scholarly journals Uncoupling protein-2 regulates lifespan in mice

2009 ◽  
Vol 296 (4) ◽  
pp. E621-E627 ◽  
Author(s):  
Zane B. Andrews ◽  
Tamas L. Horvath
Keyword(s):  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Oxygen Species ◽  
Wild Type ◽  
Long Term Effects ◽  
Mitochondrial Uncoupling ◽  
And Oxidative Stress ◽  
Superoxide Dismutase 2 ◽  
Different Tissues

The long-term effects of uncoupled mitochondrial respiration by uncoupling protein-2 (UCP2) in mammalian physiology remain controversial. Here we show that increased mitochondrial uncoupling activity of different tissues predicts longer lifespan of rats compared with mice. UCP2 reduces reactive oxygen species (ROS) production and oxidative stress throughout the aging process in different tissues in mice. The absence of UCP2 shortens lifespan in wild-type mice, and the level of UCP2 positively correlates with the postnatal survival of superoxide dismutase-2 mutant animals. Thus UCP2 has a beneficial influence on cell and tissue function leading to increased lifespan.

scholarly journals The Warburg Effect in Leukemia-Stroma Cocultures Is Mediated by Mitochondrial Uncoupling Associated with Uncoupling Protein 2 Activation

2008 ◽  
Vol 68 (13) ◽  
pp. 5198-5205 ◽  
Author(s):  
Ismael Samudio ◽  
Michael Fiegl ◽  
Teresa McQueen ◽  
Karen Clise-Dwyer ◽  
Michael Andreeff
Keyword(s):  
Warburg Effect ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Mitochondrial Uncoupling ◽  
The Warburg Effect

scholarly journals Mitochondrial Uncoupling protein‐2 regulates NLRP3 inflammasome

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Rajan babu Venugopal ◽  
Ruan Rollin Cox ◽  
prasanna Tamarappu Parthasarathy ◽  
Richard F Lockey ◽  
Narasaiah Kolliputi
Keyword(s):  
Nlrp3 Inflammasome ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein

Dissociation of obesity and insulin resistance in transgenic mice with skeletal muscle expression of uncoupling protein 1

2008 ◽  
Vol 32 (3) ◽  
pp. 352-359 ◽  
Author(s):  
Yvonne Katterle ◽  
Susanne Keipert ◽  
Jana Hof ◽  
Susanne Klaus
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Uncoupling Protein ◽  
Wild Type ◽  
Uncoupling Protein 1 ◽  
Mitochondrial Uncoupling ◽  
High Fat Diets ◽  
Fat Diets ◽  
White Fat

We evaluated the effect of skeletal muscle mitochondrial uncoupling on energy and glucose metabolism under different diets. For 3 mo, transgenic HSA-mUCP1 mice with ectopic expression of uncoupling protein 1 in skeletal muscle and wild-type littermates were fed semisynthetic diets with varying macronutrient ratios (energy % carbohydrate-protein-fat): HCLF (41:42:17), HCHF (41:16:43); LCHF (11:45:44). Body composition, energy metabolism, and insulin resistance were assessed by NMR, indirect calorimetry, and insulin tolerance test, respectively. Gene expression in different organs was determined by real-time PCR. In wild type, both high-fat diets led to an increase in body weight and fat. HSA-mUCP1 mice considerably increased body fat on HCHF but stayed lean on the other diets. Irrespective of differences in body fat content, HSA-mUCP1 mice showed higher insulin sensitivity and decreased plasma insulin and liver triglycerides. Respiratory quotient and gene expression indicated overall increased carbohydrate oxidation of HSA-mUCP1 but a preferential channeling of fatty acids into muscle rather than liver with high-fat diets. Evidence for increased lipogenesis in white fat of HSA-mUCP1 mice suggests increased energy dissipating substrate cycling. Retinol binding protein 4 expression in white fat was increased in HSA-mUCP1 mice despite increased insulin sensitivity, excluding a causal role in the development of insulin resistance. We conclude that skeletal muscle mitochondrial uncoupling does not protect from the development of obesity in all circumstances. Rather it can lead to a “healthy” obese phenotype by preserving insulin sensitivity and a high metabolic flexibility, thus protecting from the development of obesity associated disturbances of glucose homeostasis.

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