Paul Saladino· MD
and so when I was trying to talk to the guys on this podcast for mastering diabetes I said we cannot define insulin resistance independent of levels of systemic insulin because glucose pairing is low insulin and systemic pathologic insulin resistance like techno B's is very high insulin which is why we check fasting insulin why we check c-peptide and that's a very good sort of indicator whether we're in a state of low carb high fat normal or if we're or were hyperinsulinemia so if we are insulin resistant or the body's not getting a whole lot of signals at the liver at the adipocyte in the muscle when insulin is low it's still getting some and you and I have talked about how insulin signaling is not entirely driven by absolute insulin levels that things can change at that level but if there are high levels of insulin in the body and things and tissues are not responding to insulin that is physiologic insulin resistance and that is the case in which glucose hi oh that that is that is pathological in resistance right we need better terms thank you that is pathologic insulin resistance and that is it the case that you're describing where the adipocytes are releasing fat and there's all these substrates coming to the liver and gluconeogenesis does appear to be at least somewhat supply driven mm-hmm and the liver as you said is incorrectly gluconeogenesis at ease the liver has its headband on it's got a big fro and it is gluconeogenesis izing like crazy and making glucose from all this substrate and that's what I love that you pointed that out that high levels of glucose in pathologic insulin resistance are predominantly related to just the liver gluconeogenesis I'm like crazy like because of the signaling that's different so these are very different states Yeah right did I say all that right what do you think about that yeah I think that's right