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Mice without the Regulator Gene Rsc1A1 Exhibit Increased Na+-D-Glucose Cotransport in Small Intestine and Develop Obesity.
- Source :
- Molecular & Cellular Biology; Jan2005, Vol. 25 Issue 1, p78-87, 10p, 6 Color Photographs, 1 Diagram, 1 Chart, 18 Graphs
- Publication Year :
- 2005
-
Abstract
- The product of the intronless single copy gene RSC1A1, named RS1, is an intracellular 617-amino-acid protein that is involved in the regulation of the Na<superscript>+</superscript>-D-glucose cotransporter SGLT1. We generated and characterized RS1 knockout (RS1<superscript>-/-</superscript>) mice. In the small intestines of RS1<superscript>-/-</superscript> mice, the SGLT1 protein was up-regulated sevenfold compared to that of wild-type mice but was not changed in the kidneys. The upregulation of SGLT1 was posttranscriptional. Small intestinal D-glucose uptake measured in jointly perfused small bowel and liver was increased twofold compared to that of the wild-type, with increased peak concentrations of D-glucose in the portal vein. At birth, the weights of RS1<superscript>-/-</superscript> and wild-type mice were similar. At the age of 3 months, male RS1<superscript>-/-</superscript> mice had 5% higher weights and 15% higher food intakes, whereas their energy expenditures and serum leptin concentrations were similar to those of wild-type mice. At the age of 5 months, male and female RS1<superscript>-/-</superscript> mice were obese, with 30% increased body weight, 80% increased total fat, and 30% increased serum cholesterol. At this age, serum leptin was increased, whereas food intake was the same as for wild-type mice. The data suggest that the removal of RS1 leads to leptin-independent up-regulation of food intake, which causes obesity. [ABSTRACT FROM AUTHOR]
- Subjects :
- GENES
AMINO acids
PROTEINS
SODIUM ions
SMALL intestine
GLUCOSE
LABORATORY mice
Subjects
Details
- Language :
- English
- ISSN :
- 02707306
- Volume :
- 25
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Molecular & Cellular Biology
- Publication Type :
- Academic Journal
- Accession number :
- 15728349
- Full Text :
- https://doi.org/10.1128/MCB.25.1.78-87.2005