Keto Diet, Saturated Fat and Pancreatic Beta Cells?

(Domonic) #1

Hi all. I’m not asking this question to provoke anyone. I have been on the Keto Diet for some time and have had amazing benefits from it. No question about it.

This is a serious question. I have heard and read about studies about how Saturated Fatty Acids do damage to Pancreatic Beta Cells. Is that true or is it a viscous rumour?

This link is a reference to one such study. Just wondering what the Keto community knows about this and whether there’s a counter argument to this? (yes the diet works for me so I’m staying on it but that’s not the point of the question).
https://diabetes.diabetesjournals.org/content/50/1/69

(Michael - When reality fails to meet expectations, the problem is not reality.) #2

A couple of initial comments. With all rodent experiments there are always two big ifs: are the findings directly applicable to humans? and, what chow was used? The experiment got different results using saturated and monounsaturated palmitic fatty acids. What exactly are the potential health consequences of these different results? Do the results apply only to palmitic fatty acid? Are the results applicable to humans or not? Since living animals are not test tubes, we need to know what other nutrients were fed and whether any of them interacted with palmitic fatty acid in either or both forms. Or how the experiment controlled for those possible confounders.

Finally, the study linked is from 2001. Do we know any more since then? Here’s a study from 2017 that may be of interest. Again rodents, so the same questions apply. This one made a distinction between high fat high glucose and high fat low glucose.

https://www.nature.com/articles/s41598-017-16485-0

(bulkbiker) #3

I’m afraid my response is

Are you a rat?

If not then ignore…

if you are then… wow you can read!

The impairment of beta cells is now thought to be due to excess fat build up around the pancreas and liver in humans. By becoming a fat burner this fat is burnt off and insulin functions normalise. This is the basis of both a ketogenic treatment for T2 and the Newcastle Diet starvation method (in fact any starvation method such as Kempeners rice diet etc…) The benefit of keto is that you can eat satiating food and utilise your hormones rather than fight against them (which to me sounds a lot smarter than starving.)

(Bunny) #4

Wow, what is peculiar is they say “autophagy” which I would translate into not eating saturated fat 3 times a day, the human body also makes saturated fat anyway, so what difference would it make?

The saturated fat from a high carb diet could very well do the same?

If people fasted a little bit between meals there would be a lot of thin people and very few obese people.

You can fast too much and do damage and if you fast too little you can do damage?

If we ate like a gastric bypass patient we would all be looking good?

(You've tried everything else; why not try bacon?) #5

It is not true. In fact, a low-carbohydrate, high-fat diet has been shown several times to have the potential to reverse insulin resistance in human beings. Since polyunsaturated fatty acids ingested in quantity can have a systemic inflammatory effect, the healthiest fats are saturated and monounsaturated.

A couple of things to notice in the study you cite: first, it was done on rats, and rats are very hard to get into ketosis, except at the end stages of starvation. In fact, human beings are the only mammal that enters ketosis at all easily. Second, the study was performed on rat islet cells in vitro, and results are often different from what they would be in vivo. Third, what researchers consider a “low-carbohydrate” diet is often what we on these forums would consider a high-carbohydrate diet, and the results could well be confounded by the elevated blood glucose, and not the result of the fat intake at all. In all the rat studies I’ve read about ketogenic diets for rats, the formulation given to the rats was extremely high in glucose.

So it is not entirely clear that the observed results actually apply to the pancreas of a rat eating a low-carbohydrate diet, let alone whether this rat model actually applies to human beings. The most that can be claimed on the basis of this study is that the matter warrants further study.

(Jenna Ericson) #6

I think there is a distinction to made between ingesting saturated fat and having high levels of free fatty acids in your blood. The article says “Apart from hyperglycemia, plasma long-chain free fatty acid levels are often increased in states of insulin resistance, further impairing β-cell—secretory function.” I don’t think that eating more saturated fat necessarily increases pancreatic exposure to saturated fats in the way that the experiment did.

