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Abstract

Background: Type 2 diabetes (T2D) in children has increased over the past two decades. Strategies to mitigate disease progression often focus on macronutrients, overlooking micronutrients despite evidence of deficiency in children with T2D. Riboflavin, as flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), is crucial for metabolism and oxidative stress management, mainly through FAD-dependent glutathione reductase. Given that insulin-producing β-cells are vulnerable to oxidative stress, they may have unique riboflavin requirements, especially during puberty, a period characterized by β-cell expansion. The objective of my thesis was to investigate the role of riboflavin in glucose homeostasis in an adolescent mouse model. Methods: Male and female C57BL/6J mice were fed for 8-12 weeks from weaning one of the following diets: control (6mg riboflavin/kg diet), low riboflavin (1mg riboflavin/kg diet), western (45% energy fat, 6mg riboflavin/kg diet), or western low riboflavin (45% energy fat, 1mg riboflavin/kg diet). Physiological assessments of adiposity and glucose homeostasis were performed. Serum, liver, gonadal fat, and pancreatic islets were collected for metabolite analyses and functional assessment of β-cells. Results: The low riboflavin diets lowered (p