EGCG attenuates negative changes in rats given rapamycin with HFD

“EGCG reversed rapamycin exacerbated HFD-induced alterations in spermatogenesis, insulin-glucose balance, reproductive hormones, oxido-nitrergic stress, and altered serotonin, acetylcholinesterase levels, and autophagic and apoptotic activities in rats’ testes and brains respectively. EGCG significantly attenuated HFD-induced cognitive loss.”

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Onyekweli CC, Ben-Azu B, Oyovwi OM, Nwangwa EK, Ovuakporaye IS, Moke GE, Agbonifo-Chijiokwu E, Onome BO, Emojevwe V, Rotu AR. Epigallocatechin-gallate attenuates rapamycin exacerbated high fat diet-induced hormonal dysregulation, testicular and brain oxidative stress and neurochemical changes in rats. Food Chem Toxicol. 2023 Dec 12:114340. doi: 10.1016/j.fct.2023.114340. Epub ahead of print. PMID: 38097001.

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snippets of full text:
Epigallocatechin-gallate attenuates rapamycin exacerbated high fat diet-induced hormonal dysregulation, testicular and brain oxidative stress and neurochemical changes in rats
Their hypothesis is based on some dubious assumptions about the supposed bad effects of a high fat diet with rapamycin:

we therefore hypothesized that treatment with EGCG would reverse rapamycin and HFD-mediated reproductive and cognitive dysfunctions via normalization of hormonal dysregulation, reversal of testicular and brain oxidative stress and neurochemical changes in rats.

They also state that EGCG might reverse rapamycin-induced autophagy. Do I want to reverse it?

EGCG reversed rapamycin exacerbated HFD-induced alterations in spermatogenesis, insulin-glucose balance, reproductive hormones, oxido-nitrergic stress, and altered serotonin, acetylcholinesterase levels, and autophagic and apoptotic activities in rats’ testes and brains respectively.

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If you look at the Conclusion section they mention “autophagy enhancement.”

“Our findings showed that rapamycin exacerbates HFD-induced spermatogenesis deficiency and cognitive impairment. However, treatment with EGCG attenuated the rapamycin mediated HFD-induced spermatogenesis deficiency and cognitive impairment via mechanisms associated with increased reproductive hormones, inhibition of testicular and brain oxidative stress, apoptosis, autophagy enhancement, and increased serotoninergic and cholinergic transmissions in rats […]”

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