Trends in Genetics
CommentGenetics of obesity: advances from rodent studies
References (25)
- et al.
Cell
(1992) Cell
(1995)Cell
(1996)Hum. Mol. Genet.
(1995)Genetics
(1995)- et al.
Nature
(1994)Diabetologia
(1978)New Engl. J. Med.
(1996)Science
(1995)
Cell
Cited by (32)
Genetic Analysis of Rodent Obesity and Diabetes
2007, The Mouse in Biomedical ResearchGenetic Analysis of Rodent Obesity and Diabetes
2006, The Mouse in Biomedical Research: History, Wild Mice, and Genetics: Volume 1-4, Second EditionCytosolic NADP<sup>+</sup>-dependent isocitrate dehydrogenase plays a key role in lipid metabolism
2004, Journal of Biological ChemistryCitation Excerpt :This inference is also supported by the 4.4-fold up-regulation of GLUT4 expression in the epididymal fat pads of IDPc-Tg1 mice. These findings suggest that the obesity induced in IDPc-Tg1 mice is different from that observed in other rodent models (33) and may not be associated with diabetes or insulin resistance. The concurrent induction of fatty liver, hyperlipidemia, and obesity by alteration of a single IDPc gene in liver and adipose tissues without an increase in caloric intake or diet composition is unprecedented to the best of our knowledge.
Combinatorial control in ubiquitin-dependent proteolysis: Don't Skp the F-box hypothesis
1998, Trends in GeneticsTheraTRACE®: A mechanism unbiased in vivo platform for phenotypic screening and drug repositioning
2011, Drug Discovery Today: Therapeutic StrategiesCitation Excerpt :Type II diabetes is a heterogeneous disease of disrupted glucose homeostasis that is characterized by elevated blood glucose, insulin receptor insensitivity and degeneration of insulin secreting pancreatic β-cells. Selective inbreeding of animals that spontaneously develop a type II diabetes-like phenotype has generated many of the strains currently used for type II diabetes research [16]. For example, db/db mice exhibit many features of clinical stage type II diabetes including a decrease in insulin receptor sensitivity, steadily increasing blood glucose levels, compensatory elevations in serum insulin followed by a degeneration of insulin secreting pancreatic β-cells.
Chromosomal Q-heterochromatin polymorphism in patients With alimentary obesity
2016, Biology and Medicine