Maternal nutrient restriction in early pregnancy induces adipose tissue inflammation with a compensatory increase in adiponectin abundance in juvenile offspring

Abstract

1.0 0.2 1.9 0.5 0.08 MCP-1 1.0 0.2 1.0 0.2 0.57 Leptin 1.0 0.3 2.2 1.0 0.17 *Relative mRNA abundance (au). Leptin expression and plasma levels (4) were not different between the groups in keeping with their similar fat mass. Irrespective of maternal diet adiponectin abundance correlated with CD68 (r 2 0.79; P < 0.001), IL-18 (r 2 0.72; P = 0.001) and TNFa (r 2 0.66; P = 0.001). Despite early NR having no effect on birth weight, juvenile offspring show evidence of increased adipose tissue inflammation with an apparent compensatory increase in adiponectin expression. Adipose tissue inflammation is associated with the development of insulin resistance and obesity. These offspring show no evidence of insulin resistance and this outcome may reflect the compensatory increase in adiponectin thus delaying its onset. Further studies in later life could investigate whether this compensatory mechanism is overcome by on-going inflammation as a result of increasing IL-18 ultimately resulting in insulin resistance. This information may well have important implications for women with suboptimal nutrition in early pregnancy.