From the study (K J Acheson Y Schutz T Bessard K Anantharaman J P Flatt E Jéquier. Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. The American Journal of Clinical Nutrition, Volume 48, Issue 2, 1 August 1988, Pages 240–247):
Glycogen storage capacity in man is approximately 15 g/kg body weight and can accommodate a gain of approximately 500 g before net lipid synthesis contributes to increasing body fat mass.
The question then comes up – what happens when you fill up the glycogen stores from carbohydrate consumption? That’s exactly the question that the study asked. And the answer they got was:
When the glycogen stores are saturated, massive intakes of carbohydrate are disposed of by high carbohydrate-oxidation rates and substantial de novo lipid synthesis (150 g lipid/d using approximately 475 g CHO/d) without postabsorptive hyperglycemia.
Some of it burns off (the “high carbohydrate-oxidation rates”) but a lot of it gets stored as fat via DNL (de novo lipogenesis). And the storage efficiency is pretty darned good. 150g of lipids are 1350 calories of fat. The 475g of carbs provides 1900 calories. So the efficiency is 71%.
Without High Blood Sugar Levels
The most amazing part is that all of this happens, per the study “without postabsorptive hyperglycemia”. In other words, the blood sugar doesn’t go high. It all happens within the liver.
The Test Subjects were young and their livers weren’t fat to begin with.
Another study (Increased liver fat and glycogen stores after consumption of high versus low glycaemic index food: A randomized crossover study.
Stephen Bawden PhD Mary Stephenson PhD Yirga Falcone Melanie Lingaya Elisabetta Ciampi PhD Karl Hunter PhD Frances Bligh PhD Jörg Schirra PhD Moira Taylor. 4 September 2016).
Plasma glucose and insulin peak values and area under the curve were significantly greater after the HGI test meal compared with the LGI test meal, as expected. Hepatic glycogen concentrations increased more after the HGI test meal ( P < .05) and peak levels were significantly greater after 7 days of HGI dietary intervention compared with those at the beginning of the intervention ( P < .05). Liver fat fractions increased significantly after the HGI dietary intervention compared with the LGI dietary intervention (two‐way repeated‐measures analysis of variance P ≤ .05).
Compared with an LGI diet, a 1‐week HGI diet increased hepatic fat and glycogen stores. This may have important clinical relevance for dietary interventions in the prevention and management of non‐alcoholic fatty liver disease.
A Third Study
In this paper (Int J Sports Med. 1982 Feb;3(1):22-4. Muscle glycogen storage and its relationship with water. Sherman WM, Plyley MJ, Sharp RL, Van Handel PJ, McAllister RM, Fink WJ, Costill DL.):
This study examined the relationship between muscle glycogen and muscle water content. Exercise dietary manipulations were used to vary skeletal muscle glycogen levels in four groups of rodents: (1) eight animals were sedentary controls (SC); (2) ten animals were treadmill familiarized and allowed to recover 24 h before sacrifice (F); (3) ten animals were treadmill familiarized and exercised to exhaustion (E); (4) ten animals were treadmill familiarized, exercised to exhaustion, and allowed to recover with food and water ad libitum for 72 h (ER).
All animals were sacrificed in a resting state to normalize intracellular, extracellular, and interstitial water compartments; thus, the E group was sacrificed 45 m in following their run. The treatments altered skeletal muscle glycogen to values ranging from 10.0 to 30.2 mumol glucosyl units/g wet tissue weight. Neither muscle triglyceride nor protein levels were affected by the treatments.
Muscle water content expressed as mumol H2O lost/g wet tissue weight or made relative to protein content showed no consistent relationship to the glycogen content.
These data, therefore, do not support the commonly accepted muscle glycogen-to-water ratio of 1.0:2.7 (g:g). Further work is necessary to quantify the exact amount of water that is actually associated with the glycogen complex.
Impressive Fourth Study
From (Eur J Appl Physiol. 2015 Sep;115(9):1919-26. doi: 10.1007/s00421-015-3175-z. Epub 2015 Apr 25. Relationship between muscle water and glycogen recovery after prolonged exercise in the heat in humans. Fernández-Elías VE1, Ortega JF, Nelson RK, Mora-Rodriguez R.):
On two occasions, nine aerobically trained subjects ([Formula: see text] = 54.4 ± 1.05 mL kg(-1) min(-1); mean ± SD) dehydrated 4.6 ± 0.2 % by cycling 150 min at 65 % [Formula: see text] in a hot-dry environment (33 ± 4 °C). One hour after exercise subjects ingested 250 g of carbohydrates in 400 mL of water (REHLOW) or the same syrup plus water to match fluid losses (i.e., 3170 ± 190 mL; REHFULL). Muscle biopsies were obtained before, 1 and 4 h after exercise.
In both trials muscle water decreased from pre-exercise similarly by 13 ± 6 % and muscle glycogen by 44 ± 10 % (P < 0.05). After recovery, glycogen levels were similar in both trials (79 ± 15 and 87 ± 18 g kg(-1) dry muscle; P = 0.20) while muscle water content was higher in REHFULL than in REHLOW (3814 ± 222 vs. 3459 ± 324 g kg(-1) dm, respectively; P < 0.05; ES = 1.06). Despite the insufficient water provided during REHLOW, per each gram of glycogen, 3 g of water was stored in muscle (recovery ratio 1:3) while during REHFULL this ratio was higher (1:17).
Our findings agree with the long held notion that each gram of glycogen is stored in human muscle with at least 3 g of water. Higher ratios are possible (e.g., during REHFULL) likely due to water storage not bound to glycogen.
The following inferences can be drawn from the results:
1. During work, the muscle glycogen falls successively to values approaching zero, and the working capacity decreases when the glycogen store is depleted.
2. The glycogen concentration in resting muscle remains unchanged when other muscle groups in the same subject have been emptied of glycogen by exercise.
3. If glucose is infused continuously during muscular work, the glycogen consumption is significantly lower than when no glucose is administered. The difference is nevertheless small, and the consumption of muscle glycogen is responsible for the greater part of the energy production, even when the blood sugar level is high.
4. The glucose production by the liver increases towards the end of continuous muscular work, but is of relatively small magnitude in comparison to the total carbohydrate metabolism.
Shorter Study Problems
Under standard isocaloric conditions, 42% of the ingested glucose was oxidized over the 5-hour postingestive period. The remaining 58% was essentially stored as glycogen (54%), with very little net de novo lipogenesis (4% of the glucose load).
Net nonoxidative glucose disposal was consequently reduced and represented only 43% of the glucose load. Simultaneously, net glycogen synthesis was reduced and represented only 30% of ingested glucose, whereas net de novo lipogenesis increased by 296% and corresponded to 13% of ingested glucose. There was also a marked increase in fasting and postprandial plasma TG concentrations after carbohydrate overfeeding together with suppressed plasma FFA concentrations. This increase in plasma TGs may be caused by both stimulation of hepatic de novo lipogenesis (18) and a decreased clearance of very-low-density lipoprotein-TGs.
In conclusion, the present data indicate that whole body
de novo lipogenesis after glucose ingestion was markedly
enhanced by a 4-day carbohydrate overfeeding and that the
amount of lipid newly synthesized markedly exceeded the
maximal reported rates for hepatic de novo lipogenesis.
So the useful strategy is to lower the glycogen stores via low carbohydrate diet and exercise. Both of these lower glycogen quickly and can begin to drop the fat in the liver. The fat around the pancreas can then begin to drop and diabetes gets reversed.