Angiotensin-I converting enzyme genotype-dependent benefit from hormone replacement therapy in isometric muscle strength and bone mineral density

David Woods, Gladys Onambele, Roger Woledge, Dawn Skelton, Stuart Bruce, Steve E. Humphries, Hugh Montgomery

Research output: Contribution to journalArticle

Abstract

Low bone mineral density (BMD) and muscle weakness are major risk factors for postmenopausal osteoporotic fracture. Hormone replacement therapy (HRT) reverses the menopausal decline in maximum voluntary force of the adductor pollicis and reduces serum angiotensin-I converting enzyme (ACE) levels. The insertion (I) allele of the ACE gene polymorphism is associated with lower ACE activity and improved muscle efficiency in response to physical training. Therefore, we examined whether the presence of the I allele in postmenopausal women would affect the muscle response to HRT. Those taking HRT showed a significant gain in normalized muscle maximum voluntary force slope, the rate of which was strongly influenced by ACE genotype (16.0 ± 1.53%, 14.3 ± 2.67%, and 7.76 ± 4.13%, mean ± SEM for II, ID, and DD genotype, respectively; P = 0.017 for gene effect, P = 0.004 for I allele effect). There was also a significant ACE gene effect in the response of BMD to HRT in Ward’s triangle (P = 0.03) and a significant I allele effect in the spine (P = 0.03), but not in the neck of femur or total hip. These data suggests that low ACE activity associated with the I allele confers an improved muscle and BMD response in postmenopausal women treated with HRT.

Original languageEnglish
JournalJournal of Clinical Endocrinology and Metabolism
DOIs
Publication statusPublished - 1 May 2001

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Hormone Replacement Therapy
Muscle Strength
Peptidyl-Dipeptidase A
Bone Density
Minerals
Muscle
Bone
Genotype
Hormones
Alleles
Genes
Enzyme activity
Muscles
Osteoporotic Fractures
Femur Neck
Muscle Weakness
Polymorphism
Hip
Skeletal Muscle
Spine

Keywords

  • HRT
  • bone mineral density
  • hormone replacement therapy

Cite this

@article{5c1a28ff5eea4a81b13fa45d4754d838,
title = "Angiotensin-I converting enzyme genotype-dependent benefit from hormone replacement therapy in isometric muscle strength and bone mineral density",
abstract = "Low bone mineral density (BMD) and muscle weakness are major risk factors for postmenopausal osteoporotic fracture. Hormone replacement therapy (HRT) reverses the menopausal decline in maximum voluntary force of the adductor pollicis and reduces serum angiotensin-I converting enzyme (ACE) levels. The insertion (I) allele of the ACE gene polymorphism is associated with lower ACE activity and improved muscle efficiency in response to physical training. Therefore, we examined whether the presence of the I allele in postmenopausal women would affect the muscle response to HRT. Those taking HRT showed a significant gain in normalized muscle maximum voluntary force slope, the rate of which was strongly influenced by ACE genotype (16.0 ± 1.53{\%}, 14.3 ± 2.67{\%}, and 7.76 ± 4.13{\%}, mean ± SEM for II, ID, and DD genotype, respectively; P = 0.017 for gene effect, P = 0.004 for I allele effect). There was also a significant ACE gene effect in the response of BMD to HRT in Ward’s triangle (P = 0.03) and a significant I allele effect in the spine (P = 0.03), but not in the neck of femur or total hip. These data suggests that low ACE activity associated with the I allele confers an improved muscle and BMD response in postmenopausal women treated with HRT.",
keywords = "HRT, bone mineral density, hormone replacement therapy",
author = "David Woods and Gladys Onambele and Roger Woledge and Dawn Skelton and Stuart Bruce and Humphries, {Steve E.} and Hugh Montgomery",
note = "Originally published in: Journal of Clinical Endocrinology and Metabolism (2001), 86 (5), pp.2200-2204.",
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Angiotensin-I converting enzyme genotype-dependent benefit from hormone replacement therapy in isometric muscle strength and bone mineral density. / Woods, David; Onambele, Gladys; Woledge, Roger; Skelton, Dawn; Bruce, Stuart; Humphries, Steve E.; Montgomery, Hugh.

In: Journal of Clinical Endocrinology and Metabolism, 01.05.2001.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Angiotensin-I converting enzyme genotype-dependent benefit from hormone replacement therapy in isometric muscle strength and bone mineral density

AU - Woods, David

AU - Onambele, Gladys

AU - Woledge, Roger

AU - Skelton, Dawn

AU - Bruce, Stuart

AU - Humphries, Steve E.

AU - Montgomery, Hugh

N1 - Originally published in: Journal of Clinical Endocrinology and Metabolism (2001), 86 (5), pp.2200-2204.

PY - 2001/5/1

Y1 - 2001/5/1

N2 - Low bone mineral density (BMD) and muscle weakness are major risk factors for postmenopausal osteoporotic fracture. Hormone replacement therapy (HRT) reverses the menopausal decline in maximum voluntary force of the adductor pollicis and reduces serum angiotensin-I converting enzyme (ACE) levels. The insertion (I) allele of the ACE gene polymorphism is associated with lower ACE activity and improved muscle efficiency in response to physical training. Therefore, we examined whether the presence of the I allele in postmenopausal women would affect the muscle response to HRT. Those taking HRT showed a significant gain in normalized muscle maximum voluntary force slope, the rate of which was strongly influenced by ACE genotype (16.0 ± 1.53%, 14.3 ± 2.67%, and 7.76 ± 4.13%, mean ± SEM for II, ID, and DD genotype, respectively; P = 0.017 for gene effect, P = 0.004 for I allele effect). There was also a significant ACE gene effect in the response of BMD to HRT in Ward’s triangle (P = 0.03) and a significant I allele effect in the spine (P = 0.03), but not in the neck of femur or total hip. These data suggests that low ACE activity associated with the I allele confers an improved muscle and BMD response in postmenopausal women treated with HRT.

AB - Low bone mineral density (BMD) and muscle weakness are major risk factors for postmenopausal osteoporotic fracture. Hormone replacement therapy (HRT) reverses the menopausal decline in maximum voluntary force of the adductor pollicis and reduces serum angiotensin-I converting enzyme (ACE) levels. The insertion (I) allele of the ACE gene polymorphism is associated with lower ACE activity and improved muscle efficiency in response to physical training. Therefore, we examined whether the presence of the I allele in postmenopausal women would affect the muscle response to HRT. Those taking HRT showed a significant gain in normalized muscle maximum voluntary force slope, the rate of which was strongly influenced by ACE genotype (16.0 ± 1.53%, 14.3 ± 2.67%, and 7.76 ± 4.13%, mean ± SEM for II, ID, and DD genotype, respectively; P = 0.017 for gene effect, P = 0.004 for I allele effect). There was also a significant ACE gene effect in the response of BMD to HRT in Ward’s triangle (P = 0.03) and a significant I allele effect in the spine (P = 0.03), but not in the neck of femur or total hip. These data suggests that low ACE activity associated with the I allele confers an improved muscle and BMD response in postmenopausal women treated with HRT.

KW - HRT

KW - bone mineral density

KW - hormone replacement therapy

U2 - 10.1210/jc.86.5.2200

DO - 10.1210/jc.86.5.2200

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JO - Journal of Clinical Endocrinology and Metabolism

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SN - 0021-972X

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