Keyword search (4,163 papers available)

"Tam BT" Authored Publications:

Title Authors PubMed ID
1 Combating childhood overweight and obesity: The role of Olympic Movement and bodily movement Tam BT; Wan K; Santosa S; Cai Z; 39991475
SOH
2 Intramyocellular lipid use is altered with exercise in males with childhood-onset obesity despite no differences in substrate oxidation Feola S; Al-Nabelsi L; Tam BT; Near J; Morais JA; Santosa S; 39875595
HKAP
3 Age of obesity onset affects subcutaneous adipose tissue cellularity differently in the abdominal and femoral region Murphy J; Dera A; Morais JA; Tsoukas MA; Khor N; Sazonova T; Almeida LG; Cooke AB; Daskalopoulou SS; Tam BT; Santosa S; 39045668
SOH
4 Senescence markers in subcutaneous preadipocytes differ in childhood- versus adult-onset obesity before and after weight loss Murphy J; Tam BT; Kirkland JL; Tchkonia T; Giorgadze N; Pirtskhalava T; Tsoukas MA; Morais JA; Santosa S; 37194560
PERFORM
5 Sex Affects Regional Variations in Subcutaneous Adipose Tissue T Cells but not Macrophages in Adults with Obesity Murphy J; Delaney KZ; Dam V; Tam BT; Khor N; Tsoukas MA; Morais JA; Santosa S; 33179451
PERFORM
6 Acetyl-CoA regulation, OXPHOS integrity and leptin level are different in females with different onsets of obesity. Tam BT, Murphy J, Khor N, Morais JA, Santosa S 32808657
PERFORM
7 Obestatin and growth hormone reveal the interaction of central obesity and other cardiometabolic risk factors of metabolic syndrome. Yu AP, Ugwu FN, Tam BT, Lee PH, Ma V, Pang S, Chow AS, Cheng KK, Lai CW, Wong CS, Siu PM 32218464
HKAP
8 Obesity and ageing: Two sides of the same coin. Tam BT, Morais JA, Santosa S 32020741
PERFORM
9 Ghrelin Axis Reveals the Interacting Influence of Central Obesity and Hypertension. Yu AP, Ugwu FN, Tam BT, Lee PH, Lai CW, Wong CSC, Siu PM 30258404
HKAP

 

Title:Senescence markers in subcutaneous preadipocytes differ in childhood- versus adult-onset obesity before and after weight loss
Authors:Murphy JTam BTKirkland JLTchkonia TGiorgadze NPirtskhalava TTsoukas MAMorais JASantosa S
Link:https://pubmed.ncbi.nlm.nih.gov/37194560/
DOI:10.1002/oby.23745
Publication:Obesity (Silver Spring, Md.)
Keywords:
PMID:37194560 Category: Date Added:2023-05-17
Dept Affiliation: PERFORM
1 Department of Health, Kinesiology, and Applied Physiology, Concordia University, Montréal, Québec, Canada.
2 Metabolism, Obesity, and Nutrition Laboratory, PERFORM Centre, Concordia University, Montréal, Québec, Canada.
3 Centre de recherche-Axe maladies chroniques, Centre intégré universitaire de santé et de services sociaux du Nord-de-l'Ile-de-Montréal, Hôpital du Sacré-Coeur de Montréal, Montréal, Québec, Canada.
4 Department of Sport, Physical Education, and Health, Faculty of Social Sciences, Hong Kong Baptist University, Kowloon Tong, Hong Kong, China.
5 Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.
6 Division of Endocrinology and Metabolism, Department of Medicine, McGill University, Royal Victoria Hospital, McGill University Health Centre Glen Site, Montréal, Québec, Canada.
7 Division of Geriatric Medicine, Department of Medicine, McGill University, McGill University Health Centre-Montréal General Hospital, Montréal, Québec, Canada.

Description:

Objective: The aim of this study was to determine the effect of age of obesity onset on senescence-related markers in abdominal (AB) and femoral (FEM) subcutaneous adipose tissue (SAT) before and after moderate (~10%) weight loss.

Methods: AB and FEM SAT were collected from human females with childhood-onset obesity (CO) or adult-onset obesity (AO) before and after diet- and exercise-induced weight loss. Immunofluorescence analysis of ?H2AX/RAD51 (DNA damage/repair markers) and p53/p21 (senescence markers) was conducted in cultured preadipocytes, and senescence-associated ß-galactosidase (SA-ß-gal) activity was measured in SAT.

Results: CO had proportionately more AB and FEM preadipocytes with DNA damage (?H2AX+ ) and senescence markers (p53+ and/or p21+ ) than AO at baseline. The proportion of ?H2AX+ FEM preadipocytes declined with weight loss in CO and was similar between groups after weight loss. The number of ?H2AX foci in ?H2AX+ preadipocytes decreased similarly between groups and regions with weight loss in parallel with an increase in RAD51. The proportion of p53+ and p21+ preadipocytes and SA-ß-gal+ cells in SAT did not change with weight loss, but the total p21 intensity in p53+ /p21+ FEM preadipocytes declined in AO.

Conclusions: These results provide preliminary evidence that females with CO have an accelerated preadipocyte aging state that improves with weight loss in terms of DNA damage but not senescence.





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