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The aim of the present study was to clarify the mechanisms by which a sucrose-rich diet (SRD) produces an increase in the pancreatic -cell mass in the rat. Normal Wistar rats were fed for 30 weeks either an SRD (SRD rats; 63% wt/wt), or the same diet but with starch instead of sucrose in the same proportion (CD rats). We studied body weight, serum glucose and triacylglycerol levels, endocrine tissue and -cell mass, -cell replication rate (proliferating cell nuclear antigen; PCNA), islet neogenesis (cytokeratin immunostaining) and -cell apoptosis (propidium iodide). Body weight (g) recorded in the SRD rats was significantly (P<0·05) larger than that of the CD group (556·0 8·3 vs 470·0 13·1). Both serum glucose and triacylglycerol levels (mmol/l) were also significantly higher (P<0·05) in SRD than in CD rats (serum glucose, 8·11 0·14 vs 6·62 0·17; triacylglycerol, 1·57 0·18 vs 0·47 0·04). The number of pancreatic islets per unit area increased significantly (P<0·05) in SRD rats (3·29 0·1 vs 2·01 0·2). A significant increment (2·6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the -cell mass (P=0·0025). The islet cell replication rate, measured as the percentage of PCNA-labelled cells increased 6·8 times in SRD rats (P<0·03). The number of apoptotic cells in the endocrine pancreas decreased significantly (three times) in the SRD animals (P=0·03). The cytokeratin-positive area did not show significant differences between CD and SRD rats. The increase of -cell mass induced by SRD was accomplished by an enhanced replication of cells together with a decrease in the rate of -cell apoptosis, without any evident participation of islet neogenesis. This pancreatic reaction was unable to maintain serum glucose levels of these rats at the level measured in CD animals.

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The interaction between fetal programming and the post-natal environment suggests that the post-natal diet could amplify or attenuate programmed outcomes. We investigated whether dietary n-3 long-chain polyunsaturated fatty acids (n-3 PUFAs) at weaning resulted in an amelioration of dyslipidemia, adiposity and liver steatosis that was induced by a sucrose-rich diet (SRD; where the fat source is corn oil) from the onset of pregnancy up to adulthood. During pregnancy and lactation, dams were fed an SRD or the standard powdered rodent commercial diet (RD). At weaning and until 150 days of life, male offspring from SRD-dams were divided into two groups and fed an SRD or SRD-with-fish oil [where 6% of the corn oil was partially replaced by fish oil (FO) 5% and corn oil (CO) 1%], forming SRD-SRD or SRD-FO groups. Male offspring from RD-dams continued with RD up to the end of the experimental period, forming an RD-RD group. The presence of FO in the weaning diet showed the following: prevention of hypertriglyceridemia and liver steatosis, together with increased lipogenic enzyme activity caused by a maternal SRD; the complete normalization of CPT I activity and PPARα protein mass levels; a slight but not statistically significant accretion of visceral adiposity; and limited body fat content and reduced plasma free fatty acid levels. All of these results were observed even in the presence of a high-sucrose diet challenge after weaning. SRD-dams' breast milk showed a more saturated fatty acid composition. These results suggest the capacity of n-3 PUFAs to overcome some adverse outcomes induced by a maternal and post-weaning sucrose-rich diet.