Adipose tissue is a major endocrine organ responsible for the release of hormones, termed adipokines, with roles in the inflammatory response and insulin sensitivity. Of these, leptin and tumour necrosis factor (TNF) alpha increase with obesity, whilst adiponectin decreases. Adiponectin has anti-inflammatory properties and reduces insulin resistance. Although maternal nutrient restriction during pregnancy programmes offspring adipose tissue sensitivity and later adiposity, whether it regulates adipokine expression in perirenal adipose tissue (PAT) in the absence of an effect on total fat mass is currently unknown. Singleton-male-bearing Scottish Blackface ewes of similar weight were individually housed from day of mating. Eight control (C) ewes were fed 100% of total metabolisable energy requirements whilst ten nutrient restricted (NR) ewes consumed 50% of ME requirements up to 95 days of gestation. All ewes then consumed 100% of ME requirements up to term (147 days). Rams were overdosed with barbiturates at ~3 years of age to enable tissue sampling. Adiponectin, leptin and TNF alpha mRNA abundances were quantified by real time qRT-PCR with standard curves generated from isolated gene specific PCR amplicons to ensure equal PCR efficiency. Quantitative gene expression was measured using the 2−deltaCT method with the housekeeping gene 18S as an internal control. Statistical differences between nutritional groups were analysed using a Mann-Whitney U test (p<0.05). Offspring growth rate, body weight and adiposity to 3 years of age were unaffected by maternal nutrient restriction. Although there were no differences between groups in the mRNA abundances of leptin or TNF alpha in PAT, adiponectin mRNA was significantly up-regulated in NR offspring. In conclusion, although maternal nutrient restriction from 0-95 days gestation had no effect upon body or adipose tissue weight, mRNA abundance for adiponectin was up-regulated in NR adult offspring. As adiponectin is inversely related to fat mass, inflammation and insulin resistance, its up-regulation may reflect a compensatory mechanism for adult offspring following maternal nutrient restriction in early gestation. Such an adaptation in NR offspring may have prevented/ delayed increased adiposity associated with early maternal undernutrition.