High glycemic index starch promotes hypersecretion of insulin and higher body fat in rats without affecting insulin sensitivity.
I think im approaching a pretty convincing model for diabesity. Some additional clues come from this paper.
The major finding here is that 7 weeks of a high GI diet in rats leads to increased insulin secretion in response to an intravenous-glucose tolerance test. Importantly this increased insulin secretion is NOT a response to insulin resistance because glucose tolerance was not impaired.
So the insulin-hypersecretion is primary.
In the discussion the researchers are not sure why a high GI diet leads to insulin hyper-secretion and speculate that it may have to do with triglyceride accumulation in the beta cells. But from JJ's paper we learned that there is positive feedback mechanism between the pancreas and insulin secretion. More insulin can easily lead to MORE insulin during future hyperglycemic challenges from your plain boiled potatoes.
Oh, and the insulin hyper-secreting rats on the high GI diet also had increased fat mass. But im sure thats just coincidence. ( feeding regime was isocaloric, just before you CICO nutters try to jump in. )
The high GI diet promoted a high insulin response during an intravenous glucose tolerance test (IVGTT) (14), which increased with the duration of feeding (15) and eventually led to fasting hyperinsulinemia
So if the results of JJ's study says that hyperinsulinemia drives obesity, we have a connection, for the above quote says that consumption of a high GI diet leads to hyperinsulinemia.
Which, according to JJ's paper says, drives obesity.
I.E. spiking your blood sugar makes you fat.
But, most of us ( educated ) fatties already know this. So lets move on...........
It has been reported that the mRNA expression and activity of fatty acid synthase, a key lipogenic enzyme, increase in adipose tissue after only 3 wk of wheat starch feeding
hhhhhmmmm, what about 3 weeks of plain boiled potato feeding?
We speculate that this hypersecretion of insulin in response to a glucose challenge after only 7 wk of feeding may alter fuel utilization and patterns of energy disposition, irrespective of changes in insulin sensitivity.
Indeed, this study says that "fatty acid oxidation was significantly blunted as early as 3 wk after beginning of the high-GI intervention" and occurred before any significant increase in fat mass, indicating a possible causal role. ( only "possible"?! lol )
Bottom line, I think the idea that insulin feeds back positively to increase beta cell mass and insulin secretion is a missing part of the "Insulin Hypothesis".