A significant amount of research has shown that type 1 diabetes in children causes a delay in puberty. However, it is unclear how hyperglycemia contributes to this delay in puberty. Hyperglycemia, which is associated with diabetes, refers to elevated blood glucose levels. To model hyperglycemia at a molecular level, C. elegans are fed a glucose-supplemented diet and the physiological and molecular impacts are studied. We found that a glucose-supplemented diet induces a developmental delay in comparison to the control food (OP50 E. coli diet). The glucose induced developmental delay was also observed in animals fed the deltaPTS E. coli OP50 bacteria strain, which lacks a glucose transporter, indicating the phenotype is not due to metabolites produced by OP50. Developmental delay can be induced by environmental stress or genetic mutations. For example, mutations that impact ceramide biosynthesis, electron transport chain activity, ubiquinone biosynthesis, or insulin signaling (
hyl-2(
tm2031),
isp-1(
qm150),
clk-1(
e2519) and
daf-2(
e1370), respectively) lead to developmental delay. We tested if a glucose diet prolonged developmental progression in these mutants. A glucose-supplemented diet further exacerbates the developmental delay of the
hyl-2(
tm2031),
isp-1(
qm150) and
clk-1(
e2519) mutants but did not induce a developmental delay in the
daf-2(
e1370) animal. The resistance to glucose-induced developmental delay observed in the
daf-2(
e1370) animal is suppressed by
daf-16(
mu86). To further understand how glucose impacts insulin signaling and developmental progression we are using RNA sequencing and genetic analysis to identify the DAF-16 regulated genes that have a role in developmental progression. This could provide insight into how hyperglycemia and altered insulin signaling is linked to delayed puberty in children with type 1 diabetes.