Abstract
Intra-cerebroventricular (i.c.v.) injection of glucose (0.1-1.0 μmol) caused dose-dependent increases in resting oxygen consumption (VO2) of conscious rats (maximum increase of 15.4 ± 2% at 0.5 μmol). These effects were significantly attenuated by peripheral (i.p.) pretreatment with the β-adrenoceptor antagonist propranolol, indicating the importance of the sympathetic nervous system (SNS) in the response. Plasma glucose concentrations were elevated (11%) 30 min after central injection of glucose, but intravenous glucose (0.5 μmol) did not affect resting VO2. Animals which had been fasted for 12 h prior to VO2 measurements exhibited reduced basal VO2 values, but the nutritional state of the animal did not affect the metabolic response to central injections of glucose (0.5 μmol). Rats exhibiting genetic (fa/fa Zucker rats) and hypothalamic (VMH-lesioned) obesity showed similar thermogenic responses to centrally administered glucose, to their lean counterparts. These data suggest a dual action of central glucose in the regulation of energy balance, involving stimulation of energy expenditure in addition to its reported inhibition of energy intake. The defective diet-induced thermogenesis associated with VMH and genetic obesities does not appear to result from an inability to respond to changes in intracerebroventricular glucose concentrations. © 1991.
| Original language | English |
|---|---|
| Pages (from-to) | 110-114 |
| Number of pages | 4 |
| Journal | Brain research |
| Volume | 547 |
| Issue number | 1 |
| Publication status | Published - 26 Apr 1991 |
Keywords
- Genetically obese
- Glucose
- Obesity
- Thermogenesis
- Ventromedial hypothalamus-lesioned
Research Beacons, Institutes and Platforms
- Manchester Institute of Biotechnology