[foxl]

I recall a somewhat heated discussion in which it was decided that gluconeogenesis strictly involved protein as a substrate ...

Nope. Here is information to the contrary, for those who were involved ... Sorry folks, fat, too, is involved. Enjoy:

High-fat feeding has been shown to cause hepatic insulin resistance. The aims of this study were to investigate the biochemical steps responsible for enhanced gluconeogenesis as a result of increased dietary fat intake and the site or sites at which the antihyperglycemic agent metformin acts to inhibit this process. Male Hooded Wistar rats were fed either a standard chow diet (5% fat by weight) or a high-fat diet (60% fat by weight) for 14 days with or without metformin. Total endogenous glucose production and gluconeogenesis were determined using [6-3H]glucose and [U-14C]alanine, respectively. Gluconeogenic enzyme activity and, where appropriate, protein and mRNA levels were measured in liver tissues. The high-fat diet increased endogenous glucose production (21.9 ± 4.4 vs. 32.2 ± 4.8 µmol · kg1 · min1, P < 0.05) and alanine gluconeogenesis (4.5 ± 0.9 vs. 9.6 ± 1.9 µmol · kg1 · min1, P < 0.05). Metformin reduced both endogenous glucose production (32.2 ± 4.8 vs. 16.1 ± 2.1 µmol · kg1 · min1, P < 0.05) and alanine gluconeogenesis (9.6 ± 1.9 vs. 4.7 ± 0.8 µmol · kg1 · min1, P < 0.05) after high-fat feeding. These changes were reflected in liver fructose-1,6-bisphosphatase protein levels (4.5 ± 0.9 vs. 9.6 ± 1.9 arbitrary units, P < 0.05 chow vs. high-fat feeding; 9.5 ± 1.9 vs. 4.7 ± 0.8 arbitrary units, P < 0.05 high fat fed in the absence vs. presence of metformin) but not in changes to the activity of other gluconeogenic enzymes. There was a significant positive correlation between alanine gluconeogenesis and fructose-1,6-bisphosphatase protein levels (r = 0.56, P < 0.05). Therefore, excess supply of dietary fat stimulates alanine gluconeogenesis via an increase in fructose-1,6-bisphosphatase protein levels. Metformin predominantly inhibits alanine gluconeogenesis by preventing the fat-induced changes in fructose-1,6-bisphosphatase levels.

endogenous glucose production; fructose-1,6-bisphosphatase; fat feeding; hepatic insulin resistance

[yannah]

I have no idea what most of that means. but I think I get the point.

Here is what I know. fat doesn't seems to be interfering with my wieght loss. although I hestitate to say I am high fat with diet. If I put butter on on my low carb bread, I am golden, if not I spike a bit. Bs is under good control with less than half the meds I started with.

lipid profile went from high to normal and I am off my statin.

that is what I know. but again, I don't know what high fat is, but I doubt I am. I am probably moderate fat.

[foxl]

I confess I do not know either ... but I found it interesting that there is much out there on how high fat diets cause increased gluconeogenesis.

biochemistry... oh, yeah, THAT'S why I am science dropout!

[xMenace]

Protein - 58%
Fat - 10%

How Much Protein?

[yannah]

at the start of this I read about a million studies and articles.

burned frickin out on it.

my conclusion is that fat - not high fat- just some fat - is good. carbs not so much. we can get all the carbs we need eating vegatbles and chicken or whatever. but alot of protein, probably not good either. although not as evil as the carb fest we are currently in here. so, I think the foods we can grow in the garden in Ohio are probably good staple foods. which is prolly why the higher power made sure we could grwo them in the garden in Ohio. you know, like a cucumber. these are what I mainly eat. cabbage. nothing to fancy or thought out.

one of x menaces videos stressed shopping the perimeter of the grocery store. I think that is about as complicated as it needs to be.

I may eat too much high fat dairy. my fat does not come from meat. I don't eat that much meat. dairy is carby unless it is buku loaded with fat.

this is what I have concluded basically. and oh, I have been forced to admit that aeorbic excersize is necassary.

[foxl]

To my amazement, even the ADA website considers the verdict still out on higher levels of protein ... unless there is evidence of renal damage, of course.

Fat ... almost eveyone is down on HIGH fat.

And we mostly have 2 macronutrients left to us ... fat or protein.

[yannah]

Originally Posted by xMenace

Protein - 58%
Fat - 10%

How Much Protein?

I did read this.

thank you.

and I forgot to metnion that the calorie restriction thing., for T2,s....all for it.

[REDLAN]

I think you need to bear in mind that this study is done in rats.

There is also something you need to understand about nutrition in rodents. They do not tolerate high fat diets very well. Typically they eat 8% or less fat, and usually very high carbs. The researchers know that high fat diets are harmful because infant rats fed significantly more than this i.e. above 12% do not thrive, and end up smaller in size and weight than normally fed rats. Feeding rats high fat diets also will give them type 2 diabetes.

in this study they were fed 60% fat - not sure of the relevance to humans who do tolerate high fat diets very well.

what this bit means...

excess supply of dietary fat stimulates alanine gluconeogenesis via an increase in fructose-1,6-bisphosphatase protein levels

fructose-1,6-bisphosphatase is a key enzyme in gluconeogenesis - it uses pyruvate as a substrate - some amino acids can be deaminated and broken down into pyruvate. The other substrate is glycerol derived from triglycerides.

so what they are basically saying is that gluconeogenesis increases because a key enzyme in the pathway increases in concentration. Presumably to deal with the increased glycerol from triglyceride breakdown

Note if the substrate is mostly glycerol, then this may not necessarily cause ketogenesis - it is pyruvate being used for gluconeogenesis and decreasing the supply of oxaloactetate that triggers ketogenesis. Fat supply to the liver regulates the rate of ketogenesis - the more fat there is the faster it goes.

