Saturday, 11 May 2013

More on Fat Cell dynamics, - in response to weight loss/calorie restriction

cba today so ima just copy/paste

Adaptation of human adipose tissue to hypocaloric diet
  • In a study on type 2 diabetes patients submitted to 1-year dietary intervention combined with exercise, the authors stratified the adipocytes into four subfractions in respect to the cell size.16 At the end of intervention, the adipocyte size was reduced just in subfraction of ‘large’ adipocytes, while the other three remained unchanged.
  • investigations suggest that individuals with hypertrophic obesity—who are at higher metabolic risk6, 18, 19, 20—are more responsive to the adipocyte size-reducing effect of hypocaloric diets in comparison with those with small adipocytes, that is, with hyperplasic obesity.
  • In another study, using electron microscopy, the response was variable in a group of six patients submitted to 6 weeks’ LCD: in subjects with higher proportion of large adipocytes (hypertrophic obesity), the authors observed a shift from the fraction of large adipocytes towards the small ones, whereas in subjects with higher proportion of small adipocytes (hyperplasic obesity) no shift between the fractions occurred.
  • no reduction of adipocyte size in abdominal (but not in gluteal) SCAT was found after 20 weeks’ LCD in one study.15

  • insulin stimulation of de novo lipogenesis measured on isolated SCAT adipocytes was blunted after 4-weeks’ VLCD.10 However, in weight-maintenance phase, 1–3 years after initiation of the weight reducing program or after gastric banding, both, the basal- and insulin-stimulated, de novo lipogenesis measured on isolated adipocytes were increased when compared with the pre-diet condition.31

Prospective and controlled studies of the actions of insulin and catecholamine in fat cells of obese women following weight reduction.

  • Many of the adipocyte abnormalities associated with obesity improve after weight loss [1215]. Fat cell size decreases, as does basal lipolysis. Insulin and catecholamine actions are improved. However, it is not known if these actions completely return to normal. A full normalisation would suggest that the abnormalities are secondary to obesity. However, incomplete normalisation would suggest primary defects in adipocyte function that cannot be cured by weight loss
  • A prominent finding in this study was a decrease in fat cell volume below the control level in weight-reduced obese subjects. Since BMI, fat distribution and body fat content were similar in obese subjects and their controls, the results imply that adipose hyperplasia (at least in abdominal subcutaneous adipose tissue) is a major feature of weight-reduced obese subjects
  • This further strengthens the idea that insulin resistance is secondary to obesity, whereas adipose hypercellularity and low adipose lipolytic rates may be primary factors in obesity.
  • In conclusion, adipose tissue hyperplasia (many small fat cells) is present in the weight-reduced state and probably explains the low rates of adipocyte lipolysis in this condition. However, adipocyte insulin resistance is a secondary and fully reversible phenomenon in obesity.

You cant select a random obese person from the population then tell him "fat mass is only about CICO", because you have no idea of the amount of fat cell hyperplasia they are suffering from. The more fat cells you have, the fatter youll be, BY DEFAULT.

Why am I posting this? Because I want it to be apparent that people suffering from significant hyperplasia will be unable to resolve their dysfunctional metabolism with diet and exercise alone, despite what you may hear from high standing medical doctors and bloggers. More likely we will need pharmaceutical intervention or in the worst case scenario, surgery.

How can you tell if your suffering from hyperplasia? Well, while I dont have references to back up these claims, I have several ideas. Firstly, the ease with which you rebound weight gain after weight loss will signify hyperplasia. Also the degree to which you are metabolically healthy despite significant increases in weight will signify significant hyperplasia. If you was very heavy but with no clear signs of diabetes = significant hyperplasia.

Also, just look at your fat tissue, is it very "lumpy" with lots of partitions? or is it very roundish and circular? The former = hyperplasia. See pictures in this post for example. The guy in the left most likely has significantly more hyperplasia than the right.


  1. A clear sign of hyperplasia:

    -While weight reduced, your face / hands is skeletal, although other areas of your body look healthy even fat. The skeletal face is a sign that your adipocytes are extremely small, as the face is typically protected from insulin mediated adipocyte hyperplasia. Having large volume fat mass in say, legs or arms or abdomen in spite of this, suggests signfiicant hyperplasia.

    If one were to get "skin removal surgery" they will observe a trend toward ameliorating that skeletal face problem at an equal body weight, which is because "skin removal surgery" is really a misnomer and it is actually hyperplastic adipocyte surgery (which is probably the main cause of "loose skin" anyway).

    In addition to a superior aesthetic, metabolic function is normalized at a reduced weight.

  2. "Having large volume fat mass in say, legs or arms or abdomen in spite of this, suggests signfiicant hyperplasia."

    Thats very true I think, fat lumpy inner thighs, lower abdomen, and the underarm's all seem very prone to hyperplasia.

  3. check out this video from 14:00. This poor guy experienced the most gross and absurd hyperplasia from his lower abdomen I have ever seen. Apparently it weighed 8 stone alone.

    Why on earth the body lets the fat tissue grow to such a state is disturbing beyond belief.

  4. From the same group who conducted the second study:

    The postobese cases had 43% smaller fat cell volume (P = 0.0008), 68% lower adipocyte leptin production (P = 0.001), and 54% lower serum leptin levels (P = 0.0007) than control subjects, despite almost identical percent body fat in the two groups. Fat cell volume, but not percent body fat or BMI, was directly proportional to leptin secretion and serum leptin concentrations.
    CONCLUSION: Adipose tissue hyperplasia (too many small fat cells) and low leptin production resulting in relative hypoleptinemia in the fasting (basal) state are common features of the postobese state in women.

    I know it's old hat to us here but I just thought I'd mention it.

  5. I wish Jemmy Moore had a skin removal surgery. His face looks really thin lately.

    I lost weight several times in past, but somehow it was LCarbing that made my face look thinner. It could be also aging, of course.