Abstract
Epidemiological and experimental studies report associations between overweight mothers and increased obesity risk in offspring. It is unclear whether neonatal leptin regulation mediates this association between overweight mothers and offspring obesity. We investigated the effect of neonatal treatment with a leptin antagonist (LA) on growth and metabolism in offspring of mothers fed either a control or a high fat diet. Wistar rats were fed either a control (CON) or a high fat diet (MHF) during pregnancy and lactation. Male CON and MHF neonates received either saline (S) or a rat-specific pegylated LA on days 3, 5, and 7. Offspring were weaned onto either a control or a high fat (hf) diet. At day 100, body composition, blood glucose, β-hydroxybutyrate and plasma leptin and insulin were determined. In CON and MHF offspring, LA increased neonatal bodyweights compared to saline-treated offspring and was more pronounced in MHF offspring. In the post-weaning period, neonatal LA treatment decreased hf diet-induced weight gain but only in CON offspring. LA treatment induced changes in body length, fat mass, body temperature, and bone composition. Neonatal LA treatment can therefore exert effects on growth and metabolism in adulthood but is dependent upon interactions between maternal and post-weaning nutrition.
Highlights
Obesity and metabolic-related disorders are considered major health issues worldwide
Consistent with our previous observations [7], maternal High-fat diet (HF) diet during pregnancy and lactation resulted in a transient increase in caloric intake from day 2 (P < 0.001) to day 15 of gestation when intakes returned to levels similar to those observed in CON dams
Increased caloric intake in MHF dams was reflected in an increased maternal weight gain by gestational day 7 (P = 0.04, Figure 2), which persisted until birth
Summary
Obesity and metabolic-related disorders are considered major health issues worldwide. The rapid increases in the rates of obesity suggest that environmental and behavioural influences, rather than genetic causes, are fuelling the present epidemic. Increasing evidence from both clinical and animal studies has highlighted the link between altered maternal nutrition and the risk of offspring developing obesity and the metabolic syndrome [2,3,4,5]. There is accumulating evidence from human [6] and animal studies suggesting that excess maternal caloric intake has adverse effects on the health and well-being of offspring, independent of postnatal diet [7] and exerted transgenerational effects [8]
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