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An intracellular amino acid scarcity sensor tunes protein hunger

ABSTRACT: Protein is a dietary macronutrient with a strong homeostatic drive, which plays a major contribution in determining total energy intake. Most animals, including Drosophila, display compensatory preference for amino acid-rich food following dietary protein scarcity. In the CNS, peptidergic cells play an important role in adaptive feeding behaviour, by mediating the satiating effects of protein consumption. We demonstrate that protein appetite and compensatory feeding following amino acid deprivation are also under peptidergic control. Using single-nucleus RNA-sequencing, we identified gene expression changes in peptidergic neurons from amino acid-deprived flies and sated controls. One of the strongly regulated genes is Lsp2, which encodes an amino acid storage protein essential for larval development and pupation. We demonstrate that in the adult brain, specific peptidergic neurons use Lsp2 levels as a gauge to scale protein intake.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE334747 | GEO | 2026/06/15

REPOSITORIES: GEO

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Project description:High-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver. Adult male Wistar rats were fed diets with varying amounts of protein, carbohydrates and fat for 5 weeks. At the end of the experiment, rats were killed and tanscriptome analysis was performed on pooled liver samples.

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An intracellular amino acid scarcity sensor tunes protein hunger

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