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Loss of stearoyl–CoA desaturase-1 function protects mice against adiposity
It is shown that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain, suggesting that a consequence ofSCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage.
Stearoyl-Coenzyme A Desaturase 1 Deficiency Protects against Hypertriglyceridemia and Increases Plasma High-Density Lipoprotein Cholesterol Induced by Liver X Receptor Activation
It is suggested that SCD1 plays a pivotal role in the regulation of hepatic and plasma triglyceride accumulation, possibly by modulating the MUFA-to-SFA ratio.
Role for Stearoyl-CoA Desaturase-1 in Leptin-Mediated Weight Loss
Ob/ob mice with mutations in SCD-1 were significantly less obese than ob/ob controls and had markedly increased energy expenditure, suggesting that down-regulation of SCD1 is an important component of leptin's metabolic actions.
Stearoyl-CoA desaturase 1 deficiency increases fatty acid oxidation by activating AMP-activated protein kinase in liver.
The phosphorylation and activity of AMP-activated protein kinase (AMPK), a metabolic sensor that regulates lipid metabolism during increased energy expenditure is significantly increased and identified as a mediator of increased fatty acid oxidation in liver of SCD1-deficient mice.
A lipogenic diet in mice with a disruption of the stearoyl-CoA desaturase 1 gene reveals a stringent requirement of endogenous monounsaturated fatty acids for triglyceride synthesis.
Observations demonstrate that induction of triglyceride synthesis is highly dependent on SCD1 gene expression.
Role of stearoyl-coenzyme A desaturase in lipid metabolism.
Relationship between stearoyl-CoA desaturase activity and plasma triglycerides in human and mouse hypertriglyceridemia Published, JLR Papers in Press, August 16, 2002. DOI 10.1194/jlr.M200189-JLR200
It is proposed that many of the factors that influence plasma triglyceride levels do so by converging upon the regulation of SCD activity and the desaturation index explains 44% of the variance in triglycerides.
Stearoyl-CoA Desaturase 1 Gene Expression Is Necessary for Fructose-mediated Induction of Lipogenic Gene Expression by Sterol Regulatory Element-binding Protein-1c-dependent and -independent
It is demonstrated that oleate produced by SCD is necessary for fructose-mediated induction of lipogenic gene expression through SREBP-1c-dependent and -independent mechanisms and suggested that SCD1 gene expression is important in lipid and carbohydrate homeostasis.
Effects of diet and genetic background on sterol regulatory element-binding protein-1c, stearoyl-CoA desaturase 1, and the development of the metabolic syndrome.
Dietary fat and genetic background act through SREBP-1c and SCD1 to affect hepatic lipid metabolism contributing to the development of the metabolic syndrome.