Loss of stearoyl–CoA desaturase-1 function protects mice against adiposity

By J. Ntambi, M. Miyazaki, J. Stoehr, H. Lan, Christina Kendziorski, Brian S. Yandell, Yang Song, P. Cohen, J. Friedman, A. Attie. Proceedings of the National Academy of Sciences of the United States of America, 2002

1,112 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/44e54cfe1a0dac3e83cdea0804fb1a061d6ab85e

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Citations in the corpus

Knockouts model the 100 best-selling drugs—will they model the next 100? (2003, background): “and stearoyl-CoA desaturase KO mice also have lean phenotype”
An emerging role of mTOR in lipid biosynthesis (2009, positive): “Interestingly, similar increase in energy expenditure is observed in many animal models deficient for protein playing key roles in lipogenesis [40-42].”
Molecular mediators of hepatic steatosis and liver injury. (2004, positive): “The genetic deletion of SCD-1, an enzyme responsible for the synthesis of monounsaturated fatty acids, protects against the development of fatty livers and insulin resistance in mice (47, 48).”
Non-Alcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases (2017, positive): “SCD1 knockout mice were protected from diet-induced obesity and glucose intolerance (Ntambi et al., 2002).”
Enzymes of triacylglycerol synthesis and their regulation. (2004, background): “When a targeted disruption is made of SCD-1 on the Sv129 background, the knockout mice, like the asebia mice, have reduced body fat, increased sensitivity to insulin and resistance to diet-induced obesity [177].”
The Human Obesity Gene Map: The 2005 Update (2006, background): “1) Rxrg 1q22-q23 RXRG Retinoid X receptor Resistant to diet-induced obesity (545) 19(43) Scd1 10 SCD1 Stearyl-CoA desaturase 1 Reduced BW and adiposity; resistant to diet-induced obesity (508,546)”
Nonshivering thermogenesis and its adequate measurement in metabolic studies (2011, background): “Similarly, the global absence of stearoyl CoA dehydrogenase 1 (SCD1) leads to this type of apparently hypermetabolic phenotype (Ntambi et al., 2002); however, it turns out that if the knock-out of SCD1 is restricted to the skin, exactly the same phenotype is found as in the global knockout (Sampath ”
Energy Metabolism in the Liver (2014, positive): “Global knockout of SCD1, which catalyzes the synthesis of monounsaturated LCFAs, protects against obesity (39, 193).”
SIRT3 Deficiency and Mitochondrial Protein Hyperacetylation Accelerate the Development of the Metabolic Syndrome (2011, positive): “Hepatic steatosis was absent in SCD1KO mice fed a HFD, as previously reported (Ntambi et al., 2002).”
Role of Dietary Fructose and Hepatic de novo Lipogenesis in Fatty Liver Disease (2016, background): “Mice with a global knockout of stearoyl-CoA desaturase are protected from a high-carbohydrate high-fat (HCHF) diet-induced or genetically induced obesity and show decreased lipogenic gene expression coupled with increased b-oxidation [70, 71].”
Regulation of energy metabolism by long-chain fatty acids. (2014, background): “resistance to dietary induced obesity [261,257]and improved insulin sensitivity [257], caution would be required to inhibit skin lipid synthesis for treating human obesity.”
The Inflammasome-Mediated Caspase-1 Activation Controls Adipocyte Differentiation and Insulin Sensitivity (2010, background): “Since SCD-1 / animals have a reduction in adiposity due to enhanced lipid oxidation together with an improvement in insulin sensitivity (Ntambi et al., 2002), regulation of SCD-1 activity by caspase-1 in adipose tissuemay partly explain our observations.”