|Image 1: Should HE take HER estrogen birth control pills? Or should even she abstain from any exogenous estradiol? |
In their study a group of scientists from the Chiang Mai University in Thailand investigated the effects of 50µg/kg subcutaneously injected estrogen for 30 days on the negative impact a "high fat" (I am not tiring of repeating myself that this diet is not only high (60%) in fat and carbohydrates and has 33% more calories on a gram per gram base) had on a group of 40 male and female Wistar rats (Pratchaylsakul. 2011), to test the hypothesis that
the administration of estrogen in both male and female rats can reverse the impairment ofAnd as in every good study, W. Pratchayasakul et al. were able to disprove their hypothesis - at least partly. While the desired effects on neuronal insulin signaling did occur in the female mice, similar changes could not be observed in their male peers.
both insulin-induced LTD [in other words: neuronal insulin resistance] in the hippocampus and neuronal insulin signaling caused by a 12-week HF diet consumption.
|Figure 1: Changes in plasma (pg/ml) and brain (pg/mg) estrogen levels upon administration of 50µg/kg 1 to 40 male and 40 female on different dietary regimens for 30 days (data based on Pratchaylsakul. 2011)|
|Figure 2: Relative improvements in glucose and fatty acid metabolism in rats on a high fat diet after administration of 70µg/kg 17-β estradiol (data calculated based on Pratchaylsakul. 2011)|
|Figure 3: Modularory effects of 70µg/kg 17-β estradiol on increases in body weight and visceral fat mass in HFD fed rats compared to rats receiving a normal diet (data calculated based on Pratchaylsakul. 2011)|
|Illustration 1: Damaged muscle tissue will recruit quiescent satellite cells to regenerate the myofiber (img. Scime 2009)|
Now, more importantly, estrogen will also enhance 24 and 72 hours post-exercise muscle satellite cell activation and proliferation (in overiectomized rats, Enns. 2010), which is actually counterintuitive, because estrogen also blocks macrophage infiltration, which has been implicated in satellite cell activation and muscle repair, as well. The beneficial effects on estrogen on satellite cell activation is however mediated directly via estrogen receptors on skeletal muscle (Igbal .2008). As possible underlying mechanisms, Enns et al. list
- insulin-like growth factor-1 (IGF-1) signalling,
- NO signalling and
- signalling via the phospho-inositide-3 kinase/protein kinase B (PI3K/Akt) pathways