By now it seems pointless, everything that could of been discussed has already been discussed about it elsewhere. However the points about beta cell mass expansion in obesity were interesting.
Pancreas and beta cell is an area that I am under-researched in ( I have been focusing alot on the morphology of the adipose tissue ), so I was a bit surprised that learn that beta cell mass increases in obesity. Its worse than I could ever have imagined, one study reports as much 10-30% increase in beta cell mass for each 10kg in weight gain.
One of the best lines in JJ's paper is this...
Together, many lines of evidence from multiple groups support the concept that insulin acts via insulin receptors to mediate the compensatory increase in b cell mass and basal insulin release in the context of high-fat diet
Ignore the bolded part for now. What JJ says in the paper is that there appears to be some kind of positive feedback mechanism between insulin secretion and beta cell expansion. I.E. insulin acts via receptors locally on the pancreas to promote beta cell expansion. Insulin hyper-secretion feeds back positively to the beta cells telling them to increase mass, presumably so that you can become a better insulin hyper-secreter in the future.
more insulin leads to more insulin leads to more insulin.
Yeh something like that.
Ofcourse the beta cells probably dont have any idea in the meantime that all this insulin its learning to pump out is rapidly expanding your fat tissue.
In addition there is this excerpt from the 2004 paper linked above...
In conclusion, obesity is a condition of predominantly β-cell functional upregulation rather than β-cell expansion. This upregulation involves the static responses (i.e., basal and total secretion) much more than the dynamic responses (i.e., glucose sensitivity and potentiation), at least as long as glucose-tolerant subjects are concerned. The insulin hypersecretion of obesity has a primary component, which cannot be explained by adaptation to insulin resistance and can be tracked through the period of weight loss (induced by calorie reduction or restrictive bariatric surgery). The residual insulin hypersecretion of the postobese (or weight-reduced) state may be the equivalent of an inherent insulin hypersecretion of the preobese condition.
So what im getting at is this, did you become obese because your pancreas learned to become an insulin-hypersecreter? All the fucked up stuff that happens with the morphology of your adipose tissue is likely just the result of this insulin-hypersecretion.
But, what provided the positive feedback of insulin hypersecretion to get the snowball rolling in the first place? I think this is a good point to go back to the Jenkins study . Insulin-hypersecretion BEGINS in response to blood sugar spikes.
But what causes blood sugar spikes? Again as shown in the Jenkins study, it is fast absorption of lots of glucose. Jenkins shows that fast absorption of glucose alone is not enough to spike blood sugar, you must also have significant amounts for it to build up in the blood ( I suppose thats obvious really, a single glucose molecule is not going to spike your blood sugar ) . Also we have to consider the degree of hepatic insulin resistance you have and how well you can activate glucokinase in the liver in response to carb ingestion.
All in all, the physiology remains complex, but the cause remains simple. Its the fast digesting, glucose dense foods spiking your blood sugar that is making you fat.
Also what happens with weight loss? Does beta cell mass shrink along with your BMI? Even after youve lost weight, it doesnt change the fact you were an insulin-hypersecreter in the past. And you can be one again in the future. You just need to get the snowball rolling again with some potato.