Ionising radiation triggers fat accumulation in white adipose tissue

Jo, Sung-Kee; Seol, Min-A; Park, Hae‐Ran; Jung, Uhee; Roh, Changhyun

doi:10.3109/09553002.2010.537429

Cited by 13 publications

(16 citation statements)

References 21 publications

(23 reference statements)

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“…We also observed a large increase in the levels of TGs and ChoE, which has been reported in previous studies with 6 Gy of external irradiation in rats 20 and 5 Gy of whole-body external irradiation in mice 21 . Although the levels of these lipids reverted back to normal after one radiation exposure, in our current study the 90 Sr exposure-induced increases persisted until the end of the experiment, day 30 at 5.2±0.73 Gy.…”

Section: Resultssupporting

confidence: 90%

Serum Dyslipidemia Is Induced by Internal Exposure to Strontium-90 in Mice, Lipidomic Profiling Using a Data-Independent Liquid Chromatography–Mass Spectrometry Approach

et al. 2015

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Despite considerable research into the environmental risks and biological effects of exposure to external beam gamma rays, incorporation of radionuclides has largely been understudied. This dosimetry and exposure risk assessment is challenging for first responders in the field during a nuclear or radiological event. Therefore, we have developed a workflow for assessing injury responses in easily obtainable biofluids, such as urine and serum, as the result of exposure to internal emitters Cesium-137 (137Cs) and Strontium-90 (90Sr) in mice. Here we report on the results of the untargeted lipidomic profiling of serum from mice exposed to 90Sr. We also compared these results to those from previously published 137Cs exposure to determine any differences in cellular responses based on exposure type. The results of this study conclude that there is a gross increase in the serum abundance of triacylglycerides and cholesterol esters, while phostaphatidylcholines and lysophosphatidylcholines displayed decreases in their serum levels post exposure at study days 4, 7, 9, 25, and 30, with corresponding average cumulative skeleton doses ranging from 1.2±0.1 Gy to 5.2±0.73 Gy. The results show significant perturbations in serum lipidome as early as 2 days post exposure and persisting until the end of the study (day 30).

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Section: Resultssupporting

confidence: 90%

Serum Dyslipidemia Is Induced by Internal Exposure to Strontium-90 in Mice, Lipidomic Profiling Using a Data-Independent Liquid Chromatography–Mass Spectrometry Approach

et al. 2015

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“…Although many in vitro and short-term in vivo studies have shown that IR can induce premature senescence [20,23,36], long-term in vivo studies are lacking. We previously reported that IR can produce long-term alterations of immunological functions and lipid metabolism, and the fractionation scheme can modulate the effects of IR [14,25]. Therefore, the present study was performed to examine the long-term effects of IR on tissue senescence in mice up to 6 months following IR exposure.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the effect of irradiation delivery, such as single or fractionated doses, on senescence marker expression was evaluated. We previously reported that more prominent prolonged effects on immunological functions and lipid metabolism are observed when irradiation is given in fractionated doses than in a single dose [14,25]. For our investigation, mice were given single or fractionated doses of IR (in a total dose of 5 Gy), and senescence marker expression in the mouse tissues was analyzed 2, 4, and 6 months after irradiation.…”

Section: Introductionmentioning

confidence: 99%

Prolonged expression of senescence markers in mice exposed to gamma-irradiation

et al. 2012

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Although ionizing radiation is known to induce cellular senescence in vitro and in vivo, its long-term in vivo effects are not well defined. In this study, we examined the prolonged expression of senescence markers in mice irradiated with single or fractionated doses. C57BL/6 female mice were exposed to 5 Gy of γ-rays in single or 5, 10, 25 fractions. At 2, 4, and 6 months after irradiation, senescence markers including mitochondrial DNA (mtDNA) common deletion, p21, and senescence-associated β-galactosidase (SA β-gal) were monitored in the lung, liver, and kidney. Increases of mtDNA deletion were detected in the lung, liver, and kidney of irradiated groups. p21 expression and SA β-gal staining were also increased in the irradiated groups compared to the non-irradiated control group. Increases of senescence markers persisted up to 6 months after irradiation. Additionally, the extent of mtDNA deletion and the numbers of SA β-gal positive cells were greater as the number of radiation fractions increased. In conclusion, our results showed that ionizing radiation, especially that delivered in fractions, can cause the persistent upregulation of senescence marker expression in vivo. This should be considered when dealing with chronic normal tissue injuries caused by radiation therapy or radiation accidents.

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“…In adipose tissue of the irradiated rats, incorporation of 14 C-glucose into all the lipid fractions was raised throughout the time of observation (300–600% of the control value). Jo et al (17) exposed two-month-old C57BL/6 mice to whole-body radiation at a single dose (5 gray [Gy]) and found that the mRNA levels of glucose transporter 4 (GLUT4) in gonadal white fat was lower in the gamma-irradiated groups vs. un-irradiated animals.…”

Section: Discussionmentioning

confidence: 99%

Combination of Radiation and Burn Injury Alters [18F] 2-Fluoro-2-Deoxy-D-Glucose Uptake in Mice

Carter

Winter

Tolman

et al. 2012

Journal of Burn Care & Research

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Radiation exposure and burn injury have both been shown to alter glucose utilization in vivo. The present study was designed to study the effect of burn injury combined with radiation exposure, on glucose metabolism in mice using [18F] Fluorodeoxyglucose (18FDG). Groups of male mice weighing approximately 30g were studied. Group 1 was irradiated with a 137Cs source (9 Gy). Group 2 received full thickness burn injury on 25% total body surface area followed by resuscitated with saline (2mL, IP). Group 3 received radiation followed 10 minutes later by burn injury. Group 4 were sham treated controls. After treatment, the mice were fasted for 23 hours and then injected (IV) with 50 µCi of 18FDG. One hour post injection, the mice were sacrificed and biodistribution was measured. Positive blood cultures were observed in all groups of animals compared to the shams. Increased mortality was observed after 6 days in the burn plus radiated group as compared to the other groups. Radiation and burn treatments separately or in combination produced major changes in 18FDG uptake by many tissues. In the heart, brown adipose tissue (BAT) and spleen, radiation plus burn produced a much greater increase (p<0.0001) in 18FDG accumulation than either treatment separately. All three treatments produced moderate decreases in 18FDG accumulation (p<0.01) in the brain and gonads. Burn injury, but not irradiation, increased 18FDG accumulation in skeletal muscle; however the combination of burn plus radiation decreased 18FDG accumulation in skeletal muscle. This model may be useful for understanding the effects of burns + irradiation injury on glucose metabolism and in developing treatments for victims of injuries produced by the combination of burn plus irradiation.

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Ionising radiation triggers fat accumulation in white adipose tissue

Abstract: A physical agent such as γ-rays can trigger biological responses resulting in fat accumulation of gonadal white adipose tissue in mice.

Cited by 13 publications

References 21 publications

Serum Dyslipidemia Is Induced by Internal Exposure to Strontium-90 in Mice, Lipidomic Profiling Using a Data-Independent Liquid Chromatography–Mass Spectrometry Approach

Serum Dyslipidemia Is Induced by Internal Exposure to Strontium-90 in Mice, Lipidomic Profiling Using a Data-Independent Liquid Chromatography–Mass Spectrometry Approach

Prolonged expression of senescence markers in mice exposed to gamma-irradiation

Combination of Radiation and Burn Injury Alters [18F] 2-Fluoro-2-Deoxy-D-Glucose Uptake in Mice

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