" Both a high fat diet and obesity trigger insulin resistance independently, with a high fat diet contributing to overweight and obesity" :
" High saturated fats in circulation, derived mainly from diets or even from lipolysis of fat depots, lead to fatty acids and glucose competing for uptake and metabolism in tissues. With persistent hyperglycemia, increased saturated FFA induce a glucolipotoxic state that is detrimental to beta cells by increasing oxidative stress, subsequently reducing insulin synthesis and secretion thereby compromising both beta cell structure and function."
Taken from a long scientific article about how beta cells are destroyed by (amongst other things) saturated fat in the bloodstream.
High fat diet modulation of glucose sensing in the beta-cell. https://www.ncbi.nlm.nih.gov/pubmed/17179917
I'm no scientist - but from everything else I have read, what is being stated here seems to be entirely consistent with the shoddy science previously espoused for the fat is bad hypothesis. my comments in red
"Type 2 diabetes is primarily associated with beta-cell failure, insulin resistance and elevated hepatic glucose production.
I believe T2 diabetes is primarily associated with hugely elevated levels of insulin production coming from an inability to process modern foods which cause inflated glucose responses compared to natural foods.
The islet beta-cell is specialized for the synthesis, storage and secretion of insulin. Beta-cell failure is characterized by the inability of the beta-cell to secrete sufficient insulin in response to glucose, which ultimately results in hyperglycemia- the clinical hallmark of Type 2 diabetes.
I believe that beta cell failure is a function of asking it to continue to produce huge levels of insulin because of the resistance that comes from having too much circulating insulin . The clinical hall mark for T2 diabetes is simply wrong. The correct clinical hallmark should be increasing circulating insulin which precedes current actual T2 diagnosis by about 10-15 years.
Impairment in glucose sensing contributes to beta-cell dysfunction. The facilitative glucose transporter, GLUT-2, and glucose phosphorylating enzyme, glucokinase, are key for glucose sensing of the pancreatic beta-cell, the initial event in the pathway for glucose-stimulated insulin secretion.
There is an increase in dietary fat intake, particularly saturated fat, in both the developing and Westernized world, which predisposes individuals to become obese and to potentially develop insulin resistance, beta-cell dysfunction and Type 2 diabetes.
This is pure speculation - there is no particular evidence I have seen that it is dietary fat intake that predisposes one to become obese - instead there is evidence that too much circulating insulin caused by too much refined carbohydrate and industrial seed oils leads to disregulated appetite and obesity - the actual diet involved in doing this is actually not a high " saturated " fat diet - it is a "high carb, high fat" diet comprising lots of refined carbohydrates cooked in lots of industrial seed oils eaten to excess.
A high fat diet is known to reduce both GLUT-2 and glucokinase expression thereby impairing glucose-stimulated insulin secretion. How did they define a " high fat" diet - I
doubt that it was by feeding the subject high quality meats that happen to be high in saturated fat coupled with good quality fresh vegetables.
Furthermore, a high fat diet and specific free fatty acids, induces oxidative stress and apoptosis which reduces beta-cell mass and compromises beta-cell function.
All the stuff I have read suggests that oxidative stress is actually the same thing they are talking about in relation to heart disease - ie the contents of one's blood stream - leading to the fat/ heart hypothesis and the same rubbish about LDL cholesterol . A high fat diet reliably REDUCES triglycerides - ( fat ) in the blood stream
Glucose sensing is the initial event of glucose-stimulated insulin secretion therefore it is imperative to maintain adequate expression levels of GLUT-2 and GK for ensuring normal beta-cell function. The development of pharmaceutical agents that improve glucose-stimulated insulin secretion may replenish expression of these glucose sensing genes after their attenuation by high fat feeding.
Hmm so the response to having too much insulin in circulation is to find drugs that will cause you to secrete even more insulin - nice one. - entirely indicative of the fact that scientists are being blinded by their masters into looking for a pharmaceutical solution to everything as opposed to going back to the root cause ( defined by them as "high fat feeding" and by me as ( high carb, high fat, highly processed food feeding)
Now consider what happens when you adopt a low carb, high fat diet of natural foods thus getting rid of refined carbs and industrial seed oils
Your glucose levels come down, your circulating insulin levels come down. The level of triglycerides ( fat in the blood stream) comes down, your level of HDL - the good cholesterol goes up. Your level of inflammation all over your body comes down,(GGT is a good marker for this) your risk of heart attack comes down. All of these are known and reliably charted in anyone following a proper real foods low carb diet.
In those circumstances - the idea that somehow this process is having a deleterious effect on beta -cell function compared with the positive benefits it is creating on everything else is bizarre and shows how misleading this " science" is .
It is becoming very clear to me that for me personally there are a few basic markers I want to track that indicate my underlying state of metabolic health .
Hba1C - coupled with relatively steady individual glucose readings,
Low fasting insulin
High HDL
Low Triglycerides
Low GGT
I KNOW I can get all of these through a natural foods, low carb diet which includes fatty meat, diary, and fatty fish to taste.
From an obesity standpoint I am looking to get my waist to be less than 50% of my height) ( not quite there yet) all of the other markers are now well into " normal " ranges.
I will take my own personal markers over this type of " scientific" report any day of the week, not least because I have the blood tests that prove it.
D.
