ArticlePloS one2009
Altered energy homeostasis and resistance to diet-induced obesity in KRAP-deficient mice.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Gene-based meta-analysis of genome-wide association studies implicates new loci involved in obesity.Human molecular genetics · 2015Pooled it
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- KRAP tethers IPNature communications · 2021Article
- Zfat expression in ZsGreen reporter gene knock‑in mice: Implications for a novel function of Zfat in definitive erythropoiesis.International journal of molecular medicine · 2018Article
- Placental Ras Regulates Inflammation Associated with Maternal Obesity.Mediators of inflammation · 2018Article
- Lineage-specific regulation of imprinted X inactivation in extraembryonic endoderm stem cells.Epigenetics & chromatin · 2014Article
- Identification of KRAP-expressing cells and the functional relevance of KRAP to the subcellular localization of IP3R in the stomach and kidney.International journal of molecular medicine · 2012Article
- Tespa1 is a novel inositol 1,4,5-trisphosphate receptor binding protein in T and B lymphocytes.FEBS open bio · 2012Article
- Mice with a targeted deletion of the type 2 deiodinase are insulin resistant and susceptible to diet induced obesity.PloS one · 2011Article
- Three-dimensionally specific inhibition of DNA repair-related genes by activated KRAS in colon crypt model.Neoplasia (New York, N.Y.) · 2010Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity and related metabolic disorders have become leading causes of adult morbidity and mortality. KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule, however, its physiological roles remain unknown. Here we demonstrate that KRAP-deficient (KRAP(-/-)) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP(-/-) mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Notably, glucose uptake in the brown adipose tissue (BAT) in KRAP(-/-) mice is enhanced in an insulin-independent manner, suggesting that BAT is involved in altered energy homeostasis in KRAP(-/-) mice, although UCP (Uncoupling protein) expressions are not altered. Of interest is the down-regulation of fatty acid metabolism-related molecules, including acetyl-CoA carboxylase (ACC)-1, ACC-2 and fatty acid synthase in the liver of KRAP(-/-) mice, which could in part account for the metabolic phenotype in KRAP(-/-) mice. Thus, KRAP is a novel regulator in whole-body energy homeostasis and may be a therapeutic target in obesity and related diseases.
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