The mechanism of the increase in mitochondrial proton permeability induced by thyroid hormones

115

SummaryMitochondrial biogenesis is induced in response to cold temperature in many organisms. The effect is particularly pronounced in ectotherms such as fishes, where acclimation to cold temperature increases mitochondrial density. Some polar fishes also have exceptionally high densities of mitochondria. The net effect of increasing mitochondrial density is threefold. First, it increases the concentration of aerobic metabolic enzymes per gram of tissue, maintaining ATP production. Second, it elevates the density of mitochondrial membrane phospholipids, enhancing rates of intracellular oxygen diffusion. Third, it reduces the diffusion distance for oxygen and metabolites between capillaries and mitochondria. Although cold-induced mitochondrial biogenesis has been well documented in fishes, little is known about the molecular pathway governing it. In mammals, the co-transcriptional activator peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1) is thought to coordinate the three components of mitochondrial biogenesis: the synthesis of mitochondrial proteins, the synthesis of phospholipids and the replication of mitochondrial DNA. Some components of the mitochondrial biogenic pathway are conserved between fishes and mammals, yet the pathway appears more versatile in fishes. In some tissues of cold-acclimated fishes, the synthesis of mitochondrial proteins increases in the absence of an increase in phospholipids, whereas in some polar fishes, densities of mitochondrial phospholipids increase in the absence of an increase in proteins. The ability of cold-bodied fishes to fine-tune the mitochondrial biogenic pathway may allow them to modify mitochondrial characteristics to meet the specific needs of the cell, whether it is to increase ATP production or enhance oxygen diffusion.

Section: Signaling Molecules That Might Stimulate Changes In Mitochonmentioning

confidence: 99%

Mitochondrial biogenesis in cold-bodied fishes

O’Brien

2011

115

“…Second, thyroxine affects mitochondrial membrane composition (Hulbert, 2000). Thyroxine may affect the amount of inner mitochondrial membrane (Brand et al, 1992), thus resulting in more mitochondrial stain binding. In this scenario, the increase in fluorescence intensity would be due to an increase in inner mitochondria membrane surface area, rather than in mitochondrial content.…”

Section: Physiological Mechanisms Underlying Among-individual Variatimentioning

confidence: 99%

Physiological and morphological correlates of among-individual variation in standard metabolic rate in the leopard frog Rana pipiens

Steyermark

Miamen

Feghahati

et al. 2005

SUMMARY Rates of standard metabolism (SMR) are highly variable among individuals within vertebrate populations. Because SMR contributes a substantial proportion of an individual's energy budget, among-individual variation in this trait may affect other energetic processes, and potentially fitness. Here, we examine three potential proximate correlates of variation in SMR:organ mass, serum T4 thyroxine and relative mitochondrial content, using flow cytometry. Body-mass-adjusted kidney mass correlated with SMR, but liver,heart, small intestine and gastrocnemius did not. Thyroxine correlated with SMR, as did mitochondrial content. These results suggest several novel proximate physiological and morphological mechanisms that may contribute to among-individual variation in SMR. Variation in SMR may be maintained by diverse environmental conditions. Some conditions, such as low resource availability, may favor individuals with a low SMR, through small organ size,or low thyroxine or mitochondrial content. Other conditions, such as high resource availability, may favor individuals with a high SMR, through large organ size, or high thyroxine or mitochondrial content.

“…For example, hypothyroid rats have liver mitochondrial membranes containing more unsaturated phospholipid fatty acyl components (Pehowich, 1999) and are inherently less permeable to protons (Brand et al, 1992;Brand et al, 2003). Another goal of this study, therefore, was to examine the effects of dietary PUFA on mitochondrial proton leak in hibernation and to determine how this might relate to the whole-animal effects of PUFA on hibernation performance.…”

Section: Introductionmentioning

confidence: 99%

Effects of dietary polyunsaturated fatty acids on mitochondrial metabolism in mammalian hibernation

Gerson

Brown

Thomas

et al. 2008

SUMMARYThirteen-lined ground squirrels (Spermophilus tridecemlineatus) were fed one of four isocaloric, isolipemic diets containing 16, 22, 35 or 55 mg linoleic acid (18:2n-6) per gram. Mitochondrial properties were compared between hibernating and summer active states, and between diet groups. As in other studies, state 3 respiration was significantly reduced in hibernation, but only in animals fed the 22 mg g -1 18:2 diet. In the other diet groups, there was no difference in state 3 respiration between the hibernating and summer active groups. In the 22 mg g -1 18:2 diet group, there was no difference in mitochondrial proton conductance between hibernating and summer active animals, again in agreement with earlier studies. However, for all other diet groups, mitochondrial proton conductance was significantly reduced during hibernation. Mitochondrial phospholipid fatty acids changed significantly with hibernation, including increases in unsaturation indices and n-6/n-3, but no differences were found among diet groups. Mitochondrial proton conductance in hibernation showed a positive correlation with the content of linoleic acid (18:2) and arachidonic acid (20:4) in mitochondrial phospholipids. Lipid peroxidation was higher in mitochondria from hibernating animals, probably due to higher unsaturation, but there was no effect of dietary 18:2 on this pattern. Despite the dietary effects on mitochondrial metabolism, all animals hibernated with no differences in bout durations, body temperatures or whole-animal metabolic rates among the diet groups. The reduced mitochondrial proton leak in the 15, 35 and 55 mg g -1 18:2 diet groups might compensate for the inability to suppress respiration, permitting whole-animal energy savings over the hibernation season.