Abstract:
Objectives: This study aimed to determine in a rat model, whether supplementation with fish oil (rich in omega-3 fats), during the pregnancy of insulin resistant mothers, could prevent the development of insulin resistance and other aspects of metabolic dysfunction in the offspring. Methods: Virgin female rats were time-mated and randomised into four treatment groups: Con-Con, dams fed a control diet (15% calories from fat) and administered water by gavage; Con-FO, control diet with 1ml of fish oil by gavage; HF-Con, high-fat diet (45% calories from fat) and water by gavage; and HF-FO, high-fat diet and fish oil by gavage. The fish oil was independently verified to be unoxidised (peroxide value 2.7meq/kg). Dams were fed ad libitum during pregnancy and lactation, but daily gavage occurred only during pregnancy. After weaning, male offspring consumed a chow diet ad libitum until adulthood, when they underwent detailed assessments of body composition and metabolism, including dual-xray absorptiometry and an oral glucose tolerance test with calculation of the Matsuda index of insulin sensitivity. Results: Maternal high-fat diet led to increased food consumption (+89 g; p=0.044), adiposity (+6.4% body fat; p=0.008), systolic blood pressure (+12 mmHg; p<0.0001), and plasma triglyceride (+0.55mmol/l; p=0.014) and leptin (+4.1 ng/ml; p=0.002) concentrations in adult HF-Con offspring. HFCon offspring also exhibited lower insulin sensitivity than Con-Con rats (Matsuda index 38% lower; p=0.036). Male offspring from HF-FO group were similar to HF-Con regarding food consumption, adiposity, and most metabolic parameters. However, insulin sensitivity in the HF-FO group was improved relative to the HF-Con offspring (Matsuda index 85% higher; p=0.014) and similar to the Con-Con offspring. Conclusions: Supplementation of dams consuming a maternal high fat diet (an established insulin resistant model) with unoxidised n-3 PUFA rich oils prevented the development of insulin resistance, but had no impact on body composition or other metabolic parameters in adult male offspring. Future studies should assess whether this effect translates to obese human pregnancy.
