1201-P: Monocyte Reprogramming in Nonhuman Primate Mother-Child Dyads Based on Maternal Health and Obesity Status

The developmental origins of metabolic disease mechanisms are mostly unknown. Up to 40% of obese women are healthy, while roughly 15% of lean women are not. The implications for their children are difficult to disentangle from environmental factors. We assessed offspring from age-matched female African green monkeys (AMGs [n=44]) classified as metabolically healthy lean (MHL), healthy obese (MHO), unhealthy lean (MUL), and unhealthy obese (MUO) based on adjusted metabolic syndrome criteria (waist >40cm, fasting glucose (FG) >100 mg/dL, SBP >135/DBP >85mmHg and HDL-c <50mg/dL). Pre-pubertal juveniles (n=9–11/group) had weight, FG and blood pressure measured. Flow cytometry identified circulating classical, intermediate, and non-classical monocytes in mother-offspring pairs and offspring monocyte chemoattractant protein 1 (MCP1) was measured. Offspring did not differ by weight or FBG but SBP trended higher in two groups (MUL and MHO, p=0.06). MUO mothers had more non-classical monocytes compared to MHL (p=0.006), and both MUL and MUO offspring also had higher non-classical monocytes compared to MHL (p=0.05 and p=0.07). MCP1 was higher in MUO offspring (p=0.02). Maternal health and obesity influence offspring immune profiles and metabolic risk factors prior to obesity. Shifting maternal immune cells prior to pregnancy may mitigate suboptimal developmental programming.View largeDownload slideView largeDownload slide DisclosureA. D. Ruggiero: None. M. Block: None. R. Vemuri: None. M. Davis: None. D. Destephanis: None. K. Kavanagh: None.