[Real4]

Originally Posted by foxl

Male Hooded Wistar rats were fed either a standard chow diet (5% fat by weight) or a high-fat diet (60% fat by weight) for 14 days with or without metformin.

I'd suspect that not even the poster actually understood the article. One thing that jumps at me is that the overall nutrition of both diets is NOT specified. That leaves many holes as to what is actually happening; the result they proclaim is by no means what they say they have proved.

Many of you remember reading about "hungry rats" and the various experiments they were put through - usually in an attempt to prove something or other reductionist about human behavior. Do you realize that by "hungry rate" they meant a rat that had been starved to less than half of normal body weight?
Might not that fact influence your understanding of they were doing with the, in fact, tortured rats, and what the results meant?

[foxl]

Originally Posted by Real4

I'd suspect that not even the poster actually understood the article.

Might not that fact influence your understanding of they were doing with the, in fact, tortured rats, and what the results meant?

I think I made that clear, in this thread, no? I just thought it was interesting as it indicated something that was argued in another thread.

Stress is a factor controlled for in most animal studies, BTW. THAT MUCH I understand. And I do not see evidence of "torture," taking place ... we have IACUCs to prevent that, FYI. That remark smacks of a certain radicalism.

[PERKDOUG]

I read about this rat experiment and it raised a slight red flag in my mind about fat in the human diet. I leaned back in my chair and for some reason a picture of a man in a caribou fur parka and pants appeared. He was carrying a harpoon and walking on an ice flow. I understood, smiled and the red flag disappeared.

[foxl]

Originally Posted by PERKDOUG

I read about this rat experiment and it raised a slight red flag in my mind about fat in the human diet. I leaned back in my chair and for some reason a picture of a man in a caribou fur parka and pants appeared. He was carrying a harpoon and walking on an ice flow. I understood, smiled and the red flag disappeared.

Yes... and where is he getting his VITAMIN C?

[PERKDOUG]

Originally Posted by foxl

Yes... and where is he getting his VITAMIN C?

From the organ meats (liver, stomach contents ect.) of the animals he kills and eats. Also an all meat diet requires much less vitamin C than the standard balanced diet. The metabolism of carbs requires much more vitamin C. Inuits did not suffer from scurvy. Arctic Exporers trying to live off of Hardtack and canned food suffered and died of scurvy. Also, many Inuits had a few berries stored for winter they harvested the previous summer.

[REDLAN]

errata...

the alanine gluconeogenesis part above - means making glucose from amino acids, and is most likely derived from dietary protein - which has the potential for ketogenesis. If you check about half the increase in gluconeogenesis is derived from alanine.

PERKDOUG wrote
From the organ meats (liver, stomach contents ect.) of the animals he kills and eats. Also an all meat diet requires much less vitamin C than the standard balanced diet. The metabolism of carbs requires much more vitamin C. Inuits did not suffer from scurvy. Arctic Exporers trying to live off of Hardtack and canned food suffered and died of scurvy. Also, many Inuits had a few berries stored for winter they harvested the previous summer.

muktuk - raw whale skin. Eskimos eat a highly specialised diet, raw whale skin is high in vitamin C. I believe whale stomach's are also high in vitamin C too. If you eat an all meat derived diet, without ingesting raw organ meats - particularly adrenal glands/kidneys, or parts of the brain, then you too will develop scurvy.

Why is Vit C used in glucose metabolism?

It has role in carbohydrate metabolism??

According to Wiki it's main role is in preventing oxidative stress Another article I read said that it's only proven essential function is in stabilising collagen, which in deficiency causes scurvy. We have synthesis of carnitine, and involved in neurotransmitter synthesis.

Vitamin C is synthesised (in non-primates) utilising glucose, and it uses glucose transporters to cross the cell wall, but I can't find how vitamin C use is increased by glucose metabolism.

[foxl]

Originally Posted by REDLAN

errata...

the alanine gluconeogenesis part above - means making glucose from amino acids, and is most likely derived from dietary protein - which has the potential for ketogenesis. If you check about half the increase in gluconeogenesis is derived from alanine.



muktuk - raw whale skin. Eskimos eat a highly specialised diet, raw whale skin is high in vitamin C. I believe whale stomach's are also high in vitamin C too. If you eat an all meat derived diet, without ingesting raw organ meats - particularly adrenal glands/kidneys, or parts of the brain, then you too will develop scurvy.

Why is Vit C used in glucose metabolism?

It has role in carbohydrate metabolism??

According to Wiki it's main role is in preventing oxidative stress Another article I read said that it's only proven essential function is in stabilising collagen, which in deficiency causes scurvy. We have synthesis of carnitine, and involved in neurotransmitter synthesis.

Vitamin C is synthesised (in non-primates) utilising glucose, and it uses glucose transporters to cross the cell wall, but I can't find how vitamin C use is increased by glucose metabolism.

Adrenals, apart from being toxic due to high hormone concentration, are a terrific source of Vit. C. I worked on a study that entailed measuring ascorbate in kidneys exposed to various conditions.

And yes that IS it's only proven function as I recall it -- stabilizing collagen. We also compared collagen fibers in wound healing, on SEM.

Oh and as far as its role in glucose metabolism ... ascorbate glucose metabolism - Google Search It is "thought to" play a role ...