Can you explain this ^^^ by what mechanism does this work? Any studies (animal or human) that back this claim or is this just "bro knowledge"?
The bro science that "tren chews through carbs" is mediated by tren's reducing PPARγ mRNA expression. Some evidence (I believe you are familiar already with this study? This is how it can be applied):
[159] Daniel G. Donner, Grace E. Elliott, Belinda R. Beck, Andrew C. Bulmer, Alfred K. Lam, John P. Headrick, Eugene F. Du Toit, Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome, Endocrinology, Volume 157, Issue 1, 1 January 2016, Pages 368–381,
**broken link removed**
"... only TREN treatment significantly reduced HOMA-IR values..."
For recollection, HOMA-IR is defined as the fasting serum insulin (μU/mL) * fasting plasma glucose (mmol/L) / 22.5.
TBA+E2 decreased PPARγ (and SCD) mRNA expression during increased feeding [55]. Recall that PPARγ controls formation of new fat cells, FA uptake and storage, therefore insulin sensitivity.
[55] Chung, K. Y., Baxa, T. J., Parr, S. L., Luqué, L. D., & Johnson, B. J. (2012). Administration of estradiol, trenbolone acetate, and trenbolone acetate/estradiol implants alters adipogenic and myogenic gene expression in bovine skeletal muscle1. Journal of Animal Science, 90(5), 1421–1427. doi:10.2527/jas.2010-3496
There's good data on methyltrieonolone substantially reducing serum glucose concentrations to the tune of 43%... I'd reckon tren is comparable qualitatively in this regard.
[150] Didebulidze, N. A., Kakabadze, M. S., Gordadze, N. G., Latsabidze, I. N., Kordzaya, M. E., & Sikharulidze, I. T. (2015). Correction of Hormonal and Metabolic Disorders in Male Rats with Developing Experimental Diabetes. Bulletin of Experimental Biology and Medicine, 159(1), 20–23. doi:10.1007/s10517-015-2879-8