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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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38 records · Page 3

Exploring the ARNTL and RORc Genes' Impact on Lipid Accumulation in the Liver via the Circadian Rhythm

The objective of our proposed experiment is to prove the significance of the upregulation of the ARNTL gene and down regulation of the RORc gene in space, highlighting their crucial roles in causing circadian rhythm misalignment during spaceflight, ultimately resulting in liver lipid accumulation. This experiment was created by thoroughly analyzing the genetic data (UseGalaxy) in OSD-245, Transcriptional analysis of liver from mice flown on the RR-6 mission (NASA GeneLab), and making a comparison between the Flight ISS Terminal and the Ground Control ISS Terminal groups. In our study, we intend to establish experimental groups of Mus musculus (lab mice), with 4 of these groups designated for space travel, while the remaining groups will serve as ground control samples on Earth. Both the space and ground conditions are categorized into four groups according to the genetic makeup of the mice. Within each condition, there will be a control group representing the wild type genes, and the experimental groups will involve knockout mice for ARNTL and RORc. We will then compare the lipid accumulation between the ground control mice and FLT mice to understand whether or not spaceflight causes lipid accumulation, due to a misaligned circadian rhythm. The experiment is anticipated to yield two main outcomes. Firstly, the upregulation of ARNTL is expected to rectify the circadian rhythm misalignment in space, consequently heightening lipid accumulation within the liver. Secondly, the downregulation of RORc is predicted to result in a diminished immune response in the liver, thereby facilitating lipid accumulation. Our space research is expected to aid in lipid buildup countermeasures, informing scientists regarding astronaut protection and providing insights into obesity and non-alcoholic fatty liver disease.

GL4HS↗

Leptin regulates bone formation via the sympathetic nervous system

We previously showed that leptin inhibits bone formation by an undefined mechanism. Here, we show that hypothalamic leptin-dependent antiosteogenic and anorexigenic networks differ, and that the peripheral mediators of leptin antiosteogenic function appear to be neuronal. Neuropeptides mediating leptin anorexigenic function do not affect bone formation. Leptin deficiency results in low sympathetic tone, and genetic or pharmacological ablation of adrenergic signaling leads to a leptin-resistant high bone mass. beta-adrenergic receptors on osteoblasts regulate their proliferation, and a beta-adrenergic agonist decreases bone mass in leptin-deficient and wild-type mice while a beta-adrenergic antagonist increases bone mass in wild-type and ovariectomized mice. None of these manipulations affects body weight. This study demonstrates a leptin-dependent neuronal regulation of bone formation with potential therapeutic implications for osteoporosis.

NASA Discipline Regulatory Physiology↗