ArticleCellular and molecular life sciences : CMLS2024
Dietary cysteine and methionine promote peroxisome elevation and fat loss by induction of CG33474 expression in Drosophila adipose tissue.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 1 citations in OpenAlex.
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2 authors at 1 institution in 1 country.
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Abstract
The high-protein diet (HPD) has emerged as a potent dietary approach to curb obesity. Peroxisome, a highly malleable organelle, adapts to nutritional changes to maintain homeostasis by remodeling its structure, composition, and quantity. However, the impact of HPD on peroxisomes and the underlying mechanism remains elusive. Using Drosophila melanogaster as a model system, we discovered that HPD specifically increases peroxisome levels within the adipose tissues. This HPD-induced peroxisome elevation is attributed to cysteine and methionine by triggering the expression of CG33474, a fly homolog of mammalian PEX11G. Both the overexpression of Drosophila CG33474 and human PEX11G result in increased peroxisome size. In addition, cysteine and methionine diets both reduce lipid contents, a process that depends on the presence of CG33474. Furthermore, CG33474 stimulates the breakdown of neutral lipids in a cell-autonomous manner. Moreover, the expression of CG33474 triggered by cysteine and methionine requires TOR signaling. Finally, we found that CG33474 promotes inter-organelle contacts between peroxisomes and lipid droplets (LDs), which might be a potential mechanism for CG33474-induced fat loss. In summary, our findings demonstrate that CG33474/PEX11G may serve as an essential molecular bridge linking HPD to peroxisome dynamics and lipid metabolism.
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