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From:
Jean-Louis Tu <[log in to unmask]>
Date:
Mon, 29 Dec 1997 14:59:30 -0500
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Peter:

> Yet, the main function of insulin is to respond to rising blood glucose
> levels.  If you come across an explanation in simple layman's terms of what
> GIP is and how it interacts with insulin when fat is ingested with
> carbohydrate, I would be very interested in seeing it.

>From Ellenberg and Rifkin's "Diabetes Mellitus", 5th Edition, 1997,
GIP (Gastric Inhibitory Polypeptide, or Glocose dependent Insulinotropic
Polypeptide), is a gut hormone which stimulates insulin release (some
hormones stimulate, others inhibit insulin release). The effectiveness of
GIP to stimulate insulin release is dependent on the plasma glucose level
(the higher the glucose level, the higher the effectiveness). The exact
contribution of GIP to the insecretin effect is currently inclear because
its insulin-stimulating effect may vary with species.

(see below for more details concerning the experiments of Collier)

> For active people who do not need to lose weight, the zone might mean a
> 30/25/45 breakdown of macro nutrients.

Which interestingly corresponds approximately to what a Paleo-human may
have eaten.

> With such conflicting results it seems that the jury is still out on this
> issue.  I wonder which of Collier's studies on the effects of fats on
> insulin levels are considered the most conclusive.

Sorry, I was confused. There are actually several results:

[Collier et al., The effect of co-ingestion of fat on the glucose, insulin
and gastric inhibitory polypeptide responses to carbohydrate and protein,
Am J Clin Nutr 37:941]:

The effects of co-ingestion of 50 g fat (butter) with 50 g carbohydrate
(potato) compared with potato alone: markedly decreased glucose, very
slightly decreased insulin, markedly increased GIP.

These results suggest the following mechanism:
 -Fat stimulates GIP release
 -GIP stimulate insulin secretion when blood glucose level is elevated
 -therefore, despite a lower blood glucose with butter+potato than with
potato alone, the consequence of a higher level of GIP is that the insulin
curve is almost unaffected by the addition of fat.

[Collier et al., Effect of co-ingestion of fat on the metabolic responses
to slowly and rapidly absorbed carbohydrates, Diabetologia 26:50-54]

Similar experiments and results with 75 g carbohydrate (438 g potato or
121 g lentils) with or without 37.5 g fat (46.5 g butter). Of course, all
the effects are more important with the rapidly absorbed carbohydrate
(potato) than with the slowly absorbed carbohydrate (lentils).

[Collier et al., The acute effect of fat on insulin secretion, J Clin
Endocrin. Metabolism 66:323 (1988)]

The aim of that article was to test the conjecture that the RATE of rise
of GIP, rather than the STEADY STATE LEVEL achieved, stimulates insulin
secretion when fat and carbohydrate are ingested together. To do that, the
authors administered a 5 g iv bolus dose of glucose 15 minutes after the
meal, when the RATE of rise of GIP was highest but the LEVEL still LOW,
and observed the insulin response. It appears that the peak insulin after
the mixed meal was 60% higher than after the carbohydrate meal. That seems
to confirm their hypothesis.

It should be noted that, in a practical situation, nobody will inject you
some glucose after lunch, so, that the insulin peak is higher after such a
practice following a mixed meal shouldn't be of concern. More important
for us "consumers", the first two articles of Collier show that eating fat
with carbohydrate indeed prevents skyrocketing of blood glucose levels,
but that we shouldn't feel too protected by the co-ingestion of fat, since
it barely affects insulin levels.

Moreover, I would add, from [Collier et al., concurrent ingestion of fat
and reduction in starch content impairs carbohydrate tolerance to
subsequent meals, Am J Clin Nutr 45(5):963-9, 1987] that, even if
ingesting fat with carbohydrate at a meal doesn't harm you, it can at the
next meal.

> If the effect is almost zero or even positive it is not clear to me why the
> carbohydrate tolerance to future meals will be impaired.  Of course there
> is the GIP factor but I doubt that more than a handful of very educated
> scholars really understand the mechanism behind it.

Perhaps the exact mechanism hasn't been found yet. There are many
experimental data about response to different carbohydrates with various
quantities of protein and/or fat, and all of those are not consistent with
each other, nor do they provide any theorical models that I know of. For
instance, [Westphal et al., Metabolic response to glucose ingested with
various amounts of protein, Am J Clin Nutr 1990 (62):267-272] found that
protein (very lean beef) with 50 g glucose barely changes the insulin
curve, whereas [Spiller et al., Effect of protein dose on serum glucose
and insulin response to sugars, Am J Clin Nutr 1987 (46):474-80] found
that 58 grams of carbohydrates (maltodextrin+fructose+lactose) ingested
with various amounts (16,25,34,50 grams) of protein (1/3 milk proteins and
2/3 soy proteins) approximately doubles the area under the insulin curve
compared with the carbohydrates ingested alone. The reasons are unclear,
and may be due to the fact that different types of protein and different
types of carbohydrates have been used. Similarly, it appears from some
results (I haven't kept the references), the type of fat may be important;
however, Collier et al. haven't found any significant difference between
butter and peanut butter!!

You will understand that, if experimental data are already unclear, a
theorical explanation isn't yet within reach.

> A little confused.

Me too, me too! ;-)

Best wishes,

Jean-Louis
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