PEPCK

(I don't think I'm yet done with this post, but I'll just throw it up now in case I forget.)

PEPCK is important for glucose homeostasis and positively affects gluconeogenesis. Greater expression correlates with greater endogenous glucose production (EGP), and one of its many effects can be symptoms which resemble diabetes type II.

It seems there is a positive association between a high-fat-ketogenic diet and PEPCK activity, however, the calories must not be restricted, and it looks like the more excessive the intake of LCTs are, the greater the PEPCK activity.

The consumption of high fat diets led to a 1.5-fold increase of PEPCK in liver


PEPCK mice create energy chiefly by use of fatty acids rather than glucose.

This looks like the definitive site for learning more about the functions of PEPCK with respect to a ketogenic diet. excerpt: "... even if hepatic gluconeogenesis is abolished, normal blood glucose levels can be maintained in rats. "

Here's a study - that hasn't been cited by any other studies - where the results show

• less rapid weight gain 
• greater visceral lipogenesis
• body fat ratio 2.4x higher
• accompanying glucose intolerance

with ketogenic rats vs control rats. Don't overlook the phrase "weight gain" here. The abstract doesn't explicitly say this - the rats were overfed (but why?). Also the ratios nor any other details beyond "ketogenic" and "control" are available in this abstract. You'd have to purchase the full-text. These results do look consistent with my own recent past experience of overfeeding on a ketogenic diet.

The results are inconsistent with

A high-fat, ketogenic diet induces a unique metabolic state in mice

C57BL/6 mice (not Wistar Rats) on a ketogenic diet (KD), a high-fat diet (HF) like the standard american diet (SAD), low-fat chow diet, and a calorie-restricted diet (CR) diet were compared.

KD increased expression of genes in fatty acid oxidation pathways and reduction in lipid synthesis pathways.
"Animals made obese on HF and transitioned to KD lost all excess body weight, improved glucose tolerance, and increased energy expenditure"

KD consumed at least as many calories as mice fed a high-fat (HF) diet, but KD failed to gain weight despite high calories.

Compared to standard chow, KD lost weight and then stabilized at a lower weight than chow-fed animals in a pattern that was the same as that seen calorie-restricted mice.

Insulin levels were extremely low compared with both animals fed chow and animals fed high-fat diet. Furthermore, despite the consumption of saturated fat, serum lipids did not increase.

I could go on, but that's just copy-paste. Better to read the full text.

I made some additions to my last post.