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  1. Jul 2018
    1. On 2014 Jul 18, William Cawthorn commented:

      Several thoughts about this very interesting study:

      1. Larger adipocytes are often taken as a surrogate for impaired adipogenesis, whereas smaller adipocytes are seen as indicative of enhanced adipogenesis. But lipogenesis, leading to adipocyte hypertrophy, also contributes to adipose tissue expandability (perhaps more so than adipogenesis). Therefore, I wonder if the smaller adipocytes at baseline actually represent impaired lipogenesis, and therefore impaired adipose tissue expandability?

      2. Was there any association between adipocyte size at baseline, and changes in circulating lipids? I.e. the subjects with larger adipocytes had smaller change in SAT, VAT, and total fat mass, without accumulating more lipid in liver or SkM; therefore, is the excess lipid circulating instead?

      3. The adipocyte size measurements are for subcutaneous WAT. It would be interesting to see if there were similar associations for the sizes of adipocytes in visceral WAT, which tends to be more inflamed.

      4. The authors here find no association between SAT adipocyte size and expression of markers of inflammation. Another study in humans found that smaller SAT adipocytes were associated with increased inflammation (McLaughlin et al, 2010; PMID 19816674). Each of these studies are in contrast to the concept that adipocyte hypertrophy is associated with increased inflammation (e.g. Gustafson et al, 2009; PMID 19622783). Clearly, further studies in humans, both in subcutaneous and visceral WAT, are needed to determine if adipocyte hypertrophy is associated with increased WAT inflammation.


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  2. Feb 2018
    1. On 2014 Jul 18, William Cawthorn commented:

      Several thoughts about this very interesting study:

      1. Larger adipocytes are often taken as a surrogate for impaired adipogenesis, whereas smaller adipocytes are seen as indicative of enhanced adipogenesis. But lipogenesis, leading to adipocyte hypertrophy, also contributes to adipose tissue expandability (perhaps more so than adipogenesis). Therefore, I wonder if the smaller adipocytes at baseline actually represent impaired lipogenesis, and therefore impaired adipose tissue expandability?

      2. Was there any association between adipocyte size at baseline, and changes in circulating lipids? I.e. the subjects with larger adipocytes had smaller change in SAT, VAT, and total fat mass, without accumulating more lipid in liver or SkM; therefore, is the excess lipid circulating instead?

      3. The adipocyte size measurements are for subcutaneous WAT. It would be interesting to see if there were similar associations for the sizes of adipocytes in visceral WAT, which tends to be more inflamed.

      4. The authors here find no association between SAT adipocyte size and expression of markers of inflammation. Another study in humans found that smaller SAT adipocytes were associated with increased inflammation (McLaughlin et al, 2010; PMID 19816674). Each of these studies are in contrast to the concept that adipocyte hypertrophy is associated with increased inflammation (e.g. Gustafson et al, 2009; PMID 19622783). Clearly, further studies in humans, both in subcutaneous and visceral WAT, are needed to determine if adipocyte hypertrophy is associated with increased WAT inflammation.


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.