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.

6 comments:

  1. Fat people are doomed - most of them who are always hungry think about food too much which must increase insulin secretion as well.

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  2. Hi, Galina.

    We're all doomed, really. It's just a matter of whether your demise is at 40-something or 80-something. An "older" heart attack is still a heart attack, but it has a very different meaning at 90 than it does at 50.

    But, interesting about secreting insulin when just thinking about food.

    I've never been obese, and I'm sure I have no chance of it on LCHF. But I do notice that unless I've just eaten, I can whip up a bit of an appetite just thinking about something good (bacon, dark chocolate, etc).

    It's a pity we don't have insulin meters to check such things.

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  3. I still surprised to see the difference a diet AND an eating regiment made in my own behavior. I used to be that person fantasizing about food most of my waking hours back than in my "balanced" diet days. All my life I cook all my food from a scratch mainly because I enjoy all food-related activities. I strongly suspect that a love for cooking and a high culinary creativity are important markers for a hyperinsulemia. My base insulin is on a low border of normal now, but what is going on during my day - I just don't know. My food indifference is quite strong during first part of the day between my coffee with a heavy cream and a first meal. The longer I delay my first normal meal, the less I eat during the day, and after that meal triggers my interest in food even when I feel complitely full. I guess, some people could be having too high insulin response, and they should avoid reading blogs with recipes and food pictures, watching culinary shows, planning complex culinary marvels.
    I don't think I am totally doomed. My dieting activity preserved my health, and I look much better than most people my age, but I am doomed forever to be careful about what I put in my mouth. No, occasional relaxations other people enjoy are complitely out of question for me.

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  4. This is a good experiment for showing that insulin itself causes insulin resistance

    Exposure to excess insulin (glargine) induces type 2 diabetes mellitus in mice fed on a chow diet.
    Xuefeng Yang, Shuang Mei, Haihua Gu, Huailan Guo, Longying Zha, Junwei Cai, Xuefeng Li, Zhenqi Liu and Wenhong Cao.
    Journal of Endocrinology (2014) 221, 469–480

    https://www.dropbox.com/s/ecf60aemmwr0sow/Insulin%20T2DM%20mice%20Yang%202014.pdf?dl=0

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