D-galactose-induced aging aggravates obesity-induced bone dyshomeostasis
Issued Date
2022-12-01
Resource Type
eISSN
20452322
Scopus ID
2-s2.0-85130343290
Pubmed ID
35595806
Journal Title
Scientific Reports
Volume
12
Issue
1
Rights Holder(s)
SCOPUS
Bibliographic Citation
Scientific Reports Vol.12 No.1 (2022)
Suggested Citation
Imerb N., Thonusin C., Pratchayasakul W., Arunsak B., Nawara W., Ongnok B., Aeimlapa R., Charoenphandhu N., Chattipakorn N., Chattipakorn S.C. D-galactose-induced aging aggravates obesity-induced bone dyshomeostasis. Scientific Reports Vol.12 No.1 (2022). doi:10.1038/s41598-022-12206-4 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/86418
Title
D-galactose-induced aging aggravates obesity-induced bone dyshomeostasis
Other Contributor(s)
Abstract
We aimed to compare the time-course effect of D-galactose (D-gal)-induced aging, obesity, and their combined effects on bone homeostasis. Male Wistar rats were fed with either a normal diet (ND; n = 24) or a high-fat diet (HFD; n = 24) for 12 weeks. All rats were then injected with either vehicle or 150 mg/kg/day of D-gal for 4 or 8 weeks. Blood was collected to measure metabolic, aging, oxidative stress, and bone turnover parameters. Bone oxidative stress and inflammatory markers, as well as bone histomorphometry were also evaluated. Additionally, RAW 264.7 cells were incubated with either D-gal, insulin, or D-gal plus insulin to identify osteoclast differentiation capacity under the stimulation of receptor activator of nuclear factor κB ligand. At week 4, D-gal-induced aging significantly elevated serum malondialdehyde level and decreased trabecular thickness in ND- and HFD-fed rats, when compared to the control group. At week 8, D-gal-induced aging further elevated advanced glycation end products, increased bone inflammation and resorption, and significantly impaired bone microarchitecture in HFD-fed rats. The osteoclast number in vitro were increased in the D-gal, insulin, and combined groups to a similar extent. These findings suggest that aging aggravates bone dyshomeostasis in the obese condition in a time-dependent manner.