Foetal exposure to a diabetic intra-uterine environment is known to impair metabolic processes with long term consequences, a phenomenon termed foetal programming. However, the mechanisms involved has not been completely understood. Fructose feeding has been used to induce type 2 diabetes in animal models. This study aims to investigate if stress mechanism is involved in the foetal programming of diabetic pregnancies. Twenty-four female rats were randomly divided into two groups namely group A (control): rats fed with normal rat chow and group B (Fructose-induced diabetes): rats made diabetic using a diet consisting of 25% fructose. Diabetes was confirmed after 8 weeks of fructose feeding. Rats in both groups were mated, pregnancy was confirmed and rats sub-grouped into 2 namely day 19 of pregnancy and term rats. Maternal blood and amniotic fluid samples were obtained from day 19 group and assessed for glucose, insulin, corticotrophin releasing hormone (CRH) and corticosterone levels. Term rats were allowed to deliver; the offspring were weaned and fed with normal rat chow till the onset of puberty. Offspring blood samples were obtained and assessed for glucose, insulin, corticosterone, lipids and liver enzyme levels. Oral glucose and insulin tolerance tests were also conducted. Results showed that maternal and amniotic fluid glucose, insulin, CRH and corticosterone levels were significantly increased in the diabetic rats (P<0.05). The offspring of diabetic rats had a significantly increased birth weight, glucose, insulin, corticosterone and lipid levels (P<0.05) with no significant difference in liver enzyme levels. Glucose and insulin tolerance test results were deranged, while positive correlations exist between maternal and offspring glucose, insulin, and corticosterone levels in the diabetic rats. These findings show that maternal diabetes triggers stress mechanism in both maternal and foetal circulations, leading to impaired glucose and lipid metabolism in the offspring.