Bone and fat hormonal crosstalk with antiretroviral initiation.


Journal

Bone
ISSN: 1873-2763
Titre abrégé: Bone
Pays: United States
ID NLM: 8504048

Informations de publication

Date de publication:
01 2022
Historique:
received: 15 03 2021
revised: 16 08 2021
accepted: 15 09 2021
pubmed: 22 9 2021
medline: 12 3 2022
entrez: 21 9 2021
Statut: ppublish

Résumé

Bone mineral density (BMD) loss and fat gain is common in people living with HIV (PLWH), particularly after initiating combination antiretroviral therapy (cART). Given the close metabolic interaction between bone and fat, we tested the hypotheses that changes in bone-derived hormones are associated with fat accumulation and changes in fat-derived hormones are associated with BMD loss following cART initiation. HIV-seropositive subjects (n = 15) initiating fixed dose cART of tenofovir disoproxil fumarate/emtricitabine/efavirenz (TDF/FTC/EFV) underwent dual X-ray absorptiometry (DXA) assessment pre-cART and again 12-months post-cART initiation. DXA-derived measurements included BMD at the lumbar spine, femoral neck, total hip, and trochanter and the trunk and total fat. Serum undercarboxylated osteocalcin (ucOCN), sclerostin, lipocalin-2, leptin, and adiponectin were measured pre and post-cART. Spearman's rank-order correlations assessed the cross-sectional associations between hormones and bone and fat mass pre- and post-cART. Linear regression models adjusting for baseline bone or fat mass assessed the association between hormone change and BMD/fat changes following cART initiation. ucOCN (p = 0.04) and lipocalin-2 (p = 0.03) increased post-cART while sclerostin, leptin, and adiponectin remained unchanged. BMD significantly decreased post-cART at all skeletal sites. Trunk and total fat increased post-cART but not significantly, while weight and BMI remained unchanged. In models adjusting for baseline BMD and fat mass, change in ucOCN was negatively associated with change in trunk (p = 0.008) and total fat (p = 0.01) and the change in leptin was positively associated with change in total hip (p = 0.03) and trochanteric BMD (p = 0.02). The current study demonstrates bone-fat crosstalk in cART initiating PLWH.

Sections du résumé

BACKGROUND
Bone mineral density (BMD) loss and fat gain is common in people living with HIV (PLWH), particularly after initiating combination antiretroviral therapy (cART). Given the close metabolic interaction between bone and fat, we tested the hypotheses that changes in bone-derived hormones are associated with fat accumulation and changes in fat-derived hormones are associated with BMD loss following cART initiation.
METHODS
HIV-seropositive subjects (n = 15) initiating fixed dose cART of tenofovir disoproxil fumarate/emtricitabine/efavirenz (TDF/FTC/EFV) underwent dual X-ray absorptiometry (DXA) assessment pre-cART and again 12-months post-cART initiation. DXA-derived measurements included BMD at the lumbar spine, femoral neck, total hip, and trochanter and the trunk and total fat. Serum undercarboxylated osteocalcin (ucOCN), sclerostin, lipocalin-2, leptin, and adiponectin were measured pre and post-cART. Spearman's rank-order correlations assessed the cross-sectional associations between hormones and bone and fat mass pre- and post-cART. Linear regression models adjusting for baseline bone or fat mass assessed the association between hormone change and BMD/fat changes following cART initiation.
RESULTS
ucOCN (p = 0.04) and lipocalin-2 (p = 0.03) increased post-cART while sclerostin, leptin, and adiponectin remained unchanged. BMD significantly decreased post-cART at all skeletal sites. Trunk and total fat increased post-cART but not significantly, while weight and BMI remained unchanged. In models adjusting for baseline BMD and fat mass, change in ucOCN was negatively associated with change in trunk (p = 0.008) and total fat (p = 0.01) and the change in leptin was positively associated with change in total hip (p = 0.03) and trochanteric BMD (p = 0.02).
CONCLUSION
The current study demonstrates bone-fat crosstalk in cART initiating PLWH.

Identifiants

pubmed: 34547525
pii: S8756-3282(21)00374-4
doi: 10.1016/j.bone.2021.116208
pmc: PMC8671338
mid: NIHMS1743835
pii:
doi:

Substances chimiques

Anti-HIV Agents 0
Emtricitabine G70B4ETF4S

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

116208

Subventions

Organisme : NIAID NIH HHS
ID : K23 AI059884
Pays : United States
Organisme : NIAID NIH HHS
ID : K24 AI155230
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI065200
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001873
Pays : United States

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

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Auteurs

Arnold Z Olali (AZ)

Department of Cell & Molecular Medicine, Rush University Medical Center, Chicago, IL, United States of America.

Qiuhu Shi (Q)

Department of Public Health, New York Medical College, Valhalla, NY, United States of America.

Donald R Hoover (DR)

Department of Statistics and Institute for Health, Health Care Policy and Aging Research, Rutgers University, Piscataway, NJ, United States of America.

Mariana Bucovsky (M)

Columbia University Irving Medical Center, New York, NY, United States of America.

Elizabeth Shane (E)

Columbia University Irving Medical Center, New York, NY, United States of America.

Michael T Yin (MT)

Columbia University Irving Medical Center, New York, NY, United States of America.

Ryan D Ross (RD)

Department of Cell & Molecular Medicine, Rush University Medical Center, Chicago, IL, United States of America. Electronic address: Ryan_Ross@rush.edu.

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