Sex differences in the relationships between body composition, fat distribution, and mitochondrial energy metabolism: a pilot study.
Adiposity
Body composition
Fat distribution
Intermuscular fat
MRS
Mitochondria
Muscle
Journal
Nutrition & metabolism
ISSN: 1743-7075
Titre abrégé: Nutr Metab (Lond)
Pays: England
ID NLM: 101231644
Informations de publication
Date de publication:
21 May 2022
21 May 2022
Historique:
received:
06
12
2021
accepted:
09
05
2022
entrez:
21
5
2022
pubmed:
22
5
2022
medline:
22
5
2022
Statut:
epublish
Résumé
Adiposity and mitochondrial dysfunction are related factors contributing to metabolic disease development. This pilot study examined whether in vivo and ex vivo indices of mitochondrial metabolism were differentially associated with body composition in males and females. Thirty-four participants including 19 females (mean 27 yr) and 15 males (mean 29 yr) had body composition assessed by dual energy x-ray absorptiometry and magnetic resonance (MR) imaging. Monocyte reserve capacity and maximal oxygen consumption rate (OCR) were determined ex vivo using extracellular flux analysis. In vivo quadriceps mitochondrial function was measured using Mitochondrial metabolism was similar between sexes (p > 0.05). In males only, higher fat mass percent (FM%) was correlated with lower reserve capacity (r = - 0.73; p = 0.002) and reduced muscle mitochondrial function (r = 0.58, p = 0.02). Thigh subcutaneous adipose tissue was inversely related to reserve capacity in males (r = - 0.75, p = 0.001), but in females was correlated to higher maximal OCR (r = 0.48, p = 0.046), independent of FM. In females, lean mass was related to greater reserve capacity (r = 0.47, p = 0.04). In all participants, insulin (r = 0.35; p = 0.04) and HOMA-IR (r = 0.34; p = 0.05) were associated with a higher τPCr. These novel findings demonstrate distinct sex-dependent associations between monocyte and skeletal muscle mitochondrial metabolism with body composition. With further study, increased understanding of these relationships may inform sex-specific interventions to improve mitochondrial function and metabolic health.
Sections du résumé
BACKGROUND
BACKGROUND
Adiposity and mitochondrial dysfunction are related factors contributing to metabolic disease development. This pilot study examined whether in vivo and ex vivo indices of mitochondrial metabolism were differentially associated with body composition in males and females.
METHODS
METHODS
Thirty-four participants including 19 females (mean 27 yr) and 15 males (mean 29 yr) had body composition assessed by dual energy x-ray absorptiometry and magnetic resonance (MR) imaging. Monocyte reserve capacity and maximal oxygen consumption rate (OCR) were determined ex vivo using extracellular flux analysis. In vivo quadriceps mitochondrial function was measured using
RESULTS
RESULTS
Mitochondrial metabolism was similar between sexes (p > 0.05). In males only, higher fat mass percent (FM%) was correlated with lower reserve capacity (r = - 0.73; p = 0.002) and reduced muscle mitochondrial function (r = 0.58, p = 0.02). Thigh subcutaneous adipose tissue was inversely related to reserve capacity in males (r = - 0.75, p = 0.001), but in females was correlated to higher maximal OCR (r = 0.48, p = 0.046), independent of FM. In females, lean mass was related to greater reserve capacity (r = 0.47, p = 0.04). In all participants, insulin (r = 0.35; p = 0.04) and HOMA-IR (r = 0.34; p = 0.05) were associated with a higher τPCr.
CONCLUSIONS
CONCLUSIONS
These novel findings demonstrate distinct sex-dependent associations between monocyte and skeletal muscle mitochondrial metabolism with body composition. With further study, increased understanding of these relationships may inform sex-specific interventions to improve mitochondrial function and metabolic health.
Identifiants
pubmed: 35597962
doi: 10.1186/s12986-022-00670-8
pii: 10.1186/s12986-022-00670-8
pmc: PMC9123728
doi:
Types de publication
Journal Article
Langues
eng
Pagination
37Subventions
Organisme : NIH HHS
ID : P30 ES019776
Pays : United States
Organisme : NIH HHS
ID : P30 DK056336
Pays : United States
Organisme : NIH HHS
ID : K24 DK096574
Pays : United States
Organisme : NIH HHS
ID : R03 DK117246
Pays : United States
Organisme : NIH HHS
ID : T32 CA093423
Pays : United States
Organisme : NIH HHS
ID : UL1TR002378
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES019776
Pays : United States
Organisme : NIH HHS
ID : K01 DK102851
Pays : United States
Informations de copyright
© 2022. The Author(s).
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