Antioxidant Enzymes, Free-Radical Damage, and Response to Paraquat in Liver and Kidney of Long-Living Growth Hormone Receptor/Binding Protein Gene-Disrupted Mice

2002 ◽  
Vol 34 (9) ◽  
pp. 481-486 ◽  
Author(s):  
S. J. Hauck ◽  
J. M. Aaron ◽  
C. Wright ◽  
J. J. Kopchick ◽  
A. Bartke
Keyword(s):  
Growth Hormone ◽  
Antioxidant Enzymes ◽  
Free Radical ◽  
Growth Hormone Receptor ◽  
Protein Gene ◽  
Free Radical Damage ◽  
Liver And Kidney ◽  
Binding Protein Gene ◽  
Radical Damage ◽  
Receptor Binding Protein

scholarly journals Protection against Diabetes-Induced Nephropathy in Growth Hormone Receptor/Binding Protein Gene-Disrupted Mice1

Endocrinology ◽  
2000 ◽  
Vol 141 (1) ◽  
pp. 163-168 ◽  
Author(s):  
Linda L. Bellush ◽  
Sophie Doublier ◽  
Amy N. Holland ◽  
Liliane J. Striker ◽  
Gary E. Striker ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Receptor Binding ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Protein Gene ◽  
Binding Protein ◽  
Binding Protein Gene ◽  
Receptor Binding Protein

scholarly journals Interaction of growth hormone receptor/binding protein gene disruption and caloric restriction for insulin sensitivity and attenuated aging

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 256 ◽  
Author(s):  
Oge Arum ◽  
Jamal Saleh ◽  
Ravneet Boparai ◽  
Jeremy Turner ◽  
John Kopchick ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Caloric Restriction ◽  
Gene Disruption ◽  
Growth Hormone Receptor ◽  
Protein Gene ◽  
Binding Protein Gene ◽  
Ad Libitum ◽  
Insulin Responsiveness ◽  
Glycemic Regulation ◽  
Receptor Binding Protein

The correlation of physiological sensitivity to insulin (vis-à-vis glycemic regulation) and longevity is extensively established, creating a justifiable gerontological interest on whether insulin sensitivity is causative, or even predictive, of some or all phenotypes of slowed senescence (including longevity). The growth hormone receptor/ binding protein gene-disrupted (GHR-KO) mouse is the most extensively investigated insulin-sensitive, attenuated aging model. It was reported that, in a manner divergent from similar mutants, GHR-KO mice fail to respond to caloric restriction (CR) by altering their insulin sensitivity. We hypothesized that maximized insulin responsiveness is what causes GHR-KO mice to exhibit a suppressed survivorship response to dietary (including caloric) restriction; and attempted to refute this hypothesis by assessing the effects of CR on GHR-KO mice for varied slow-aging-associated phenotypes. In contrast to previous reports, we found GHR-KO mice on CR to be less responsive than their ad libitum (A.L.) counterparts to the hypoglycemia-inducing effects of insulin. Further, CR had negligible effects on the metabolism or cognition of GHR-KO mice. Therefore, our data suggest that the effects of CR on the insulin sensitivity of GHR-KO mice do not concur with the effects of CR on the aging of GHR-KO mice.

scholarly journals Interaction of growth hormone receptor/binding protein gene disruption and caloric restriction for insulin sensitivity and attenuated aging

F1000Research ◽  
2015 ◽  
Vol 3 ◽  
pp. 256
Author(s):  
Oge Arum ◽  
Jamal Saleh ◽  
Ravneet Boparai ◽  
Jeremy Turner ◽  
John Kopchick ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Caloric Restriction ◽  
Gene Disruption ◽  
Growth Hormone Receptor ◽  
Protein Gene ◽  
Binding Protein Gene ◽  
Ad Libitum ◽  
Insulin Responsiveness ◽  
Glycemic Regulation ◽  
Receptor Binding Protein

The correlation of physiological sensitivity to insulin (vis-à-vis glycemic regulation) and longevity is extensively established, creating a justifiable gerontological interest on whether insulin sensitivity is causative, or even predictive, of some or all phenotypes of slowed senescence (including longevity). The growth hormone receptor/ binding protein gene-disrupted (GHR-KO) mouse is the most extensively investigated insulin-sensitive, attenuated aging model. It was reported that, in a manner divergent from similar mutants, GHR-KO mice fail to respond to caloric restriction (CR) by altering their insulin sensitivity. We hypothesized that maximized insulin responsiveness is what causes GHR-KO mice to exhibit a suppressed survivorship response to dietary (including caloric) restriction; and attempted to refute this hypothesis by assessing the effects of CR on GHR-KO mice for varied slow-aging-associated phenotypes. In contrast to previous reports, we found GHR-KO mice on CR to be less responsive than their ad libitum (A.L.) counterparts to the hypoglycemia-inducing effects of insulin. Further, CR had negligible effects on the metabolism or cognition of GHR-KO mice. Therefore, our data suggest that the effects of CR on the insulin sensitivity of GHR-KO mice do not concur with the effects of CR on the aging of GHR-KO mice.

Sign in / Sign up

Export Citation Format

Share Document