Tuesday, 8 January 2013

Random papers on Insulin and FFA

im feeling very cba today, not gonna write anything comprehensive.

The Taubes talk that sidereal linked to sent me on a pubmed crusade and I found some interesting papers im just gonna link here and drop some short thoughts,

Dose-dependent effect of insulin on plasma free fatty acid turnover and oxidation in humans.

If anyone can link the full text of this paper I would very grateful. This is the paper where in the talk, Taubes shows how FFA turnover is strongly activated below a certain insulin threshold.

Role of free fatty acids and insulin in determining free fatty acid and lipid oxidation in man.

Insulin inhibits net lipid oxidation. Nothing new, but I will read the full paper later.

Insulin causes endothelial dysfunction in humans: sites and mechanisms.

Does insulin cause atherosclerosis?

Modulation of the hepatic malonyl-CoA-carnitine palmitoyltransferase 1A partnership creates a metabolic switch allowing oxidation of de novo fatty acids.

Im not really interested in this study but the stuff in the introduction is relevant. Glucose and insulin inhibit liver fatty acid oxidation, and as I blogged on previously inhibition of liver fat oxidation increases appetite via vagal nerve stimulation ( see Hepatic Oxidation Theory in the literature ).

This is why grazing on carbohydrates is such a vicious cycle, small quantities of carbs inhibit liver fat oxidation stimulating appetite but if you only eat a small portion of food you wont secrete enough incretins to offset that increase in appetite.

I think this is also a prime reason mice get fat on "high-fat diets" ( apart from peter's hypothalamic injury idea ), because usually, they are given Ad Libitum access to the food and tend to graze on it throughout the day, the small amount of carbs in this high-fat diet immediately inhibits liver fat oxidation, so all that fat they are eating is not oxidized and is instead packaged up as triglycerides/cholesterol and exported from the liver.

As demonstrated in the time-restricted feeding study, if you dont give the mice ad libitum access to the food, and make them do some intermittent fasting, their PPAR(alpah) shoots up indicative of increased fat oxidation, which is what you want on a high-fat diet.

BTW im sure animals dont have access to food Ad Libitum in nature, they get sick on such a protocol because there has been no evolutionary selective pressure to adapt to Ad Libitum food access.

Bottom line, if your gonna eat carbs, you gotta get some Intermittent fasting in your protocol.

Increased secretion of very low density lipoprotein triglyceride following inhibition of long chain fatty acid oxidation in isolated rat liver.

Increased secretion of triglyceride and cholesterol following inhibition of long-chain fatty acid oxidation in rat liver.

How do we inhibit liver fat oxidation? I just told you above, you eat carbs and spike insulin.


  1. "if your gonna eat carbs, you gotta get some Intermittent fasting in your protocol", unless of course, you have adrenal issues and then it all falls apart and it describes ME. I honestly don't know how all these people do it. Dr. K says no IF when leptin resistant. Whatever people think about whether leptin resistance exists, he is the only one in the (ex)paleosphere who is putting the brakes on IF.

    1. 16/8 should be do-able by the majority, either way, I recommend breakfast skipping. but if you are gonna eat breakfast, definitely make sure its a lowcarb one.

  2. I have a pdf of the insulin paper you requested, but have no idea how to post a link to it. Email?

    1. email me please kindke55@gmail.com


    2. Kindke, if you wouldn't mind sending it on, thanks a mil.