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        Maternal nutrient restriction in early pregnancy induces adipose tissue inflammation with a compensatory increase in adiponectin abundance in juvenile offspring
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        Maternal nutrient restriction in early pregnancy induces adipose tissue inflammation with a compensatory increase in adiponectin abundance in juvenile offspring
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        Maternal nutrient restriction in early pregnancy induces adipose tissue inflammation with a compensatory increase in adiponectin abundance in juvenile offspring
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Early-pregnancy nutrition is often unbalanced and suboptimal, with excess carbohydrate, and more importantly can be lacking in adequate protein(Reference Godfrey, Robinson and Barker1, Reference Moore, Davies and Willson2). This outcome may in part be secondary to nausea and vomiting that can affect 50–90% of pregnancies in the first trimester. Reduced protein intake in early pregnancy can reduce birth weight and placental size and this outcome may predispose the offspring to later adult diseases such as diabetes and CVD(Reference Godfrey, Robinson and Barker1). Adiponectin, a potent insulin sensitiser secreted by adipocytes, decreases with increasing adiposity with a concurrent rise in adipose tissue inflammation induced by cytokines and macrophage accumulation. IL-18 is elevated in obese individuals and is known to suppress adiponectin expression(Reference Chandrasekar, Patel and Mummidi3). The extent to which maternal nutrient restriction (NR) in early pregnancy can alter the inflammatory response in adipose tissue of non-obese juvenile offspring has not be studied.

The aims of the current study were to establish the effects of maternal NR during early pregnancy (0–30 d) on subsequent adipose tissue dysregulation in juvenile offspring. It has previously been shown in sheep that late NR but not early NR offspring are insulin resistant and glucose intolerant at 1 year of age(Reference Gardner, Tingey and Van Bon4).

Singleton-bearing sheep were randomised to receive either 100% metabolisable energy (ME) (controls; n 8) throughout pregnancy or 50% ME on days 0–30 (early NR; n 5). Offspring were reared by their mother until 3 months, weaned and fed at pasture until 1 year when they were humanely killed. Real-time PCR was used to measure the mRNA abundance of adiponectin, CD68 (macrophage marker), IL-18, TNFα, monocyte chemoattractant protein-1 (MCP-1) and leptin in perirenal adipose tissue. Expression was normalised to 18s rRNA using the 2−Δct method(Reference Pfaffl5) and expressed relative to the control value. Results were analysed using Student's t test and Pearson's correlation coefficient. All animal procedures were performed in accordance with UK legislation.

Birth weight (kg; controls, 4.3 (se 0.3); NR, 4.5 (se 0.2)), weight at 1 year (kg; controls, 50.7 (se 3.7); NR, 49.8 (se 4.3)) and relative fat mass (g/kg; controls, 7.7 (se 1.3); NR, 9.7 (se 0.6)) were not different between groups.

* Relative mRNA abundance (au).

Leptin expression and plasma levels(Reference Gardner, Tingey and Van Bon4) 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 TNFα (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.

1. Godfrey, K, Robinson, S, Barker, DJ et al. . (1996) Br Med J 312, 410414.
2. Moore, VM, Davies, MJ, Willson, KJ et al. . (2004) J Nutr 134, 18201826.
3. Chandrasekar, B, Patel, DN, Mummidi, S et al. . (2008) J Biol Chem 283, 42004209.
4. Gardner, DS, Tingey, K, Van Bon, BW et al. . (2005) Am J Physiol Regul Integr Comp Physiol 289, R947R954.
5. Pfaffl, MW (2001) Nucleic Acids Res 29(9), e45.