Can someone explain to me the difference between the de novo lipogenesis that occurs in the liver and “extrahepatic DNL”? I don’t understand what is meant by this term and when this process occurs.
Also, does anyone know what the regular rate of DNL is for a non-diabetic person on maintanance calories. Dr. Mercola says 40% of carbs (non-excess) turn into fat for the insulin SENSITIVE! Where did he get this info?
Thanks,
Brian
Review the “issue of de novo” thread for related info
I just reviewed it. Damn, I forgot what a great thread that was. But I didn’t spot any references/allusions to “extrahepatic DNL” or DNL rates on a non-ketogenic maintenance diet. Also, the thread deals with carb loads/refeeds in a ketogenic situation, not regular carb consumption in a maintanence or hypercaloric.
One thing that might bear consideration in keeping the rate of DNL low when bulking bulking on 33-50% carbs is carb cycling. Chris Aceto, I know, lowers carbs (and increases protein) for 3 days every 3 weeks. Is this long enough to keep DNL rate constant?
Instead of worrying about if carbs are converted into fat or not, why not look at overall fat balance?
Just based on semantics, my guess is that extrahepatic dnl takes place outside the liver and dnl takes place inside the liver.
No clue about the other part.
I gathered that as well, JW, but I where outside the liver, and when? Does “extrahepatic DNL” mean carbs that have been deposited in fat cells, having been unused, turned into fat? That’s just a wild guess.
Varying the fat intake…hmmm…I guess because the glycogen stores would still be moving toward being topped off. (In fact, I don’t know why Aceto says 3 lower carb days and up the protein, since much of that will be converted to glucose to fill the liver.)
It seems that “extrahepatic DNL” usually means “adipose DNL”, i.e. glucose in fat cells turning to fat. I found some good studies, some new like this one:
"Am J Clin Nutr. 2003 Jan;77(1):43-50.
Hepatic de novo lipogenesis in normoinsulinemic and hyperinsulinemic subjects consuming high-fat, low-carbohydrate and low-fat, high-carbohydrate isoenergetic diets.
Schwarz JM, Linfoot P, Dare D, Aghajanian K.
BACKGROUND: Hypertriglyceridemia is associated with increased risk of cardiovascular disease. Until recently, the importance of hepatic de novo lipogenesis (DNL) in contributing to hypertriglyceridemia was difficult to assess because of methodologic limitations. OBJECTIVE: We evaluated the extent of the contribution by DNL to different conditions associated with hypertriglyceridemia. DESIGN: After 5 d of an isoenergetic high-fat, low-carbohydrate diet, fasting DNL was measured in normoinsulinemic (<or= 85 pmol/L) lean (n = 9) and obese (n = 6) and hyperinsulinemic (>or= 115 pmol/L) obese (n = 8) subjects. Fasting DNL was measured after a low-fat, high-carbohydrate diet in normoinsulinemic lean (n = 5) and hyperinsulinemic obese (n = 5) subjects. Mass isotopomer distribution analysis was used to measure the fraction of newly synthesized fatty acids in VLDL-triacylglycerol. RESULTS: With the high-fat, low-carbohydrate diet, hyperinsulinemic obese subjects had a 3.7-5.3-fold higher fractional DNL (8.5 +/- 0.7%) than did normoinsulinemic lean (1.6 +/- 0.5%) or obese (2.3 +/- 0.3%) subjects. With the low-fat, high-carbohydrate diet, normoinsulinemic lean and hyperinsulinemic obese subjects had similarly high fractional DNL (13 +/- 5.1% and 12.8 +/- 1.4%, respectively). Compared with baseline, consumption of the high-fat, low-carbohydrate diet did not affect triacylglycerol concentrations. However, after the low-fat, high-carbohydrate diet, triacylglycerols increased significantly and DNL was 5-6-fold higher than in normoinsulinemic subjects consuming a high-fat diet. The increase in triacylglycerol after the low-fat, high-carbohydrate diet was correlated with fractional DNL (P < 0.01), indicating that subjects with high DNL had the greatest increase in triacylglycerols. CONCLUSIONS: These results support the concept that both hyperinsulinemia and a low-fat diet increase DNL, and that DNL contributes to hypertriglyceridemia."
And this was the title of an interesting, and very complicated, review study: “Disordered Fat Storage and Mobilization in the Pathogenesis of Insulin Resistance and Type 2 Diabetes” It explores the complexities and un-answered questions of the relationship between fatty acid flux and insulin resistance.