Related Experiment Videos
Abnormal glucose homeostasis due to chronic hyperresistinemia
Shamina M Rangwala1, A Sophie Rich, Ben Rhoades
1Department of Medicine, The Penn Diabetes Center, Philadelphia, Pennsylvania, USA.
Diabetes
|June 11, 2004
Summary
Chronic high resistin levels in normal-weight mice impair glucose metabolism. This study shows hyperresistinemia increases blood glucose and reduces glucose tolerance, impacting metabolic health.
Area of Science:
- Metabolic research
- Endocrinology
- Obesity research
Background:
- Resistin is an adipocyte-secreted protein linked to obesity.
- Acute resistin administration negatively affects glucose tolerance.
- The long-term impact of elevated resistin (hyperresistinemia) remains unclear.
Purpose of the Study:
- To investigate the effects of chronic hyperresistinemia on glucose metabolism.
- To characterize transgenic mice with sustained high resistin levels.
Main Methods:
- Generation and characterization of resistin-transgenic mice.
- Measurement of fasted blood glucose and glucose tolerance tests.
- Hyperinsulinemic-euglycemic clamp studies to assess glucose production.
- Analysis of hepatic phosphoenolpyruvate carboxykinase (PEPCK) expression.
Main Results:
- Resistin-transgenic mice exhibited higher fasted blood glucose levels compared to controls.
- Glucose tolerance was significantly impaired in mice with chronic hyperresistinemia.
- Metabolic studies revealed elevated hepatic glucose production in hyperresistinemic mice.
- Increased hepatic PEPCK expression was observed, potentially contributing to higher glucose production.
Conclusions:
- Chronic hyperresistinemia, even in the absence of obesity, impairs glucose metabolism.
- Sustained high resistin levels disrupt normal glucose homeostasis.
- This suggests resistin plays a critical role in regulating glucose production and tolerance.