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Food insecurity promotes adiposity in mice

ABSTRACT: Food insecurity promotes adiposity in mice

PROVIDER: PRJNA1145292 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR30160720_1.fastq.gz	Fastqsanger.gz
	SRR30160720_2.fastq.gz	Fastqsanger.gz
	SRR30160722_1.fastq.gz	Fastqsanger.gz
	SRR30160722_2.fastq.gz	Fastqsanger.gz

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Food insecurity promotes adiposity in mice

Project description:The obesity epidemic continues to challenge global health, driven by multifaceted environmental and biological factors. Here, we investigate the impact of food insecurity, characterized by unpredictable food access, on body weight, food intake, and body composition in mice. Male and female C57BL/6J mice were subjected to a combination of intermittent fasting and 5% calorie restriction to resemble food insecurity situations. Our results reveal that this novel food insecurity model promotes fat accumulation and decreases lean mass in both sexes on a standard chow diet. While food insecurity did not exacerbate fat gain in male mice fed a high-fat diet, it further reduced lean mass. RNA sequencing of epididymal white adipose tissue from food-insecure male mice identified upregulated lipid metabolism genes and downregulated immune response genes, suggesting adipocyte expansion and potential immunity dysfunction. These results challenge the traditional view that obesity is solely driven by positive energy balance. Instead, our findings highlight the role of food insecurity in promoting metabolic adaptations favouring fat storage. Our data provide biological mechanisms that may explain the dramatic rise in obesity, underscoring the importance of socio-economic factors, beyond diet composition and energy balance, in understanding the complex etiology of obesity.

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Project description:The high prevalence of obesity has focused attention on defining the pathophysiological processes that underlie susceptibility or resistance to its deleterious metabolic consequences. Mice lacking translin (Tsn), a gene implicated in a variety of biological functions from transcription to microRNA degradation, display extremely high levels of adiposity, comparable to those found in well-known genetic models of obesity, such as melanocortin 4 receptor or leptin knockout (KO) mice. Although translin KO mice display increased adiposity they retain normal glucose tolerance. In contrast, wild-type (WT) mice placed on a high-fat diet until they match translin KO adiposity levels are glucose intolerant, as expected. Conversely, translin KO mice display prominent hepatic steatosis that is more severe than that of adiposity-matched WT mice. The ability of translin KO mice to retain normal glucose tolerance in the face of massive tissue expansion may be due to three factors: preferential accumulation of subcutaneous fat, reduced levels of TNF mRNA in both adipose and hepatic tissue, and elevated levels of plasma adiponectin. Further studies aimed at defining the molecular bases for these phenotypes may yield new approaches to limit the adverse metabolic consequences of obesity.

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