一項研究發(fā)現(xiàn)，上半身和下半身的脂肪組織增加的重量不同,，這部分是由于脂肪細胞前體的差異,。此前的研究提示上半身脂肪增加會提高代謝疾病的風險,，而下半身脂肪的增加會減少這種風險,，但是其中的原因尚不清楚。為了確定人體脂肪積累如何增長,，Michael D. Jensen及其同事檢驗了過度進食對于人的上半身和下半身皮下脂肪組織的影響,。這組作者招募了28位健康的成年志愿者，在8周的時間里要求他們進食直到比平常的程度飽很多,。
此外,，這組志愿者食用了冰激凌奶昔、大號士力架和Boost Plus能量飲料等補充食物,。這組作者發(fā)現(xiàn),，在經(jīng)過8周之后，這組志愿者上半身脂肪增加了大約2千克,，下半身的脂肪增加了大約1.5千克,。這組作者報告說，上半身脂肪細胞的平均尺寸而非細胞數(shù)量在過度進食之后增加,，而大腿脂肪細胞的情況正好相反,。上半身而非大腿的脂肪細胞前體顯示出了參與脂肪合成的蛋白質(zhì)的RNA信息濃度更高。這組作者說,，這些發(fā)現(xiàn)可能為所謂的大腿脂肪的有益作用提供一個可能的解釋,。（生物谷Bioon.com）
生物谷推薦英文摘要：
PNAS doi: 10.1073/pnas.1005259107
Regional differences in cellular mechanisms of adipose tissue gain with overfeeding
Yourka D. Tchoukalovaa,b, Susanne B. Votrubaa, Tamara Tchkoniac, Nino Giorgadzec, James L. Kirklandc, and Michael D. Jensena,1
aEndocrine Research Unit and
cRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905; and
bPennington Biomedical Research Center, Baton Rouge, LA 70808
Body fat distribution is an important predictor of the metabolic consequences of obesity, but the cellular mechanisms regulating regional fat accumulation are unknown. We assessed the changes in adipocyte size (photomicrographs) and number in response to overfeeding in upper- and lower-body s.c. fat depots of 28 healthy, normal weight adults (15 men) age 29 ± 2 y. We analyzed how these changes relate to regional fat gain (dual energy X-ray absorptiometry and computed tomography) and baseline preadipocyte proliferation, differentiation [peroxisome proliferator-activated receptor-γ2 (PPARγ2) and CCAAT/enhancer binding protein-α (C/EBPα) mRNA]), and apoptotic response to TNF-α. Fat mass increased by 1.9 ± 0.2 kg in the upper body and 1.6 ± 0.1 kg in the lower body. Average abdominal s.c. adipocyte size increased by 0.16 ± 0.06 μg lipid per cell and correlated with relative upper-body fat gain (r = 0.74, P < 0.0001). However, lower-body fat responded to overfeeding by fat-cell hyperplasia, with adipocyte number increasing by 2.6 ± 0.9 × 109 cells (P < 0.01). We found no depot-differences in preadipocyte replication or apoptosis that would explain lower-body adipocyte hyperplasia and abdominal s.c. adipocyte hypertrophy. However, baseline PPARγ2 and C/EBPα mRNA were higher in abdominal than femoral s.c. preadipocytes (P < 0.005 and P < 0.03, respectively), consistent with the ability of abdominal s.c. adipocytes to achieve a larger size. Inherent differences in preadipocyte cell dynamics may contribute to the distinct responses of different fat depots to overfeeding, and fat-cell number increases in certain depots in adults after only 8 wk of increased food intake.
