The above picture is from Fig. 4 of Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers.
I've posted the above picture to show that leptin secretion increases non-linearly with increasing culture period. As adipocyte content almost certainly increases non-linearly with increasing culture period (like THIS), leptin secretion almost certainly increases very non-linearly with increasing adipocyte content. As adipocyte content increases, there's no/minimal leptin secretion up to a certain level of fullness. Above this level of fullness, leptin secretion increases rapidly. What this means is that reducing adipocyte content by x% reduces leptin secretion by much more than x%.
If somebody's adipocytes become 100% full due to caloric excess, there are two extreme possibilities.
1a: If there is continued caloric excess, no preadipocytes are converted into adipocytes. There is no storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed - BAD.
1b: If there is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been completely destroyed in the meantime). The relatively full adipocytes secrete plenty of leptin, so metabolic rate is high and hunger is low - GOOD.
2a: If there is continued caloric excess, pre-adipocytes are converted into adipocytes. This is adipocyte hyperplasia. There is storage capacity available for excess nutrients, so T2DM doesn't develop - GOOD.
2b: If there is subsequent caloric deficit, adipocytes start to deplete. However, there are more adipocytes than in 1), so for a given fat mass, adipocytes are emptier than in 1). The greater number of emptier adipocytes secrete less leptin than in 1), so metabolic rate is lower and hunger is higher than in 1) - BAD.
Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. I believe that growing children are much more likely to get adipocyte hyperplasia than adults. Therefore, childhood obesity is highly likely to result in misery after subsequent fat mass loss. This is why I believe that growing children should be protected from the
EDIT: Jane Karlsson just e-mailed me a link to the following study:- Adipocyte Turnover: Relevance to Human Adipose Tissue Morphology.
"Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P < 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P < 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P < 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology."
So, if you want to remain slim, high fasting serum insulin (due to hepatic and/or muscular insulin resistance) is bad mmm-kay?
