Dataset Information

Food insecurity in young rats induces metabolic remodeling in a sex- and diet- dependent manner

ABSTRACT: A growing segment of the world’s population is confronted with food insecurity (FI), which includes sporadic access to food, caloric insufficiency and poor nutritional quality. There is growing evidence that early-in-life exposure to FI can lead to an increase in risk for later-in-life cardiometabolic disease phenotypes, including obesity, type 2 diabetes, and cardiovascular diseases. In an effort to fully understand how acute FI exposure leads to metabolic reprogramming, we exposed very young rats (4 weeks old) to an acute (20 day) FI intervention compared to al-lib feeding, using either standard chow (SC) or high fat/high sucrose (HF/HS) diets, followed by continued ad-lib feeding of those diets for a follow-up period of 8 weeks. We found that male, but not female rats fed the HF/HS diet and subjected to FI exhibited increases in percent fat mass, weight of specific fat depots, and fat cell size, as well as alterations in hepatic and adipose tissue metabolomic and transcriptomic profiles consistent with reduced fatty acid oxidation in the liver and increased inflammation and maladaptive remodeling of adipose tissue. In contrast, these changes in liver and adipose tissue cellular and molecular profiles were not observed in male or female rats when fed SC diet during and after the FI intervention. In summary, we have developed a preclinical model of FI and used it to demonstrate sex- and diet-dependent effects of acute FI on development of early-stage cardiometabolic disease phenotypes that may presage increased latent risk for obesity and cardiometabolic diseases.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE319276 | GEO | 2026/09/30

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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.

Dataset Information

Food insecurity in young rats induces metabolic remodeling in a sex- and diet- dependent manner

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets