TY - JOUR
T1 - Maternal diet and obesity shape offspring central and peripheral inflammatory outcomes in juvenile non-human primates
AU - Dunn, Geoffrey A.
AU - Mitchell, A. J.
AU - Selby, Matthew
AU - Fair, Damien A.
AU - Gustafsson, Hanna C.
AU - Sullivan, Elinor L.
N1 - Publisher Copyright:
© 2022 Elsevier Inc.
PY - 2022/5
Y1 - 2022/5
N2 - The obesity epidemic affects 40% of adults in the US, with approximately one-third of pregnant women classified as obese. Previous research suggests that children born to obese mothers are at increased risk for a number of health conditions. The mechanisms behind this increased risk are poorly understood. Increased exposure to in-utero inflammation induced by maternal obesity is proposed as an underlying mechanism for neurodevelopmental alterations in offspring. Utilizing a non-human primate model of maternal obesity, we hypothesized that maternal consumption of an obesogenic diet will predict offspring peripheral (e.g., cytokines and chemokines) and central (microglia number) inflammatory outcomes via the diet's effects on maternal adiposity and maternal inflammatory state during the third trimester. We used structural equation modeling to simultaneously examine the complex associations among maternal diet, metabolic state, adiposity, inflammation, and offspring central and peripheral inflammation. Four latent variables were created to capture maternal chemokines and pro-inflammatory cytokines, and offspring cytokine and chemokines. Model results showed that offspring microglia counts in the basolateral amygdala were associated with maternal diet (β = −0.622, p < 0.01), adiposity (β = 0.593, p < 0.01), and length of gestation (β = 0.164, p < 0.05) but not with maternal chemokines (β = 0.135, p = 0.528) or maternal pro-inflammatory cytokines (β = 0.083, p = 0.683). Additionally, we found that juvenile offspring peripheral cytokines (β = −0.389, p < 0.01) and chemokines (β = −0.298, p < 0.05) were associated with a maternal adiposity-induced decrease in maternal circulating chemokines during the third trimester (β = −0.426, p < 0.01). In summary, these data suggest that maternal diet and adiposity appear to directly predict offspring amygdala microglial counts while maternal adiposity influences offspring peripheral inflammatory outcomes via maternal inflammatory state.
AB - The obesity epidemic affects 40% of adults in the US, with approximately one-third of pregnant women classified as obese. Previous research suggests that children born to obese mothers are at increased risk for a number of health conditions. The mechanisms behind this increased risk are poorly understood. Increased exposure to in-utero inflammation induced by maternal obesity is proposed as an underlying mechanism for neurodevelopmental alterations in offspring. Utilizing a non-human primate model of maternal obesity, we hypothesized that maternal consumption of an obesogenic diet will predict offspring peripheral (e.g., cytokines and chemokines) and central (microglia number) inflammatory outcomes via the diet's effects on maternal adiposity and maternal inflammatory state during the third trimester. We used structural equation modeling to simultaneously examine the complex associations among maternal diet, metabolic state, adiposity, inflammation, and offspring central and peripheral inflammation. Four latent variables were created to capture maternal chemokines and pro-inflammatory cytokines, and offspring cytokine and chemokines. Model results showed that offspring microglia counts in the basolateral amygdala were associated with maternal diet (β = −0.622, p < 0.01), adiposity (β = 0.593, p < 0.01), and length of gestation (β = 0.164, p < 0.05) but not with maternal chemokines (β = 0.135, p = 0.528) or maternal pro-inflammatory cytokines (β = 0.083, p = 0.683). Additionally, we found that juvenile offspring peripheral cytokines (β = −0.389, p < 0.01) and chemokines (β = −0.298, p < 0.05) were associated with a maternal adiposity-induced decrease in maternal circulating chemokines during the third trimester (β = −0.426, p < 0.01). In summary, these data suggest that maternal diet and adiposity appear to directly predict offspring amygdala microglial counts while maternal adiposity influences offspring peripheral inflammatory outcomes via maternal inflammatory state.
KW - Chemokines
KW - Cytokines
KW - Maternal Obesity
KW - Microglia
KW - Neuroinflammation
KW - Non-Human Primates
KW - Nutrition
KW - Western-Style Diet
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U2 - 10.1016/j.bbi.2022.02.024
DO - 10.1016/j.bbi.2022.02.024
M3 - Article
C2 - 35217175
AN - SCOPUS:85125631373
SN - 0889-1591
VL - 102
SP - 224
EP - 236
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
ER -