ArticleProceedings of the National Academy of Sciences of the United States of America2009
aP2-Cre-mediated inactivation of acetyl-CoA carboxylase 1 causes growth retardation and reduced lipid accumulation in adipose tissues.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 54 citations in OpenAlex.
- A non-invasive method for light-inducible knockout across all cell types in mouse subcutaneous adipose tissue.Adipocyte · 2026Article
- Causal Relationship Between Blood Metabolites and Osteoporosis: A Two-Sample Mendelian Randomization and Genetic Correlation Analysis.Bioengineering (Basel, Switzerland) · 2025Article
- Diet and deprivation in pregnancy: a rat model to investigate the effects of the maternal diet on the growth of the dam and its offspring.The British journal of nutrition · 2024Article
- Article
- Obesity promotes lipid accumulation in mouse cartilage-A potential role of acetyl-CoA carboxylase (ACC) mediated chondrocyte de novo lipogenesis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
- Lipogenesis inhibitors: therapeutic opportunities and challenges.Nature reviews. Drug discovery · 2022Review
- Review
- De Novo Lipogenesis as a Source of Second Messengers in Adipocytes.Current diabetes reports · 2019Review
- aP2-Cre Mediated Ablation of GHS-R Attenuates Adiposity and Improves Insulin Sensitivity during Aging.International journal of molecular sciences · 2018Article
- Early Inhibition of Fatty Acid Synthesis Reduces Generation of Memory Precursor Effector T Cells in Chronic Infection.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Adipose tissue: between the extremes.The EMBO journal · 2017Review
- Effects of Low-Dose Developmental Bisphenol A Exposure on Metabolic Parameters and Gene Expression in Male and Female Fischer 344 Rat Offspring.Environmental health perspectives · 2017Article
- Article
- Mitochondrial homeostasis in adipose tissue remodeling.Science signaling · 2017Review
- High-Fat Diet Induces Unexpected Fatal Uterine Infections in Mice with aP2-Cre-mediated Deletion of Estrogen Receptor Alpha.Scientific reports · 2017Article
- Functional characterization of AMP-activated protein kinase signaling in tumorigenesis.Biochimica et biophysica acta · 2016Review
- Role of Exchange Protein Directly Activated by Cyclic AMP Isoform 1 in Energy Homeostasis: Regulation of Leptin Expression and Secretion in White Adipose Tissue.Molecular and cellular biology · 2016Article
- Article
- HMGA1 overexpression in adipose tissue impairs adipogenesis and prevents diet-induced obesity and insulin resistance.Scientific reports · 2015Article
- Regulator of fatty acid metabolism, acetyl coenzyme a carboxylase 1, controls T cell immunity.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
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.
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