Genetically Modified Mouse Models of Insulin Resistance

2005 ◽  
pp. 133-153 ◽  
Author(s):  
Gema Medina-Gomez ◽  
Christopher Lelliott ◽  
Antonio J. Vidal-Puig
Keyword(s):  
Insulin Resistance ◽  
Mouse Models ◽  
Genetically Modified

Genetically modified mouse models in studies of luteinising hormone action

2006 ◽  
Vol 252 (1-2) ◽  
pp. 126-135 ◽  
Author(s):  
Ilpo Huhtaniemi ◽  
Petteri Ahtiainen ◽  
Tomi Pakarainen ◽  
Susana B. Rulli ◽  
Fu-Ping Zhang ◽  
...  
Keyword(s):  
Mouse Models ◽  
Luteinising Hormone ◽  
Genetically Modified ◽  
Hormone Action

scholarly journals Oxidative stress and diabetes: What can we learn about insulin resistance from antioxidant mutant mouse models?

2012 ◽  
Vol 52 (1) ◽  
pp. 46-58 ◽  
Author(s):  
JennaLynn Styskal ◽  
Holly Van Remmen ◽  
Arlan Richardson ◽  
Adam B. Salmon
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Mouse Models ◽  
Mutant Mouse

Hepatic miRNA expression profiling in genetically modified mouse models of different atherosclerosis susceptibility

2016 ◽  
Vol 252 ◽  
pp. e206-e207
Author(s):  
S. Manzini ◽  
M. Busnelli ◽  
M. Chiara ◽  
C. Parolini ◽  
F. Dellera ◽  
...  
Keyword(s):  
Mouse Models ◽  
Mirna Expression ◽  
Expression Profiling ◽  
Genetically Modified ◽  
Mirna Expression Profiling

scholarly journals Apoptosis of hematopoietic progenitor-derived adipose tissue–resident macrophages contributes to insulin resistance after myocardial infarction

2020 ◽  
Vol 12 (553) ◽  
pp. eaaw0638 ◽  
Author(s):  
Sathish Babu Vasamsetti ◽  
Emilie Coppin ◽  
Xinyi Zhang ◽  
Jonathan Florentin ◽  
Sasha Koul ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Mouse Models ◽  
De Novo ◽  
Hematopoietic Progenitor ◽  
Resident Macrophage ◽  
Systemic Insulin Resistance ◽  
Macrophage Apoptosis ◽  
St Elevation

Patients with insulin resistance have high risk of cardiovascular disease such as myocardial infarction (MI). However, it is not known whether MI can initiate or aggravate insulin resistance. We observed that patients with ST-elevation MI and mice with MI had de novo hyperglycemia and features of insulin resistance, respectively. In mouse models of both myocardial and skeletal muscle injury, we observed that the number of visceral adipose tissue (VAT)–resident macrophages decreased because of apoptosis after these distant organ injuries. Patients displayed a similar decrease in VAT-resident macrophage numbers and developed systemic insulin resistance after ST-elevation MI. Loss of VAT-resident macrophages after MI injury led to systemic insulin resistance in non-diabetic mice. Danger signaling–associated protein high mobility group box 1 was released by the dead myocardium after MI in rodents and triggered macrophage apoptosis via Toll-like receptor 4. The VAT-resident macrophage population in the steady state in mice was transcriptomically distinct from macrophages in the brain, skin, kidney, bone marrow, lungs, and liver and was derived from hematopoietic progenitor cells just after birth. Mechanistically, VAT-resident macrophage apoptosis and de novo insulin resistance in mouse models of MI were linked to diminished concentrations of macrophage colony-stimulating factor and adiponectin. Collectively, these findings demonstrate a previously unappreciated role of adipose tissue–resident macrophages in sensing remote organ injury and promoting MI pathogenesis.

Genetically modified mouse models in cancer studies

2008 ◽  
Vol 10 (12) ◽  
pp. 794-803 ◽  
Author(s):  
Javier Santos ◽  
Pablo Fernández-Navarro ◽  
María Villa-Morales ◽  
Laura González-Sánchez ◽  
José Fernández-Piqueras
Keyword(s):  
Mouse Models ◽  
Genetically Modified ◽  
Cancer Studies
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