|Image 1: Steaming would be the preferable |
cooking method to preserve all the good
ingredients in your vegetables.
(image from Wikipedia)
In a placebo controlled rodent study (Chang. 2011), Chang et al. fed a group of eighteen initially normal-weight male mice the standard high fat diet (of which I am not getting tired to say that it is hypercaloric and by far not as low in carbohydrates as one might expect, cf. figure 1) on which millions of laboratory rats before them have become just as fat and insulin resistant as their fast-food loving mammalian relative, homo sapiens.
|Figure 1: Components of basal and high fat chow in g/kg|
(data adapted from Chang. 2011)
[c]ompared with the HF group, the HFI group had improved glucose tolerance, a higher serum adiponectinserum glucose, triacylglycerol, insulin, and leptin concentrations concentration, lower , and less F4/80 expression in epididymal adipose tissue (P < 0.001). Furthermore, I3C treatment decreased acetyl coenzyme A carboxylase mRNA expression [ACC] (P < 0.05) and increased peroxisome proliferator-activated receptor-γ protein expression (P < 0.05) in epididymal adipose tissue of DIO [diet induced obese] mice.With F4/80 being a marker of macrophage infiltration or, in other words, inflammation of adipose tissue, these findings suggest that indole-3-carbinol improves resistance to (high fat) overfeeding by three closely related mechanisms:
- Indole-3-carbinol decreases adipose tissue inflammation (effects on F4/80) and thus prevents insulin resistance
- by preventing insulin resistance, I3C prevents the development of full blown diabetes, keeps "normal" blood glucose levels and (thus) reduces the production of triglycerides
- with high triglyceride levels, on the other hand, being associated with leptin resistance / lower leptin expression, I3C lastly enhances the expression / activity of leptin, which is intricately tied to the downregulation of the lipogenic (promoting fat storage) enzyme acetyl coenzyme A carboxylase (ACC) and the increased expression of the lipolytic ppar-gamma pathway.