The past, present, and future of National Aeronautics and Space Administration spaceflight diet in support of microgravity rodent experiments

Sun, Gwo-Shing; Tou, Janet C.; Yu, Diane Sau Mun; Girten, B.; Cohen, Jacob

doi:10.1016/j.nut.2013.04.005

Cited by 23 publications

(15 citation statements)

References 17 publications

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“…This component had a negligible effect on the CH band; it did not affect the 3010 cm -1 peak (= C-H) and the unsaturation ratio (I3010/I2850) did not change between AEM and FLT mice. A strong candidate for this chemical component is the highly conjugated dietary fatty acid retinol (Vitamin A), present in the NASA foodbar given to both groups [ 12 , 13 , 38 ]. Retinol is almost exclusively stored in HSC lipid droplets and is released when HSCs are initially activated [ 39 – 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…The NASA NuRFB powdered diet is custom ordered from Harlan Teklad (TD 04197) and is comprised of 47% carbohydrate, 17.9% protein, 3.9% lipids, 2.8% fiber, and 28% water. Long and short-term ground studies show no difference in physiological response between mice fed the NuRFB vs. the AIN-93G Growth Purified Diet recommended by the American Institute of Nutrition (18.7% protein, 16.4% fat, 65.1% carbohydrates, 3.89 kcal/g) [ 12 , 13 ]. AEM control mice were placed into the same housing used in flight and environmental parameters were matched as closely as possible based on 48-hour delayed telemetry data.…”

Section: Methodsmentioning

confidence: 99%

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Spaceflight Activates Lipotoxic Pathways in Mouse Liver

et al. 2016

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Spaceflight affects numerous organ systems in the body, leading to metabolic dysfunction that may have long-term consequences. Microgravity-induced alterations in liver metabolism, particularly with respect to lipids, remain largely unexplored. Here we utilize a novel systems biology approach, combining metabolomics and transcriptomics with advanced Raman microscopy, to investigate altered hepatic lipid metabolism in mice following short duration spaceflight. Mice flown aboard Space Transportation System -135, the last Shuttle mission, lose weight but redistribute lipids, particularly to the liver. Intriguingly, spaceflight mice lose retinol from lipid droplets. Both mRNA and metabolite changes suggest the retinol loss is linked to activation of PPARα-mediated pathways and potentially to hepatic stellate cell activation, both of which may be coincident with increased bile acids and early signs of liver injury. Although the 13-day flight duration is too short for frank fibrosis to develop, the retinol loss plus changes in markers of extracellular matrix remodeling raise the concern that longer duration exposure to the space environment may result in progressive liver damage, increasing the risk for nonalcoholic fatty liver disease.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Spaceflight Activates Lipotoxic Pathways in Mouse Liver

et al. 2016

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“…Moreover, samples were collected from seven C57BL/6 female mice, 9 wk of age, flown on space shuttle Atlantis (STS‐135) for 13 d, along with four ground (control) mice housed in AEMs for the same length of time. All mice were provided with food (NASA rodent food bars) and water ad libitum.…”

Section: Methodsmentioning

confidence: 99%

Response of the mouse sublingual gland to spaceflight

Dagdeviren

Beallias

Khan

et al. 2018

European J Oral Sciences

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The ultrastructure and immunohistochemistry of secretory proteins of sublingual glands were studied in mice flown on the US space shuttles Discovery [Space Transportation System (STS)-131] and Atlantis (STS-135). No differences in mucous acinar or serous demilune cell structure were observed between sublingual glands of ground (control) and flight mice. In contrast, previous studies showed autophagy and apoptosis of parotid serous acinar cells in flight mice. The expression of parotid secretory protein (PSP) in sublingual demilune cells of STS-131 flight mice was significantly increased compared with ground (control) mice but decreased in STS-135 flight mice. Similarly, expression of mucin (MUC-19) in acinar cells and expression of the type II regulatory subunit of protein kinase A (PKA-RII) in demilune cells were increased in STS-131 flight mice and decreased in STS-135 flight mice, but not significantly. Demilune cell and parotid protein (DCPP) was slightly decreased in mice from both flights, and nuclear PKA-RII was slightly increased. These results indicate that the response of salivary glands to spaceflight conditions varies among the different glands, cell types, and secretory proteins. Additionally, the spaceflight environment, including the effects of microgravity, modifies protein expression. Determining changes in salivary proteins may lead to development of non-invasive methods to assess the physiological status of astronauts.

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“…Mice were assessed for specific pathogen free (SPF) compliance prior to shipment from Taconic, within a week of arrival at NASA KSC and at 10 days before launch (L-10 days). After arrival at KSC, mice were adapted to spaceflight cage conditions including wire-mesh floors, spring operated Lixit drinking mechanism and NASA-provided nutrient food bar diet [28]. At 1 week prior to launch mice were caged at double density of n = 10 mice/cage to adjust to launch housing conditions.…”

Section: Mice and Live Phase Operationsmentioning

confidence: 99%

Inhibition of myostatin prevents microgravity-induced loss of skeletal muscle mass and strength

et al. 2020

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The microgravity conditions of prolonged spaceflight are known to result in skeletal muscle atrophy that leads to diminished functional performance. To assess if inhibition of the growth factor myostatin has potential to reverse these effects, mice were treated with a myostatin antibody while housed on the International Space Station. Grip strength of ground control mice increased 3.1% compared to baseline values over the 6 weeks of the study, whereas grip strength measured for the first time in space showed flight animals to be-7.8% decreased in strength compared to baseline values. Control mice in space exhibited, compared to ground-based controls, a smaller increase in DEXA-measured muscle mass (+3.9% vs +5.6% respectively) although the difference was not significant. All individual flight limb muscles analyzed (except for the EDL) weighed significantly less than their ground counterparts at the study end (range-4.4% to-28.4%). Treatment with myostatin antibody YN41 was able to prevent many of these space-induced muscle changes. YN41 was able to block the reduction in muscle grip strength caused by spaceflight and was able to significantly increase the weight of all muscles of flight mice (apart from the EDL). Muscles of YN41-treated flight mice weighed as much as muscles from Ground IgG mice, with the exception of the soleus, demonstrating the ability to prevent spaceflight-induced atrophy. Muscle gene expression analysis demonstrated significant effects of microgravity and myostatin inhibition on many genes. Gamt and Actc1 gene expression was modulated by microgravity and YN41 in opposing directions. Myostatin inhibition did not overcome the significant reduction of microgravity on femoral BMD nor did it increase femoral or vertebral BMD in ground control mice. In summary, myostatin inhibition may be an effective countermeasure to detrimental consequences of skeletal muscle under microgravity conditions.

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The past, present, and future of National Aeronautics and Space Administration spaceflight diet in support of microgravity rodent experiments

Cited by 23 publications

References 17 publications

Spaceflight Activates Lipotoxic Pathways in Mouse Liver

Spaceflight Activates Lipotoxic Pathways in Mouse Liver

Response of the mouse sublingual gland to spaceflight

Inhibition of myostatin prevents microgravity-induced loss of skeletal muscle mass and strength

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