Results After 6 months on the HP diet, 100% of the subjects had remission of their pre-diabetes to normal glucose tolerance, whereas only 33.3% of subjects on the HC diet had remission of their pre-diabetes. The HP diet group exhibited significant improvement in (1) insulin sensitivity (p=0.001), (2) cardiovascular risk factors (p=0.04), (3) inflammatory cytokines (p=0.001), (4) oxidative stress (p=0.001), (5) increased percent lean body mass (p=0.001) compared with the HC diet at 6 months.
A dialog in the 2KetoDudes Facebook group has me thinking more deeply about Gluconeogenesis (GNG). One of the folks there challenged my belief that GNG is a culprit with respect to Protein consumption. The person pointed me to a site which had a couple of articles, but this was the key one to represent his POV (Protein, Gluconeogenesis, and Blood Sugar).
It is the contention of the article that for a Keogenic (LCHF) diet the effects of Gluconeogensis from protein consumption are not significant to blood glucose levels. In fact, the article argues GNG and blood glucose levels are negatively correlated.
We haven’t found any solid evidence to support the idea that excess protein is turned into glucose.
Another interesting quote:
On the input side, blood sugar can come from three sources:
– We can eat carbohydrates, and have sugar enter the blood through digestion.
– We can make glucose out of glycogen (the limited amount of glucose stored in persistent form in the liver). This process is called glycogenolysis.
– Thirdly, we can produce new glucose by GNG.
Here’s where it gets even more interesting:
Even on a keto diet, there is still a substantial proportion of glucose production from glycogenolysis. Ultimately, of course, the glycogen in keto dieters also comes from GNG that happened previously.
Here’s a different article (Effect of long-term dietary protein intake on glucose metabolism in humans).
Glucose-stimulated insulin secretion was increased in the high protein group “516 45 pmol/l vs 305 32,p = 0.012) due to reduced glucose threshold of the endocrine beta cells “4.2 0.5 mmol/l vs 4.9 0.3, p = 0.031). Endogeneous glucose output was increased by 12% “p = 0.009) at 40 pmol/l plasma insulin in the high protein group, but not at higher insulin concentration whereas overall glucose disposal was reduced.
In the present study, we have determined prehepatic insulin production in six normal men throughout a day that included three typical 750-cal meals. Total insulin secretion for the 24 h was 45.4 ∪, secreted as 10.6 ∪ with breakfast, 13.4 ∪ with lunch, and 13.8 ∪ with dinner. The remaining 7.6 ∪ was secreted during the 9 h night at a rate of 0.85 ∪/h.
This may be why the transition down from 20 units a day to 8 units a day has been a more stressful one (with a couple of “higher” Blood Glucose levels) than any of the previous steps. I am now down into the range my body needs as a baseline.
If my LC-HF diet is keeping me from needing mealtime insulin then the remaining rate of approx .85 U/h would mean approx 20 U/day are needed for the background rate. I am far from a normal man (in so many ways) but I have to imagine that these were people substantially smaller than myself. Maybe 2/3 my weight so my requirements should be proportionately higher. Not a biologist so who knows?
An interesting additional factor is the question of gluconeogenesis during fasting. There was a study done on this as well (Quantitative contributions of gluconeogenesis to glucose production during fasting in type 2 diabetes mellitus).
Contributions of gluconeogenesis to glucose production were determined between 14 to 22 hours into a fast in type 2 diabetics (n = 9) and age-weight-matched controls (n = 7); ages, 60.4 ± 2.3 versus 55.6 ± 1.2 years and body mass indices (BMI) 28.6 ± 2.3 versus 26.6 ± 0.8 kg/m2.
The results were interesting.
Thus, gluconeogenesis contributed more to glucose production in the diabetic than control subjects. Production and the contribution of gluconeogenesis declined more in the diabetic subjects during the fast.