Why Fat Thighs Are Probably Better Than Fat Belly, Where Metabolic Disease Is Concerned

Why Fat Thighs Are Probably Better Than Fat Belly, Where Metabolic Disease Is Concerned



After observing weight gain in volunteers, US researchers found fat growth in the lower body such as the thighs was biologically different to fat growth in the abdomen, and this may explain why bigger thighs pose a lower risk of metabolic disease than a big belly.

You can read about the study, from researchers at the Mayo Clinic in Rochester, Minnesota, online in the 4 October early issue of theĀ Proceedings of the National Academy of Sciences (PNAS).

Fat in the abdomen tends to be visceral fat, comprising several types of deposited fat (depots) around the organs, while fat in the lower body such as the thighs and buttocks is subcutaneous, that is under the skin.

The researchers wrote in their background information that while we already know that different types of body fat and where it is situated affects the risk of metabolic disease in obesity, the underlying biology of fat gain is somewhat of a mystery.

Endocrinologist and lead author Dr Michael Jensen told the press in their study they found that in the abdomen, extra body fat appears to result from individual cells getting bigger, while in the femoral or lower body, extra fat seems to result from an increase in the number of fat cells.

“So, different mechanism, different impact,” said Jensen.

Jensen and colleagues recruited 28 volunteers (15 men and 13 women, aged 27 to 31) who overfed themselves for 8 weeks. They were encouraged to eat and drink almost anything they wanted including high calorie drinks, giant candy bars and ice cream shakes.

Both before and after the eight weeks of overeating, the researchers measured body fat, fat cell size, and other fat cell characteristics.

They used dual energy X-ray absorptiometry and computed tomography (CT) scans to assess regional fat gain, and photomicrographs to measure adipocyte (fat cell) size and they also tested various biological reactions at the cellular level. One of the reactions they tested was the turnover (replication and apoptosis) in preadipocytes (potential fat cells before they mature and become adipocytes).

They found:

    • The average upper body fat weight gain was 2.5 kg (5.5 lbs) per participant.
    • The average lower body fat weight gain was 1.5 kg (3.3 lbs) per participant.
    • There was a significant correlation between increased fat cell size and upper-body fat gain.
    • But in the lower body, the significant correlation was with increase in fat cell numbers.
    • No differences between upper and lower body fat depots in turnover of preadipocytes that would explain these findings.
  • However, there was a significantly higher rate, even before the fat gain started, of RNA messages that trigger proteins to start making fat in the abdominal preadipocytes than in the lower body ones, and this was consistent with the ability of the abdominal fat cells to achieve a larger size.

The researchers concluded that:

“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. “

They said in a statement that this finding challenges the idea that the number of fat cells in the body does not change once a person reaches adulthood.

It also supports the suggestion that having the ability to increase the number of fat cells in the lower body affords some protection to the upper body, thus lessening the risk of developing metabolic disease, which can lead to diabetes and other health problems.

Funds form the National Institutes of Health, the US. Public Health Service, The Noaber Foundation and Mayo Clinic, including the Robert and Arlene Kogod Center on Aging, helped pay for the study.

“Regional differences in cellular mechanisms of adipose tissue gain with overfeeding.”
Yourka D. Tchoukalova, Susanne B. Votruba, Tamara Tchkonia, Nino Giorgadze, James L. Kirkland, and Michael D. Jensen.
PNAS, published ahead of print 4 October 2010

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