Wednesday, 30 January 2013

High glycemic index starch promotes hypersecretion of insulin

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".


  1. Ah, but you forgot, it is all the extra salt and spices you add that drive up the glycemic index of potatoes. Otherwise, nice post.

  2. But, but it's right there in the word! High gi equals high reward!!

    I'm pretty sure the low gi mice exercised more. sneaky bastards!

    Anyway, nice study that underlines the truthfulness of the dans plan affiliate.. I mean low food reward diet!

  3. Kindke, did they control for salt and other herbs/spices/seasoning content of the diets? It is conceivable that the high GI diet was more palatable than the other.

    What's with this pre-WW2 science/endocrinology quackery? Don't you know that the majority of the research community looked at the insulin hypothesis and said it was false because the Atkins diet is gonna give you heart disease and make your kidneys explode?

    Other than that I completely agree with your post.

  4. Unrelated.. I listened to the JJ-interview on superhumanradio yesterday.. Did you people know that the hyperinsulinemia study took 7ish (?) years to complete, and cost about 100k to 200k dollars per year?
    And thats only a mouse study...

    1. ah I had not listened to that yet. JJ really does make it sound like its all about beta cell growth and fasting hyperinsulemia. And according to paper at top of my post long-term high GI diet leads to fasting hyperinsulemia.

      Along with the graph Taubes had, showing a switch for fat oxidation once insulin gets below a certain threshold hhmmmmm.

      The postprandial insulin spikes surely must be important, that must be what gets the beta cells to start expanding in the first place, which leads to the hyperinsulemia.

      I need to start looking at weight loss and if/how it reduces the increased beta cell mass to accompanies ( causes? ) obesity.

  5. Interesting. I think it's likely that the 'hyper-secretion' isn't really hyper-secretion--the metabolism is just trained to expect glucose to come into the system at a certain rate, and puts out insulin appropriate to control blood glucose at that rate. Counter-regulatory hormones probably explain why this resulted in decent glucose tolerance rather than a hypoglycemic reaction. (I guess some of the counter-regulatory effect is probably due to physiological insulin resistance from elevated free fatty acids--making increased fat storage a possible reasonable adaptation by the metabolism to better control post-meal blood glucose).

    This sort of jumps out from table 3:

    Clamp hepatic glucose output;
    low glycemic index; 36 ± 14
    high glycemic index' 12 ± 13
    high fat 45 ± 8

    Not only is the liver not insulin-resistant, by this measure, it seems it might even be over-sensitive.

  6. It is a dilemma for somebody like me with a liver producing glucose too enthusiastically. The striker my LC is, the more efficient the liver gets. For a while I tried to add some starch into my evening meal(I am ashamed to admit the "safe starch" ideas got into my head then), but it was just messing up my evenings in different ways, FBS indeed went down, but weight went slightly up. It looks like very small amount of metformin (like 1/2 of pill once a day) could be a better option. I found out it is enough to do it in periods, like 3 - 4 day, and the effect lasts for days.

  7. This is a great article! The only thing that seems missing is a clarification around why higher GI foods should be avoided...

    In simple terms, because of glucose's high affinity to react with other molecules, our bodies strictly regulate blood glucose levels to a limited amount of only 5 grams in total.

    Insulin is secreted to manage glucose levels in the blood (insulin also does many other things). More importantly, studies have shown that insulin has 3 effects as it relates to weight management: 1. insulin stimulates lipogenesis. 2. insulin inhibits gluconeogenesis. 3. insulin inhibits autophagy.

    Each of these 3 effects contribute to the chronic deterioration of your body's metabolic processes. I recommend all readers look each one of them up on Google (or whatever search engine you use) and learn more about them.