Early life exposures play a significant role in shaping health and disease susceptibility. Maternal obesity influences the offspring’s long-term risk of colorectal cancer, yet the understanding of the impact on developmental programming of intestinal stem cells and later risk of colorectal cancer remains limited. This has highlighted the growing need for a model that studies the influence of the maternal environment on the developing colon. The goal is to optimize a platform that generates human colon organoids (hCOs) from embryonic stem cells (hESCs) reliably and reproducibly and use it as a model to study colonic developmental patterning in an obesogenic environment. The organoids are derived by multi-step directed differentiation trajectory of embryonic stem cells, definitive endoderm, mid/hind gut, to fetal colon. The protocol was optimized to ensure consistent production of colonic organoids in contrast to small intestinal or urothelial cells which follow similar differentiation paths. To model an obesogenic environment on the platform, both the intrinsic and extrinsic properties of the developing colon were leveraged: 1) pharmacologically activating the transcription factor Peroxisome Proliferator-Activated Receptors Delta (PPARd) to mimic the cell-autonomous response to a pro-obesity maternal high fat diet, and 2) exposing the developing colon organoids to pro-inflammatory cytokine IL-17a to mimic the pre-pathological inflammatory state. The hESC-to-HCO model demonstrates the utility of ESC-derived organoids in studying the impact of maternal environmental factors on colonic development, generating a platform to explore factors that affect human development and maturation.