Food insecurity promotes adiposity in mice
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ABSTRACT:
PROVIDER: PRJNA1145292 | ENA |
REPOSITORIES: ENA
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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:Obesity is linked to the development of metabolic disorders. Expansion of white adipose tissue (WAT) from hypertrophy of pre-existing adipocytes and/or differentiation of precursors into new mature adipocytes contributes to obesity. We found that Nck2 expression is largely restricted to WAT, raising the hypothesis that it may play a unique function in that tissue. Using mice lacking Nck2, we found that Nck2 regulates adipocyte hypertrophy thus contributing to increased adiposity and progressive glucose intolerance, insulin resistance and hepatic steatosis. These findings were recapitulated in humans such that Nck2 expression in omental WAT was inversely correlated with the degree of obesity. Mechanistically, Nck2 deficiency promoted the induction of an adipocyte differentiation program and signaling by the PERK-eIF2α-ATF4 pathway in agreement with a role for the unfolded protein response in adipogenesis. These findings uncover Nck2 as a novel regulator of adipogenesis and that perturbation in its functionality contributes to adiposity-related metabolic disorders.
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