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Hyperinsulinemic yellow KK mice and norepinephrine turnover
H Nishioka1, T Yoshida, K Yoshioka
1First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
Endocrinologia Japonica
|August 1, 1987
Summary
Hyperinsulinemia did not accelerate sympathetic nervous system (SNS) activity in yellow KK mice. Reduced norepinephrine turnover in brown adipose tissue may contribute to obesity development in these mice.
Area of Science:
- Metabolic research
- Neuroendocrinology
- Obesity research
Background:
- Hyperinsulinemia is associated with obesity and metabolic dysfunction.
- The sympathetic nervous system (SNS) plays a role in regulating energy balance and metabolism.
- Norepinephrine (NE) turnover is a key indicator of SNS activity.
Purpose of the Study:
- To investigate the relationship between hyperinsulinemia and SNS activity.
- To determine if hyperinsulinemia accelerates NE turnover in specific tissues.
- To explore the role of NE turnover in brown adipose tissue (BAT) in obesity development.
Main Methods:
- Measurement of NE turnover in interscapular brown adipose tissue (IBAT) and heart.
- Utilized hyperinsulinemic yellow KK mice and normoinsulinemic C57BL control mice.
- Administered alpha-methyl-p-tyrosine (alpha-MPT) to block NE synthesis for turnover assessment.
Main Results:
- Yellow KK mice exhibited significantly higher plasma glucose and insulin levels compared to controls.
- NE turnover in IBAT was significantly slower in yellow KK mice than in C57BL mice.
- No significant difference in NE turnover was observed in the heart between the two groups.
Conclusions:
- Hyperinsulinemia does not consistently increase NE turnover.
- Reduced NE turnover in IBAT of yellow KK mice may be a contributing factor to obesity.
- Defects in brown adipose tissue function, a key thermogenic effector, can predispose to obesity.