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膳食肥胖小鼠中 n-3 脂肪酸对脂肪细胞增殖的抑制作用。

The inhibition of fat cell proliferation by n-3 fatty acids in dietary obese mice.

机构信息

Department of Adipose Tissue Biology, Institute of Physiology Academy of Sciences of Czech Republic v.v.i., Prague, Czech Republic.

出版信息

Lipids Health Dis. 2011 Aug 2;10:128. doi: 10.1186/1476-511X-10-128.

Abstract

BACKGROUND

Long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) of marine origin exert multiple beneficial effects on health. Our previous study in mice showed that reduction of adiposity by LC n-3 PUFA was associated with both, a shift in adipose tissue metabolism and a decrease in tissue cellularity. The aim of this study was to further characterize the effects of LC n-3 PUFA on fat cell proliferation and differentiation in obese mice.

METHODS

A model of inducible and reversible lipoatrophy (aP2-Cre-ERT2 PPARγL2/L2 mice) was used, in which the death of mature adipocytes could be achieved by a selective ablation of peroxisome proliferator-activated receptor γ in response to i.p. injection of tamoxifen. Before the injection, obesity was induced in male mice by 8-week-feeding a corn oil-based high-fat diet (cHF) and, subsequently, mice were randomly assigned (day 0) to one of the following groups: (i) mice injected by corn-oil-vehicle only, i.e."control" mice, and fed cHF; (ii) mice injected by tamoxifen in corn oil, i.e. "mutant" mice, fed cHF; (iii) control mice fed cHF diet with15% of dietary lipids replaced by LC n-3 PUFA concentrate (cHF+F); and (iv) mutant mice fed cHF+F. Blood and tissue samples were collected at days 14 and 42.

RESULTS

Mutant mice achieved a maximum weight loss within 10 days post-injection, followed by a compensatory body weight gain, which was significantly faster in the cHF as compared with the cHF+F mutant mice. Also in control mice, body weight gain was depressed in response to dietary LC n-3 PUFA. At day 42, body weights in all groups stabilized, with no significant differences in adipocyte size between the groups, although body weight and adiposity was lower in the cHF+F as compared with the cHF mice, with a stronger effect in the mutant than in control mice. Gene expression analysis documented depression of adipocyte maturation during the reconstitution of adipose tissue in the cHF+F mutant mice.

CONCLUSION

Dietary LC n-3 PUFA could reduce both hypertrophy and hyperplasia of fat cells in vivo. Results are in agreement with the involvement of fat cell turnover in control of adiposity.

摘要

背景

海洋来源的长链 n-3 多不饱和脂肪酸 (LC n-3 PUFA) 对健康有多种有益作用。我们之前在小鼠中的研究表明,LC n-3 PUFA 对肥胖的影响与脂肪组织代谢的转变和组织细胞减少有关。本研究的目的是进一步研究 LC n-3 PUFA 对肥胖小鼠脂肪细胞增殖和分化的影响。

方法

使用可诱导和可逆脂肪减少(aP2-Cre-ERT2 PPARγL2/L2 小鼠)模型,通过腹腔注射他莫昔芬选择性消融过氧化物酶体增殖物激活受体 γ,可使成熟脂肪细胞死亡。在注射前,通过 8 周的玉米油基高脂肪饮食(cHF)喂养诱导雄性小鼠肥胖,随后将小鼠随机分配(第 0 天)至以下组之一:(i)仅用玉米油载体注射的小鼠,即“对照”小鼠,喂食 cHF;(ii)用他莫昔芬在玉米油中注射的小鼠,即“突变”小鼠,喂食 cHF;(iii)用 15%膳食脂质被 LC n-3 PUFA 浓缩物替代的 cHF 喂养的对照小鼠(cHF+F);和(iv)用 cHF+F 喂养的突变小鼠。在第 14 天和第 42 天收集血液和组织样本。

结果

突变小鼠在注射后 10 天内体重减轻最多,随后体重恢复,与 cHF+F 突变小鼠相比,cHF 中的体重恢复更快。在对照小鼠中,膳食 LC n-3 PUFA 也抑制了体重增加。在第 42 天,所有组的体重均稳定,各组之间的脂肪细胞大小无显著差异,尽管与 cHF 小鼠相比,cHF+F 组的体重和肥胖程度较低,且突变小鼠比对照小鼠的效果更强。基因表达分析记录了在 cHF+F 突变小鼠的脂肪组织重建过程中脂肪细胞成熟的抑制。

结论

膳食 LC n-3 PUFA 可减少体内脂肪细胞的肥大和增生。结果与脂肪细胞周转在肥胖控制中的参与一致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ece2/3162548/113d333de8d8/1476-511X-10-128-1.jpg

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