Fat Cells May Retain a Memory of Obesity
Which could be why weight regain is so common The post Fat Cells May Retain a Memory of Obesity appeared first on Nautilus .
A recent study published in Cell Reports may have uncovered the molecular mechanisms behind why weight regain is so common after using GLP-1 medications for weight loss. While these medications are effective at reducing body weight, once discontinued, the weight tends to return. This phenomenon is not unique to humans but has also been observed in mice.
Previous research has shown that mouse fat cells retain a kind of "memory" of obesity, which is epigenetically imprinted and persists even after weight loss. In this new study led by geneticists at Case Western University, researchers discovered that a cytokine called transforming growth factor beta 1 (TGF-β1) could be responsible for this rewiring.
TGF-β1 increased the production of asprosin, a hormone that stimulates appetite during fasting. When mice were exposed to TGF-β1, even for a brief period, they showed increased food intake and subsequent weight gain. However, only a small amount of TGF-β1 was required to produce these effects that persisted for weeks. The researchers further found that TGF-β1 modifies the chromatin in adipose tissue, exposing the gene that produces the precursor to asprosin.
This discovery suggests that TGF-β1 could be a key factor in preventing weight regain after treatment ends. Additionally, the study hints at a potential explanation for obesity being passed from mother to child, as TGF-β1 can cross the placenta. In a study where female mice with induced obesity were mated with normal-weight males, their offspring had elevated asprosin levels despite normal TGF-β1 levels.
This suggests that TGF-β1-induced changes in fat cells may contribute to the intergenerational transmission of obesity. While the findings present a bleak outlook, the researchers are hopeful that these insights could lead to new therapeutic targets for obesity. They are particularly interested in investigating whether blocking asprosin could prevent weight rebound following the discontinuation of GLP-1 treatments. However, further research is needed to confirm these findings in humans.
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