Tuesday, 16 August 2016

Insulin Resistance shenanigans

IR is such a bogeyman. I am quite certain it is an effect of 99% of the things it is associated with, not a cause. Glucose disposal is usually the main proxy used to state IR.

Anyway, I thought this was interesting

A subcutaneous adipose tissue-liver signalling axis controls hepatic gluconeogenesis.

As some people may be aware, a big hallmark and feature of T2D and IR is the failure of insulin to suppress hepatic glucose output during glucose ingestion. In this study they are saying subQ fat can help suppress hepatic glucose output by releasing IL6 which is downstream of cAMP in adipocytes.

We also have this study

Insulin disrupts beta-adrenergic signalling to protein kinase A in adipocytes.

So putting 2 and 2 together, what should we do to attack the IR causing us to be fat sick and diabetic?
How can we attack IR ?

By lowering insulin secretion!

it seems plausible that high ( and chronic ) insulin secretion activates PDE3B in adipocytes which degrades cAMP, causing catecholamine resistance in adipcoytes which makes you fat, but also IR through reduced IL6 levels and increased hepatic glucose output.

In theory lowering your insulin secretion should lower PDE3B in adipocytes and increase cAMP there, making you slimmer and lowering blood sugar.

This is why I think IR is the bogeyman, it is insulin secretion causing the problems. And the last thing youll probably want to do is inject yourself with more insulin to lower your blood glucose levels.