Department of Adipose Tissue Biology, Institute of Physiology Academy of Sciences of Czech Republic v.v.i., Prague, Czech Republic.
Lipids Health Dis. 2011 Aug 2;10:128. doi: 10.1186/1476-511X-10-128.
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.
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.
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.
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.
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。
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。
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。
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。