Bioactive fatty acids: role in bone biology and bone cell function

Watkins, Bruce A.; Lippman, Hugh E; Bouteiller, L Le; Li, Y; Seifert, Mark F.

doi:10.1016/s0163-7827(00)00016-3

Cited by 167 publications

(128 citation statements)

References 140 publications

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“…Interestingly, the conversion of ALA to EPA and DHA is greater in women compared to men, possibly due to a regulatory effect of oestrogen [17]. greater specificity for AA than EPA therefore preferentially synthesise 2-series rather than 3-series prostaglandins [24].…”

Section: Figurementioning

confidence: 99%

“…During the past 10 years several authors have reviewed various studies investigating the effects of PUFAs on bone health in animals [11,24,29,[33][34][35][36][37]. However, few studies in humans have been done despite the strong evidence gleaned from work on animal models.…”

Section: Figurementioning

confidence: 99%

“…PUFAs could thus have a positive effect on bone growth and development [24,33,36,[105][106][107][108][109].…”

Section: Effects Of Polyunsaturated Fatty Acids and Metabolites On Cymentioning

confidence: 99%

See 2 more Smart Citations

Long-chain polyunsaturated fatty acids: Selected mechanisms of action on bone

Kruger

Coetzee

Haag

et al. 2010

Progress in Lipid Research

145

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Section: Figurementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

See 1 more Smart Citation

Long-chain polyunsaturated fatty acids: Selected mechanisms of action on bone

Kruger

Coetzee

Haag

et al. 2010

Progress in Lipid Research

145

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“…4C). Combined and cooperative activities of osteoblasts (for bone formation) and osteoclasts (for bone resorption) determine the impact on the bone architecture (16). Toluidine blue staining on the plastic-embedded slides of 6-week-old mouse vertebrae L5 showed fewer osteoblasts in FACC1KO mice compared with WT cohort mice, that is, 44.1% less for osteoblast surface per bone surface, Ob.S/BS, and 41.1% less for number of osteoblasts per bone perimeter, N.Ob/B.Pm, (Fig.…”

Section: Facc1ko Mice Show Decreased Osteoblastogenesismentioning

confidence: 99%

“…Bone growth and homoeostasis is achieved by modeling and remodeling that are carried out by primary skeletal cell types-chondrocytes, osteoblasts, and osteoclasts-which are responsible for the formation of cartilage and bone (16). These cells are influenced by many regulatory hormones and molecules.…”

Section: Facc1ko Mice Show Decreased Osteoblastogenesismentioning

confidence: 99%

aP2-Cre-mediated inactivation of acetyl-CoA carboxylase 1 causes growth retardation and reduced lipid accumulation in adipose tissues

Mao¹,

Yang²,

Gu³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Adipose tissue is one of the major sites for fatty acid synthesis and lipid storage. We generated adipose (fat)-specific ACC1 knockout (FACC1KO) mice using the aP2-Cre/loxP system. FACC1KO mice showed prenatal growth retardation; after weaning, however, their weight gain was comparable to that of wild-type (WT) mice on a normal diet. Under lipogenic conditions of fasting/re-feeding a fat-free diet, lipid accumulation in adipose tissues of FACC1KO mice was significantly decreased; this is consistent with a 50 -66% reduction in the ACC activity in these tissues compared with that of WT mice. Surprisingly, FACC1KO mice manifested skeletal growth retardation phenotype accompanied by decreased chondrocyte proliferation in the growth plate and lower trabecular bone density. In addition, there was about a 30% decrease in serum insulin-like growth factor I (IGF1), and while the serum leptin level was decreased by about 50%, it did not counteract the osteopenic effects of IGF1 on the bone. Fatty acid analyses of mutant bone lipids revealed relatively higher levels of C18:2n-6 and C18:3n-3 and lower levels of their elongation C20 homologs than that of WT cohorts, leading to lower levels of C20 homologs and bone development. Moreover, aP2-Cre-mediated ACC1 inactivation in bone tissue led to a decreased number of osteoblasts but not of osteoclasts. The downregulation of ACC1 on osteoblastogenesis may be the cause for the osteopenia phenotype of FACC1KO bone homeostasis.fat-specific ACC1 knockout ͉ osteoblastogenesis A cetyl-CoA carboxylase 1 (ACC1) catalyzes the synthesis of malonyl-CoA, the committed step toward de novo synthesis of long-chain fatty acids from acetyl-CoA (1). Deletion of ACC1 in mice resulted in embryonic lethality, indicating that fatty acid synthesis is essential for embryonic development (2). To understand the importance of de novo fatty acid synthesis and the role of ACC1 in adult mouse tissues, we generated tissue-specific knockout mice using the Cre-loxP system (3). Mice with liverspecific knockout of ACC1 (LACC1KO) fed normal chow did not exhibit any significant physiological differences from wildtype (WT) mice (3). But when fed a fat-free diet, they accumulated significantly less triglyceride (TG) in the liver compared with their WT cohorts. Although inactivation of ACC1 resulted in 70-75% lower ACC activity in the liver, it did not affect either glucose homeostasis or hepatic fatty acid oxidation (3). When the LACC1KO mice were fed a fat-free diet for 10 days, there was an upregulation of PPAR␥ and several lipogenic enzymes in the liver, including a 2-fold increase in fatty acid synthase (FAS) mRNA, protein, and activity. However, syntheses of fatty acid and TG were reduced significantly. Upregulated ACC2 gene expression did not compensate for the loss of ACC1 function, an observation similar to that noted in Acc2 Ϫ/Ϫ mice in which the cytosolic ACC1 did not compensate for the mitochondrialassociated ACC2 and its product malonyl-CoA (4).Adipose tissues are active lipogenic and fat storage tissues,...

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Nutrition and Development

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Bioactive fatty acids: role in bone biology and bone cell function

Cited by 167 publications

References 140 publications

Long-chain polyunsaturated fatty acids: Selected mechanisms of action on bone

Long-chain polyunsaturated fatty acids: Selected mechanisms of action on bone

aP2-Cre-mediated inactivation of acetyl-CoA carboxylase 1 causes growth retardation and reduced lipid accumulation in adipose tissues

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