The sympathetic nervous system as a target for intervention in obesity

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The sympathetic nervous system as a target for intervention in obesity. / Astrup, Arne.

In: International Journal of Obesity, Vol. 19, No. Suppl. 7, 1995, p. S24-S28.

Research output: Contribution to journalConference articleResearchpeer-review

Harvard

Astrup, A 1995, 'The sympathetic nervous system as a target for intervention in obesity', International Journal of Obesity, vol. 19, no. Suppl. 7, pp. S24-S28.

APA

Astrup, A. (1995). The sympathetic nervous system as a target for intervention in obesity. International Journal of Obesity, 19(Suppl. 7), S24-S28.

Vancouver

Astrup A. The sympathetic nervous system as a target for intervention in obesity. International Journal of Obesity. 1995;19(Suppl. 7):S24-S28.

Author

Astrup, Arne. / The sympathetic nervous system as a target for intervention in obesity. In: International Journal of Obesity. 1995 ; Vol. 19, No. Suppl. 7. pp. S24-S28.

Bibtex

@inproceedings{b48ed090dec2411ebb736cb21b527aea,
title = "The sympathetic nervous system as a target for intervention in obesity",
abstract = "The sympathoadrenal system plays an important role in the regulation of both energy intake and energy expenditure (EE), and the sympathetic nervous system (SNS) offers a dual target for pharmacological intervention directed at weight loss in obese patients. The sizes of the fat-free mass and fat mass are the major determinants of resting EE, but studies using different techniques have shown that differences in sympathetic activity can account for an additional proportion of the variation between individuals. Differences in thermogenic responses to food can also be explained by different abilities to activate the sympathoadrenal system. A low resting EE for a given body composition is one manifestation of the genetically determined predisposition to obesity. A low sympathetic activity may be one factor responsible but, as yet, no conclusive evidence has been found. In dietary treatment programmes of obesity, patients with high levels of EE and greater SNS activity achieve greater long-term weight loss than those with lower levels. Pharmacological stimulation with sympathomimetic compounds suppresses appetite and increases energy expenditure through stimulation of β1, β2 and β3 - receptor subtypes. During chronic treatment, the β3-mediation may predominate due to down-regulation of β1 - and β2 -receptors. An improved understanding of the aetiological role of the SNS in the development of obesity in genetically susceptible individuals may permit tailoring of pharmacological intervention.",
keywords = "Appetite, Dietary treatment, Energy intake, Energy metabolism, Obesity, Pharmacological therapy, Sympathetic nervous system",
author = "Arne Astrup",
year = "1995",
language = "English",
volume = "19",
pages = "S24--S28",
journal = "International Journal of Obesity",
issn = "0307-0565",
publisher = "nature publishing group",
number = "Suppl. 7",

}

RIS

TY - GEN

T1 - The sympathetic nervous system as a target for intervention in obesity

AU - Astrup, Arne

PY - 1995

Y1 - 1995

N2 - The sympathoadrenal system plays an important role in the regulation of both energy intake and energy expenditure (EE), and the sympathetic nervous system (SNS) offers a dual target for pharmacological intervention directed at weight loss in obese patients. The sizes of the fat-free mass and fat mass are the major determinants of resting EE, but studies using different techniques have shown that differences in sympathetic activity can account for an additional proportion of the variation between individuals. Differences in thermogenic responses to food can also be explained by different abilities to activate the sympathoadrenal system. A low resting EE for a given body composition is one manifestation of the genetically determined predisposition to obesity. A low sympathetic activity may be one factor responsible but, as yet, no conclusive evidence has been found. In dietary treatment programmes of obesity, patients with high levels of EE and greater SNS activity achieve greater long-term weight loss than those with lower levels. Pharmacological stimulation with sympathomimetic compounds suppresses appetite and increases energy expenditure through stimulation of β1, β2 and β3 - receptor subtypes. During chronic treatment, the β3-mediation may predominate due to down-regulation of β1 - and β2 -receptors. An improved understanding of the aetiological role of the SNS in the development of obesity in genetically susceptible individuals may permit tailoring of pharmacological intervention.

AB - The sympathoadrenal system plays an important role in the regulation of both energy intake and energy expenditure (EE), and the sympathetic nervous system (SNS) offers a dual target for pharmacological intervention directed at weight loss in obese patients. The sizes of the fat-free mass and fat mass are the major determinants of resting EE, but studies using different techniques have shown that differences in sympathetic activity can account for an additional proportion of the variation between individuals. Differences in thermogenic responses to food can also be explained by different abilities to activate the sympathoadrenal system. A low resting EE for a given body composition is one manifestation of the genetically determined predisposition to obesity. A low sympathetic activity may be one factor responsible but, as yet, no conclusive evidence has been found. In dietary treatment programmes of obesity, patients with high levels of EE and greater SNS activity achieve greater long-term weight loss than those with lower levels. Pharmacological stimulation with sympathomimetic compounds suppresses appetite and increases energy expenditure through stimulation of β1, β2 and β3 - receptor subtypes. During chronic treatment, the β3-mediation may predominate due to down-regulation of β1 - and β2 -receptors. An improved understanding of the aetiological role of the SNS in the development of obesity in genetically susceptible individuals may permit tailoring of pharmacological intervention.

KW - Appetite

KW - Dietary treatment

KW - Energy intake

KW - Energy metabolism

KW - Obesity

KW - Pharmacological therapy

KW - Sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=0029586729&partnerID=8YFLogxK

M3 - Conference article

C2 - 8963368

AN - SCOPUS:0029586729

VL - 19

SP - S24-S28

JO - International Journal of Obesity

JF - International Journal of Obesity

SN - 0307-0565

IS - Suppl. 7

ER -

ID: 209797531