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      Diet-induced changes in stearoyl-CoA desaturase 1 expression in obesity-prone and -resistant mice.

      Obesity research
      Animals, Body Composition, Body Weight, Calorimetry, Indirect, Dietary Fats, administration & dosage, Eating, Energy Intake, Energy Metabolism, Gene Expression, Genetic Predisposition to Disease, Insulin, blood, Leptin, Liver, enzymology, Male, Mice, Mice, Inbred C57BL, Obesity, genetics, Proteins, RNA, Messenger, analysis, Reverse Transcriptase Polymerase Chain Reaction, Stearoyl-CoA Desaturase

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          Abstract

          To investigate stearoyl-coenzyme A desaturase (SCD) 1 expression in obesity-prone C57BL/6 mice and in obesity-resistant FVB mice to explore the relationship of SCD1 expression and susceptibility to diet-induced obesity. Nine-week-old C57BL/6 and FVB mice were fed either a high- or low-fat diet for 8 weeks. Body weight and body composition were measured before and at weeks 4 and 8 of the study. Energy expenditure was measured at weeks 1 and 5 of the study. Hepatic SCD1 mRNA was measured at 72 hours and at the end of study. Plasma leptin and insulin concentrations were measured at the end of study. When C57BL/6 mice were switched to a calorie-dense high-fat diet, animals gained significantly more body weight than those maintained on a low-calorie density diet primarily due to increased fat mass accretion. Fat mass continued to accrue throughout 8 weeks of study. Increased calorie intake did not account for all weight gain. On the high-fat diet, C57BL/6 mice decreased their energy expenditure when compared with mice fed a low-fat diet. In response to 8 weeks of a high-fat diet, SCD1 gene expression in liver increased >2-fold. In contrast, feeding a high-fat diet did not change body weight, energy expenditure, or SCD1 expression in FVB mice. Our study showed that a high-fat hypercaloric diet increased body adiposity first by producing hyperphagia and then by decreasing energy expenditure of mice susceptible to diet-induced obesity. Consumption of a high-fat diet in species predisposed to obesity selectively increased SCD1 gene expression in liver.

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