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Transcriptomic analysis of sarcopenic obese mice reveals alterations in regulators of muscle force production, such as extracellular matrix remodeling and shifts in muscle fiber type

ABSTRACT: Sarcopenic obesity (SO) is the combined condition of sarcopenia and obesity most commonly occurring in the older adult population. SO is associated with poor physical function, increased risk of musculoskeletal injury, and reduced quality of life and independence. There is little information on the molecular underpinnings of this condition. The aim of this study was to provide a transcriptomic analysis characterizing SO and to provide deeper understanding to the etiology of the condition. Young (Y) (6 mo) and aged (A) (21-24 mo) mice were fed either normal chow (L) (12% kcal from fat) or high-fat (O) (60% kcal from fat) diets ad libitum. Through multiple analyses, we observed genes related to ECM remodeling are downregulated with aged-obesity compared with young obesity, providing insight to the effects of age in a life-long obese condition. Furthermore, genes related to slow-twitch muscle contraction and fast-to-slow muscle fiber type transitions were upregulated in with obesity in the aged condition. Together, our results demonstrate avenues of dysregulation in SO skeletal muscle, providing the molecular building blocks expanding our understanding of the etiology of poor muscle function in this condition. Further understanding and exploration of these dysregulations is critical to identify therapeutic treatments targeting the source of muscle functional impairment, reducing the risk of musculoskeletal injury, and improving quality of life and independence SO individuals.

ORGANISM(S): Mus musculus

PROVIDER: GSE290570 | GEO | 2025/08/05

REPOSITORIES: GEO

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Project description:To profile the expression of circulating miRNAs in a mouse model of diet-induced obesity (DIO) with subsequent weight-reduction with low-fat diet (LFD), eighteen C57BL/6 male mice were grouped into three subgroups as: (1) Control: the mice fed with the standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice fed with 58 kcal% high-fat diet for 12 wks; (3) DIO+LFD: the mice fed with high-fat diet for 8 wks to induce obesity, then changed to 10.5 kcal% low-fat diet for subsequent 4 wks. C57BL/6 mice were purchased from BioLasco (Taipei, Taiwan). All housing conditions were maintained, and surgical procedures, including analgesia, were performed in an Association for Assessment and Accreditation of Laboratory Animal Care International (AAALAC)-accredited SPF facility according to national and institutional guidelines. In this experiment, eighteen C57BL/6 wild type male mice were randomly grouped into three subgroups (n=6 in each group): (1) Control: the control mice were fed ad libitum a standard AIN-76A (fat: 11.5 kcal%) diet for 12 wks; (2) DIO: the mice were fed ad libitum a 58 kcal% HFD (D12331; Research Diets Inc., New Brunswick, NJ) for 12 wks to induce obesity; (3) DIO+LFD: the mice fed ad libitum a 58 kcal% HFD (D12331) for 8 wks to induce obesity, then continued the feeding of 10.5 kcal% LFD (D 12329; Research Diets Inc.) for additional 4 wks. Weight measurements were performed on a weekly basis to for these three groups of mice. Evaluation of blood glucose levels was performed at the beginning and in the end of the experiment to confirm that the HFD-fed mice developed an obese and insulin resistant phenotype. After the end of experiment at 12w, all mice were killed. The abdominal WAT of each mice was removed and weighted. Paraffin-embedded abdominal WAT was sectioned at 5 M-NM-<m and stained with hematoxylin and eosin to measure mean adipocyte area. A volume of 1 mL of whole blood was collected into a plain tube and allowed to clot for 1 hour. The sera samples were aliquoted after centrifugation at 3,000 M-CM-^W g for 10 minutes and stored at M-bM-^HM-^R80M-BM-0C until further analysis.

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Transcriptomic analysis of sarcopenic obese mice reveals alterations in regulators of muscle force production, such as extracellular matrix remodeling and shifts in muscle fiber type

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