Mitochondrial function is enhanced by thyroid hormones during zebra finch development.

An organism's response to its environment is largely determined by changes in the energy supplied by aerobic mitochondrial metabolism via adenosine triphosphate (ATP) production. ATP is especially important under energy-demanding conditions, such as during rapid growth. It is currently poorly understood how environmental factors influence energy metabolism and mitochondrial functioning, but recent studies suggest the role of thyroid hormones (TH). TH are key regulators of growth and metabolism and can be flexibly adjusted to environmental conditions, such as environmental temperature or food availability. To test whether TH enhancement is causally linked to mitochondrial function and growth, we provided TH orally at physiological concentrations during the main growth phase in zebra finch (Taeniopygia guttata) nestlings reared in a challenging environment. TH treatment accelerated maximal mitochondrial working capacity-a trait that reflects mitochondrial ATP production, without affecting growth. To our knowledge, this is the first study to characterize the regulation of mitochondria by TH during development in a semi-naturalistic context and to address implications for fitness-related traits, such as growth.

Dietary nucleotides can prevent glucocorticoid-induced telomere attrition in a fast-growing wild vertebrate.

Telomeres are chromosome protectors that shorten during eukaryotic cell replication and in stressful conditions. Developing individuals are susceptible to telomere erosion when their growth is fast and resources are limited. This is critical because the rate of telomere attrition in early life is linked to health and life span of adults. The metabolic telomere attrition hypothesis (MeTA) suggests that telomere dynamics can respond to biochemical signals conveying information about the organism's energetic state. Among these signals are glucocorticoids, hormones that promote catabolic processes, potentially impairing costly telomere maintenance, and nucleotides, which activate anabolic pathways through the cellular enzyme target of rapamycin (TOR), thus preventing telomere attrition. During the energetically demanding growth phase, the regulation of telomeres in response to two contrasting signals - one promoting telomere maintenance and the other attrition - provides an ideal experimental setting to test the MeTA. We studied nestlings of a rapidly developing free-living passerine, the great tit (Parus major), that either received glucocorticoids (Cort-chicks), nucleotides (Nuc-chicks) or a combination of both (NucCort-chicks), comparing these with controls (Cnt-chicks). As expected, Cort-chicks showed telomere attrition, while NucCort- and Nuc-chicks did not. NucCort-chicks was the only group showing increased expression of a proxy for TOR activation (the gene TELO2), of mitochondrial enzymes linked to ATP production (cytochrome oxidase and ATP-synthase) and a higher efficiency in aerobically producing ATP. NucCort-chicks had also a higher expression of telomere maintenance genes (shelterin protein TERF2 and telomerase TERT) and of enzymatic antioxidant genes (glutathione peroxidase and superoxide dismutase). The findings show that nucleotide availability is crucial for preventing telomere erosion during fast growth in stressful environments.