Blood glucose and fat breakdown

#1

I have a question for our science geeks. I have been fasting for 54 hours. I test my bg and it came back 134. My fasting bg has been running less than 100. I remember hearing Dr Fung answer a question once about an unexpected spike in glucose and if I remember correctly his answer was basically yeah it is just fat cells releasing their content. I was wondering if there is any science supporting this explanation or if there is something else going on. I have been working really hard to get my bg down to this level and sure hope I don’t have to spend weeks burning it down again. Thanks for all your geekiness!

2.5 mo. & still not fat adapted, but its ok and here is why
(Doug) #2

I’ve had the same thing, IrishRed. While I don’t have any sure opinion on all the causes, I’m not worried about it. I see it as a sometime side-effect of a process that is enormously beneficial in other ways (and usually, in the end, very beneficial for blood sugar control as well). One reading of 134 - I’d say keep going and keep tracking it. No imminent emergency. My opinion.

It’s fairly complicated, at least at times, how the body regulates blood sugar. Insulin has a lot of name recognition, and there are also Glucagon, Amylin, and the Incretins. As I understand Glucagon, it tells the liver and other tissue like muscle to use stored energy and make glucose (I’m seeing the effects of Glucagon as opposite the other three) - normally in response to declining blood sugar, as one would normally think of occurring during a fast. So, I’m thinking that if one has a little too much Glucagon, that could result in a raised blood glucose number.

#3

Thanks Doug. I was not particularly worried as I know this woe will work slowly but surely. I just find the seemingly random bg spike in the middle of an extended fast odd. It did drop back down into the 90s a few hours later. The body is a wonderfully complicated thing.

#4

I also heard Megan Ramos say that fat cells release glucose when you’re losing weight and wondered what research backs that up. Hmmmm…

#5

Gatita, that is exactly what I am questioning. What is the basis of that assertion.

#6

I did find this research showing glucose goes into fat cells, so is it logical to assume that what goes in must come out?

#7

I’'l try an explanation to the limits of my understanding.

Yes, the glut4 transporters on adipose cells are activated by insulin to allow glucose into the cells. The glucose is then converted into fat through a process called de novo lipogenesis (DNL) which is very similar to what your liver does, but produces a different fatty acid (palmitoleate). When insulin is high, glucose is stored this way and blocked from returning to the bloodstream. When insulin is low enough, the stored fat is allowed back into circulation.

After years of overstuffing a fat cell, and high insulin to keep it from being used, the cell eventually becomes enlarged (hypertrophic) and the glut4 transporter stops working. At this point, fatty acids flow back into the bloodstream and get converted to glucose again. This is when diabetes shows up as inability to control blood glucose levels after years of elevated insulin.

So, it may be possible that some of the gluose in the adipose cell did not go through DNL for whatever reason and remains there as a sugar. But I suspect a lot of the increase and fluctuations are caused by the outflow of fat as insulin decreases on keto or on a fast.

#8

Update:

Thanks to @erdoke for finding a study that confirms there can be glucose, stored in the form of glycogen, in adipose tissue. It is a symptom of inflamed fat cells in obese subjects. Note: this is a mutant mouse study, but I believe [some of] it would also apply to humans.

Transgenic overexpression of PTG in adipose tissue increases glucose flux into the glycogen synthesis pathway, indicating that adipocytes are capable of storing high levels of glycogen. Interestingly, although adipocyte function appeared to be maintained in these animals, leptin, but not adiponectin, protein content in adipose tissue was increased, and the associated hyperleptinemia was independent of fat mass [15]. Further studies showed that upon caloric excess-induced expansion of adipose tissue mass, the elevated levels of glycogen in this model inhibited the mobilization of triglyceride and impeded weight loss following the return to chow feeding [16].

The study goes on to describe adipose glycogen storage in humans.

(Gabor Erdosi) #9

In brief: glucose to DNL is insulin sensitivity, while glucose to glycogen is IR in adipose tissue. I’m not aware of studies showing glucose dumping by fat cells, but I haven’t looked for this kind of data.

#10

Thank you Carol and erdoke!