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.Read more »
2. Excess NEFA leads to insulin resistance in the tissues, including the adipocytes
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