Tchoukalova · Proceedings of the National Academy of Sciences of the United States of America 2010 · prospective interventional cohort study · n=28

Regional differences in cellular mechanisms of adipose tissue gain with overfeeding.

Cited 371 times in the scientific literature.

Level 3 - non-randomized controlled study

Prospective single-arm interventional cohort study with pre- and post-overfeeding comparisons.

PubMed 20921416 · doi:10.1073/pnas.1005259107 · record verified 2026-08-29

What was done

Twenty-eight healthy, normal-weight adults (15 men, age 29 ± 2 y) underwent an 8-week overfeeding protocol. Regional fat gain in upper- and lower-body subcutaneous fat depots was measured using dual energy X-ray absorptiometry and computed tomography. The authors assessed changes in subcutaneous adipocyte size via photomicrographs and calculated adipocyte number, relating these changes to baseline preadipocyte proliferation, differentiation markers (PPARγ2 and C/EBPα mRNA), and apoptotic response to TNF-α.

What was found

Fat mass increased by 1.9 ± 0.2 kg in the upper body and 1.6 ± 0.1 kg in the lower body. Abdominal subcutaneous 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). In contrast, lower-body subcutaneous fat increased through hyperplasia, adding 2.6 ± 0.9 × 10(9) adipocytes (P < 0.01). Preadipocyte replication and apoptotic responses did not differ between depots, but baseline PPARγ2 and C/EBPα mRNA were significantly higher in abdominal than femoral preadipocytes (P < 0.005 and P < 0.03, respectively).

Why it matters

This study shows that adult human adipose tissue depots respond differently to caloric excess, demonstrating that lower-body fat can undergo rapid hyperplasia within 8 weeks.

Limits

The study had a small sample size (n = 28) limited to young, healthy, normal-weight adults, so findings may not generalize to older individuals or those with baseline obesity. It was an uncontrolled single-arm intervention, and cellular changes in visceral fat depots were not assessed.

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