Abstract |
A reduced thermic response and an impaired activation of the sympathetic nervous system (SNS) has been reported after oral glucose in human obesity. It is, however, not known whether the reduced SNS activity returns to normal along with weight reduction. The thermic effect of glucose was lower in eight obese patients than in matched control subjects (1.7% vs 9.2%, p less than 0.002). The increase in arterial norepinephrine after glucose was also blunted in the obese patients. After a 30-kg weight loss their glucose and lipid profiles were markedly improved but the thermic effect of glucose was still lower than that of the control subjects (4.2%, p less than 0.001). The glucose-induced arterial norepinephrine response remained diminished in the reduced obese patients whereas the changes in plasma epinephrine were similar in all three groups. The results suggest that a defective SNS may be a cause in the development of obesity.
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Authors | A Astrup, T Andersen, N J Christensen, J Bülow, J Madsen, L Breum, F Quaade |
Journal | The American journal of clinical nutrition
(Am J Clin Nutr)
Vol. 51
Issue 3
Pg. 331-7
(Mar 1990)
ISSN: 0002-9165 [Print] United States |
PMID | 2178388
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Blood Glucose
- C-Peptide
- Insulin
- Glucagon
- Glucose
- Norepinephrine
- Epinephrine
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Topics |
- Adult
- Blood Glucose
(analysis)
- Body Temperature Regulation
(drug effects)
- C-Peptide
(blood)
- Energy Metabolism
- Epinephrine
(blood)
- Female
- Glucagon
(blood)
- Glucose
(pharmacology)
- Humans
- Insulin
(blood)
- Male
- Middle Aged
- Norepinephrine
(blood)
- Obesity
(blood, diet therapy, physiopathology)
- Sympathetic Nervous System
(drug effects, physiopathology)
- Weight Loss
(physiology)
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