Biguanides and Glitazones
01:23Dipeptidyl Peptidase 4 Inhibitors
01:17Oral Hypoglycemic Agents: Sulfonylureas
01:06Oral Hypoglycemic Agents: Glinides