Research Topics
Genomes and Genes | Katrine AlmindSummaryAffiliation: Harvard University Country: USA Publications
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Publications
[Genetic defects in insulin signalling proteins. Implications for the pathogenesis of type 2 diabetes]Katrine Almind
Research Division, Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
Ugeskr Laeger 164:1021-6. 2002....
Identification of interactive loci linked to insulin and leptin in mice with genetic insulin resistanceKatrine Almind
Research Division, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
Diabetes 52:1535-43. 2003....
Impact of genetic background on development of hyperinsulinemia and diabetes in insulin receptor/insulin receptor substrate-1 double heterozygous miceRohit N Kulkarni
Research Division, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
Diabetes 52:1528-34. 2003....
Genetic determinants of energy expenditure and insulin resistance in diet-induced obesity in miceKatrine Almind
Research Division, Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
Diabetes 53:3274-85. 2004..e., the "thrifty gene," is a dominant-acting genetic determinant of diet-induced obesity in mice and can be linked to a locus on chromosome 14, including genes linked to adipose development and insulin sensitivity...
Effects of diet and genetic background on sterol regulatory element-binding protein-1c, stearoyl-CoA desaturase 1, and the development of the metabolic syndromeSudha B Biddinger
Research Division, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
Diabetes 54:1314-23. 2005..Thus, dietary fat and genetic background act through SREBP-1c and SCD1 to affect hepatic lipid metabolism contributing to the development of the metabolic syndrome...
Ectopic brown adipose tissue in muscle provides a mechanism for differences in risk of metabolic syndrome in miceKatrine Almind
Research Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA
Proc Natl Acad Sci U S A 104:2366-71. 2007..Thus, ectopic deposits of brown adipose tissue in intermuscular depots with regulatable expression of UCP1 provide a genetically based mechanism of protection from weight gain and metabolic syndrome between strains of mice...
A systems biology approach identifies inflammatory abnormalities between mouse strains prior to development of metabolic diseaseMarcelo A Mori
Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, USA
Diabetes 59:2960-71. 2010..Our goal was to identify early molecular signatures predicting genetic risk to these metabolic diseases using two strains of mice that differ greatly in disease susceptibility...
Characterization of the Met326Ile variant of phosphatidylinositol 3-kinase p85alphaKatrine Almind
Research Division, Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
Proc Natl Acad Sci U S A 99:2124-8. 2002..Thus, the Met-326Ile variant of p85alpha is functional for intracellular signaling and adipocyte differentiation but has small alterations in protein expression and activity that could play a role in modifying insulin action...
Mitochondrial proton leak in obesity-resistant and obesity-prone miceBrian D Fink
University of Iowa, Iowa City Veterans Affairs Medical Center, Iowa City, IA 52242, USA
Am J Physiol Regul Integr Comp Physiol 293:R1773-80. 2007..But, this is only achieved only at a higher body mass and, therefore, may be adaptive rather than preventative. Neither obesity-prone nor resistant mice respond to HF feeding by expressing more UCP1 in ectopic BAT within muscle tissue...