I also found it interesting that elevated glucose levels both induce Beta Cell death and induce proliferation of Beta Cells. This seems to mean there is generally a faster turnover rate of Beta Cells and probably a faster death than proliferation rate.

(Bunny) #7

Just add sugar?

”…Free fatty acids (FFAs) are important to the pancreatic β-cell for its normal function, its capacity to compensate for insulin resistance, and its failure in type 2 diabetes (1–3). Fatty acid (FA) deprivation of islet tissue causes loss of glucose-stimulated insulin secretion (GSIS), a process rapidly reversible by replacement with exogenous FFAs (4). In contrast, elevated FFA supply augments GSIS (5,6); however, if chronically in excess, particularly in association with elevated glucose (7), saturated FFAs can reduce insulin biosynthesis (8) and secretion (3) and induce β-cell apoptosis (2,3,7,9). …” …More

From the short chained fatty acid angle:

Short-chain fatty acids and regulation of pancreatic endocrine secretion in mice

”…The intestinal microbiota has been demonstrated to influence host metabolism, and has been proposed to affect the development of obesity and type 2 diabetes (T2D), possibly through short-chain fatty acids (SCFAs) produced by fermentation of dietary fiber. There are some indications that SCFAs inhibit glucose-stimulated insulin secretion (GSIS) in rodents, but research on this subject is sparse. However, it has been reported that receptors for SCFAs, free fatty acid receptor 2 (FFAR2) and FFAR3 are expressed not only on gut endocrine cells secreting GLP-1 and PYY, but also on pancreatic islet cells. We hypothesized that SCFAs might influence the endocrine secretion from pancreatic islets similar to their effects on the enteroendocrine cells. We studied this using isolated perfused mouse pancreas which responded adequately to changes in glucose and to infusions of arginine. None of the SCFAs, acetate, propionate and butyrate, influenced glucagon secretion, whereas they had weak inhibitory effects on somatostatin and insulin secretion. Infusions of two specific agonists of FFAR2 and FFAR3, CFMB and Compound 4, respectively, did not influence the pancreatic secretion of insulin and glucagon, whereas both induced strong increases in the secretion of somatostatin. In conclusion, the small effects of acetate, propionate and butyrate we observed here may not be physiologically relevant, but the effects of CFMB (core facilitator molecular biology) and Compound 4 (YouTube video below) on somatostatin secretion suggest that it may be possible to manipulate pancreatic secretion pharmacologically with agonists of the FFAR2 and 3 receptors, a finding which deserves further investigation. …” …More

Organic compounds - 4 main types described

Footnotes:

[1] agonists: BIOCHEMISTRY: a substance which initiates a physiological response when combined with a receptor.

[2] ”…Currently, a high fat diet has been considered as one of the causative factors in the decline of β -cell survival and function. The absorption of excess fatty acids can result in an elevated free fatty acid (FFA) level in blood and is worthy of close attention, as the extra FFAs that are not able to be appropriately metabolized can produce many negative effects via multiple pathways in pancreatic β-cells and may lead to β-cell apoptosis. …” …More

(Bob M) #8

One must place this into context: the saturated fatty acid of palmitic acid is the DEVIL. It’s EVIL!! Meanwhile, monounsaturated fatty acids are ANGELIC. Everyone knows this. :grinning:

Seriously, your career will be over if you say palmitic acid is beneficial.

And this is a freaking test tube study.

How much palmitic acid do we have floating around able to get to the pancreas and where does it come from?

(You've tried everything else; why not try bacon?) #9

In fact, it was known in the 1960’s that hyperlipaemia (excessive fat in the blood serum) is the result of excessive carbohydrate in the diet. Dr. Phinney has research to suggest that a low-carbohydrate, high-fat, ketogenic diet promotes fatty acid metabolism, and therefore, the level of fat in the blood is lower, despite the higher fat intake. As a number of researchers have said, “We are not what we eat, we are what our body does with what we eat.”