Type 2 Ketogenic Diet Question

[bulkbiker]

You can either remain doubtful and cynical and diabetic forever, or try to keep an open mind and help yourself.

Well how kind... thank you I might just do that.. oh wait..!

 

[JohnEGreen]

The answer is NO.
Ketone bodies are being formed from fat inside every cell containing mitochondria (most cells except red blood cells). This mechanism does NOT depend on insulin.

Please read the link I posted above this will show you where you are wrong Insulin has a roll to play in the process

"The rate of ketogenesis depends upon the activity of three enzymes. One is hormone-sensitive lipase (or triglyceride lipase), which is found in peripheral adipocytes. The other two are acetyl CoA carboxylase and 3-hydroxy-3-methylglutaryl-CoA synthase (HMG CoA synthase), which are found in the liver. Hormone-sensitive lipase catalyzes the conversion of triglycerides to diglycerides for further degradation to the free fatty acids (lipolysis) that serve as substrates for ketogenesis. On the other hand, acetyl CoA carboxylase catalyzes the conversion of acetyl CoA to malonyl CoA, increasing the hepatic level of the primary substrate of fatty acid biosynthesis. Malonyl CoA levels vary in the liver directly according to the rate of fatty acid synthesis and inversely with the rate of fatty acid oxidation. Therefore, malonyl CoA plays a pivotal role in the regulation of ketogenesis. Low levels of malonyl CoA stimulate transport of fatty acids into the mitochondria via the carnitine shuttle for oxidation to ketone bodies (see lipolysis and lipogenesis for details). Malonyl CoA normally inhibits carnitine palmitoyltransferase , the enzyme that transports fatty acyl CoA across the mitochondrial membrane.

Hormone-sensitive lipase and acetyl CoA carboxylase, are exquisitely controlled by the level of circulating insulin (which acts to inhibit ketogenesis), and epinephrine and glucagon (which act to stimulate ketogenesis). Thus in fasting or diabetes the high levels of glucagon and low levels of insulin favor ketogenesis through the promotion of lipolysis in the adipocyte and the stimulation of fatty acid oxidation in the liver

Insulin inhibits lipolysis and ketogenesis and stimulates lipogenesis by triggering the inhibitory dephosphorylation of hormone-sensitive lipase and the activating dephosphorylation of acetyl CoA carboxylase. In the adipocytes, dephosphorylation of hormone-sensitive lipase inhibits the breakdown of triglycerides to fatty acids and glycerol, the rate-limiting step in the release of free fatty acids (lipolysis) from the adipocyte. This thereby reduces the amount of substrate that is available to generate acetyl CoA (via fatty acid oxidation) for ketogenesis. In addition, insulin-mediated dephosphorylation of inhibitory sites on hepatic acetyl CoA carboxylase increases the production of malonyl CoA and simultaneously reduces the rate at which fatty acids can enter hepatic mitochondria for oxidation and ketone body production"

 

[AdamJames]

Please read the link I posted above this will show you where you are wrong Insulin has a roll to play in the process

"The rate of ketogenesis depends upon the activity of three enzymes. One is hormone-sensitive lipase (or triglyceride lipase), which is found in peripheral adipocytes. The other two are acetyl CoA carboxylase and 3-hydroxy-3-methylglutaryl-CoA synthase (HMG CoA synthase), which are found in the liver. Hormone-sensitive lipase catalyzes the conversion of triglycerides to diglycerides for further degradation to the free fatty acids (lipolysis) that serve as substrates for ketogenesis. On the other hand, acetyl CoA carboxylase catalyzes the conversion of acetyl CoA to malonyl CoA, increasing the hepatic level of the primary substrate of fatty acid biosynthesis. Malonyl CoA levels vary in the liver directly according to the rate of fatty acid synthesis and inversely with the rate of fatty acid oxidation. Therefore, malonyl CoA plays a pivotal role in the regulation of ketogenesis. Low levels of malonyl CoA stimulate transport of fatty acids into the mitochondria via the carnitine shuttle for oxidation to ketone bodies (see lipolysis and lipogenesis for details). Malonyl CoA normally inhibits carnitine palmitoyltransferase , the enzyme that transports fatty acyl CoA across the mitochondrial membrane.

Hormone-sensitive lipase and acetyl CoA carboxylase, are exquisitely controlled by the level of circulating insulin (which acts to inhibit ketogenesis), and epinephrine and glucagon (which act to stimulate ketogenesis). Thus in fasting or diabetes the high levels of glucagon and low levels of insulin favor ketogenesis through the promotion of lipolysis in the adipocyte and the stimulation of fatty acid oxidation in the liver

Insulin inhibits lipolysis and ketogenesis and stimulates lipogenesis by triggering the inhibitory dephosphorylation of hormone-sensitive lipase and the activating dephosphorylation of acetyl CoA carboxylase. In the adipocytes, dephosphorylation of hormone-sensitive lipase inhibits the breakdown of triglycerides to fatty acids and glycerol, the rate-limiting step in the release of free fatty acids (lipolysis) from the adipocyte. This thereby reduces the amount of substrate that is available to generate acetyl CoA (via fatty acid oxidation) for ketogenesis. In addition, insulin-mediated dephosphorylation of inhibitory sites on hepatic acetyl CoA carboxylase increases the production of malonyl CoA and simultaneously reduces the rate at which fatty acids can enter hepatic mitochondria for oxidation and ketone body production"

I have to admit I'm well out of my depth, but since it was an interesting question, I read through that link to see if I could work out the answer.

I got the impression that insulin regulates the creation of ketones (i.e. its presence inhibits their creation), but has no role in transporting them to the cells for energy.

 

[Lamont D]

No, it's not I have just created my profile today and had to pick either T1 or T2. I hope to change it in near future, sorry to confusu you. I'm diabetes free, so are people I work with (diabetics cured by diet adjustments).

Update: my status has been successfully changed.

Edited by Mod

I hope you have a cure for me!
I have adjusted my diet to be in ketosis continually, to stave off my insulin response.
But I will never be cured, but I am in total control and all my other health issues have improved dramatically because of my being in ketosis.
I do hope, that control does not mean cure!

 

[JohnEGreen]

Insulin is a hormone it transports nothing it triggers the cell membrane to allow glucose to enter the cell, insulin in its self is a control mechanism it merely unlocks the door.