Showing posts with label Glucagon. Show all posts
Showing posts with label Glucagon. Show all posts

Thursday, October 20, 2011

Hormonal & Appetite Response to Macronutrients

I came across this paper recently and thought I would share it here on my blog.  I think it is rather eye-opening as to the postprandial hormone responses to meals rich in each of the macros (and alcohol) and the ultimate effect on satiety.


This study was done in normal weight healthy humans (9 women, 10 men) in their early 20's.  They fed them a meal containing the same calories, but high in one of each nutrient.  Each subject was given each diet with a 4-8 week "washout" in between, a standard diet the day before each test day, and subjects fasted 10 hour overnight before testing.   Hormones, etc. were measured for 5 hours postprandially, and then were provided an ad libitum meal.   Here are the diets tested:

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Friday, September 9, 2011

You're as Hyperinsulinemic as You Need to Be †

Recent comments by Todd Becker (Getting Stronger blog) have prompted me to write yet another post on the (infamous on this blog) Grey & Kipnis study.  Perhaps, part of the problem in discussing these issues is a failure to define what it is we're talking about.  For instance with IR, we have chronic/pathologic IR, glucose-sparing IR (physiologic, fasting/carb restriction), and postprandial IR (usually impaired glucose clearance following a high fat meal or large fructose load).  With hyperinsulinemia we can talk about basal insulin levels vs. postprandial insulin levels.  It appears to me, that if we combine the observations in G&K with those of the long term fasting study, with the hypothesis of G&K -- that diet can play a role in basal hyperinsulinemia and therefore contribute to obesity -- perhaps basal insulin levels are comprised of both a chronic component (I would suggest related to NEFA) and a more transient component due to the diet of the previous day(s).  

So, Todd wrote:   Forgive me if I oversimplify the argument in your above post:
1. Obesity leads to spilling of excess fat as NEFA.
2. Excess NEFA leads to insulin resistance in the tissues, including the adipocytes

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