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Metabolic programming is a concept used to assess the effects of nutrition and other environmental factors in the early stages of development on short- and long-term health. Exclusive and on-demand lactation is associated with several health benefits, and may modulate gut microbiota composition and NLRP3 inflammasome activation. Both lactation and dietary patterns in early childhood affect adaptive responses and may be related to the development of chronic diseases in adulthood, and a high-sugar diet (HSD) favors hyperinsulinemia and impairs body composition. However, the mechanisms by which lactation promotes these effects are still not fully understood. The NLRP3 inflammasome is an oligomeric protein complex of the innate immune system, responsible for the cleavage of pro-inflammatory interleukins (IL-18 and IL-1β), IL-1β is associated with the pathogenesis of type 1 and type 2 diabetes mellitus, and the IL-18 has an effect on energy metabolism and insulin sensitivity. in addition, both increased and decreased levels of this IL are associated with obesity and insulin resistance (IR). These effects suggest a role of the inflammasome as an important metabolic and IR regulator. Given the above, this work aims to clarify the effect of metabolic programming induced by manipulation of litter size on the activation of the NLRP3 inflammasome and the modulation of the intestinal microbiome in an experimental model of HSD-induced IR in young rats.
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Metagenomic analysis of the project: "Metabolic programmimg for resilience small litter size preserves gut microbiota diversity and SCFA output despite high-sucrose diet"