UNIGE document Scientific Article
previous document  unige:83951  next document
add to browser collection
Title

Fat and Sucrose Intake Induces Obesity-Related Bone Metabolism Disturbances: Kinetic and Reversibility Studies in Growing and Adult Rats

Authors
Martin, Aline
Linossier, Marie-Thérèse
Vanden Bossche, Arnaud
Laroche, Norbert
Thomas, Mireille
Gerbaix, Maude
show hidden authors show all authors [1 - 12]
Published in Journal of Bone and Mineral Research. 2016, vol. 31, no. 1, p. 98-115
Abstract Metabolic and bone effects were investigated in growing (G, n¼45) and mature (M, n¼45) rats fed a high-fat/high-sucrose diet(HFS)isocaloric to the chow diet of controls (C, n¼30 per group). At week 19, a subset of 15 rats in each group (HFS or C, at both ages)was analyzed. Then one-half of the remaining 30 HFS rats in each groups continued HFS and one-half were shifted to C until week 27. Although no serum or bone marrow inflammation was seen, HFS increased visceral fat, serum leptin and insulin at week 19 and induced further alterations in lipid profile, serum adiponectin, and TGFb1, TIMP1, MMP2, and MMP9, suggesting a prediabetic phenotype and cardiovascular dysfunction at week 27 more pronounced in M than G. These events were associated with dramatic reduction of osteoclastic and osteoid surfaces with accelerated mineralizing surfaces in both HFS age groups. Mineral metabolism and its major regulators were disturbed, leading to hyperphosphatemia and hypocalcemia. These changes were associated with bone alterations in the weight-bearing tibia, not in the non-weight-bearing vertebra. Indeed in fat rats, tibia trabecular bone accrual increased in G whereas loss of trabecular bone inMwas alleviated. At diaphysis cortical porosity increased in G and even more inMat week 27. After the diet switch, metabolic and bone cellular disturbances fully reversed in G, but not in M. Trabecular benefit of the obese was preserved in both age groups and inMthe age-related bone loss was even lighter after the diet switch than in prolonged HFS. At the diaphysis, cortical porosity normalized in G but not in M. Hypocalcemia in G and M was irreversible. Thus, the mild metabolic syndrome induced by isocaloric HFS is able to alter bone cellular activities and mineral metabolism, reinforce trabecular bone, and affect cortical bone porosity in an irreversible manner in older rats. © 2015 American Society for Bone and Mineral Research.
Keywords ObesityDiabetesCalcium-Phosphate metabolismHistomorphometryBOone Strength
Identifiers
Full text
Article (Published version) (451 Kb) - document accessible for UNIGE members only Limited access to UNIGE
Other version: http://doi.wiley.com/10.1002/jbmr.2596
Structures
Research group Etudes précliniques de l'ostéoporose (606)
Citation
(ISO format)
LAVET, Cedric et al. Fat and Sucrose Intake Induces Obesity-Related Bone Metabolism Disturbances: Kinetic and Reversibility Studies in Growing and Adult Rats. In: Journal of Bone and Mineral Research, 2016, vol. 31, n° 1, p. 98-115. https://archive-ouverte.unige.ch/unige:83951

90 hits

2 downloads

Update

Deposited on : 2016-05-30

Export document
Format :
Citation style :