In the comments of SCD1 CAUSES Humans to Store Fat, David N posted a link to a paper​​1​ that I referenced in The SCD1 Theory of Obesity Part Two where liver fat accumulation and insulin resistance in rats fed a high fructose diet were prevented by supplementing with sterculia oil. I hadn’t looked at the paper in awhile, but it’s very interesting!
Sterculia Oil Prevents Insulin Resistance, Visceral Fat and Fatty Liver in Fructose-fed Rats
In the paper they gave rats either standard rat chow plus water or rat chow plus water containing 30% fructose as the sole source of drinking water for 8 weeks. Another group of rats got regular rat chow, fructose in the drinking water and 0.5% of their diet as sterculia oil. Some of the results are quite striking. (HOMA-IR is a number that represents overall insulin resistance. A higher number indicates MORE insulin resistance.)
| Control | Fructose | Fructose + SO | |
| HOMA-IR | 1.6 | 2.2 | 1.4 |
| Triglycerides | 97 | 203 | 65 |
| Liver Weight (g) | 12.5 | 14.6 | 12.4 |
| Visceral Fat (g) | 3.2 | 5.4 | 3.9 |
Sterculia Oil causes Substitution of PUFA with Saturated Fats and Stearic Acid
SCD1 converts saturated 18-Carbon stearic acid into monounsaturated oleic acid and it converts saturated 16-Carbon palmitic acid into the monounsaturated palmitoleic acid. The ratio of oleic acid to stearic acid is known as the Desaturase Index (DI18). The ratio of palmitoleic to palmitic is the OTHER Desaturase Index (DI16). Both DI16 and DI18 reflect the activity of SCD1, which sterculia oil inhibits. Look at the changes in fat composition in the rats:
| Control | Fructose | Fructose + SO | |
| Palmitic Acid | 21.3 | 23.7 | 26.7 |
| Palmitoleic Acid | 5 | 9.4 | 3.8 |
| Stearic Acid | 8.4 | 6.3 | 14.2 |
| Oleic Acid | 24 | 32 | 29 |
| Total Saturated | 33 | 33 | 46 |
| Total Monounsaturated | 38 | 53 | 40 |
| Total PUFA | 27 | 12.3 | 12.4 |
| DI18 | 2.9 | 5.1 | 2.0 |
| DI16 | 0.24 | 0.4 | 0.14 |
These tables show some very important points:
- Consumption of large amounts of fructose leads to a torpid metabolism characterized by high levels of SCD1 (high DI18 and DI16). Along with this comes accumulation of visceral and liver fat, and insulin resistance.
- Sterculia Oil effectively blocks SCD1 – as demonstrated by the low DI compared to fructose fed mice – and prevents torpor, liver fat accumulation and insulin resistance.
- Fructose feeding leads to accumulation of monounsaturated fats at the expense of PUFA (this is torpor – high expression of the PPAR gamma/ELOVL6/SCD1 group of lipogenic or “fat making” genes); Fructose plus sterculia oil leads to accumulation of saturated fat at the expense of PUFA (compared to the control) and MUFA (compared to the normal fructose fed rats)
- Stearic acid is particularly enhanced in the sterculia oil fed Vs. the fructose fed mice
What Might This Mean For Humans
I suspect that many modern humans have a torpid metabolism. I suspect that linoleic acid consumption from vegetable oils, poultry and commercial pork combined with sugar was the trigger that got us into torpor. I suspect that torpor is causing a lot of our metabolic problems, including insulin resistance and obesity.
Using sterculia oil to break the positive feedback loop of “lipogenic genes leading to lots of MUFA leading to higher expression of lipogenic genes” prevents rats from getting into fructose induced torpor.
Can a human get back out of torpor by minimizing linoleic acid consumption, throttling back on sugar and blocking the positive feedback loop of lipogenic genes? Time will tell.
How long will it take? Probably a lot longer than 8 weeks, unfortunately.
- 1.RamÃrez-Higuera A, Peña-Montes C, Herrera-Meza S, Mendoza-López R, Valerio-Alfaro G, Oliart-Ros RM. Preventive Action of Sterculic Oil on Metabolic Syndrome Development on a Fructose-Induced Rat Model. Journal of Medicinal Food. Published online March 1, 2020:305-311. doi:10.1089/jmf.2019.0177
Would it be similar with other sugars or is fructose unique in the effect?
Experimental method in this research used composition of fats in crushed adipocytes. How does those measures correspond to the more indirect erythrocyte membrane numbers?
MRI spectroscopy of body fat in any compartment could e analyzed in humans without biopsy.
Brad:
Thanks for all this heavy lifting. I was having a real hard time choking down the Dobromylsky work and you got me over the hump.
My comment is pertaining to Berberine which you have pointed out paves the way for Sterculia via PPAR action.
A conflict I am reflecting on is the observation that Berberine is a complex 1 inhibitor and has been demonstrated to lower ROS at that level.
I appreciate that there are a lot of balls in the air and that many of these molecules have multiple actions. Part of the answer to this might come from your experience so far using Berberine at 3 grams for a while now I expect.
I am in the midst of a fairly intensive look at Berberine and would like to hope I can fit it in to my nutritional plan.
Bob Minty
Actually, I’ve moved away from berberine and am now using 12mg astaxanthin – great stuff! Post coming – hopefully tomorrow.
Loving your stuff Brad.
Purchased a few bottle of Sterculia Oil. Do you have a preference or recommendation on when to take it? I am doing OMAD and attempting to determine when it would most effective to consume. Thanks
I would take it with the meal.