This review will focus on how differing developmental processes in the intestinal epithelium affect the macromolecular passage in different species and the possible impact of such passage on the establishment of immunity during the critical perinatal period in young mammals.

The present investigation characterized the effect of red kidney bean lectin exposure on gut maturation and function in young piglets. Eleven suckling pigs were given by stomach tube a crude red kidney bean lectin preparation (containing about 25% lectin, 400 mg/kg BW) (lectin-treated pigs) at 10, 11, and 12 d of life, and an additional 16 pigs (control pigs) were given saline instead. On the next day, the intestinal absorptive capacity was determined in vivo, and on the 14th d of life the piglets were killed and organs and small intestine samples were collected for analyses and in vitro permeability experiments. The lectin-treated pigs showed an increase in stomach weights and mucosa thickness, whereas no weight effect was found for the small intestine, spleen, liver, or adrenals. Morphometric analyses of the small intestine in lectin-treated pigs showed a decrease in villus heights, an increase in crypt depths and crypt cell mitotic indices, and fewer vacuolated enterocytes per villus and reduced vacuole size. Lectin treatment also resulted in a decrease in the absorption of different-sized marker molecules after gavage feeding, a decrease in intestinal marker permeability, and a change in small intestinal disaccharidase activities, with increased maltase and sucrase activities. The size of the pancreatic acini was also greater in the lectin-treated pigs, but no increases in enzyme content or pancreatic weight could be determined. In addition, the blood plasma levels of cholecystokinin were higher in the lectin-treated than in the control pigs. The results indicate that exposure to crude red kidney bean lectin induces structural and functional maturation of the gut and pancreatic growth in young suckling piglets. This possibility of inducing gut maturation may lead to an improvement in the piglets' ability to adapt to weaning and to an increase in the growth and health of these animals.

The most frequently used and effective treatment for morbid obesity is Roux-en-Y gastric bypass surgery (RYGB), which results in rapid remission of type 2 diabetes in most cases. To what extent this is accounted for by weight loss or other factors remains elusive. To gain insight into these mechanisms, we investigated the effects of RYGB on b-cell function and b-cell mass in the pig, a species highly reminiscent of the human. RYGB was performed using linear staplers during open surgery. Sham-operated pigs were used as controls. Both groups were fed a low-calorie diet for 3 weeks after surgery. Intravenous glucose tolerance tests were performed 2 weeks after surgery. Body weight in RYGB pigs and sham-operated, pair-fed control pigs developed similarly. RYGB pigs displayed improved glycemic control, which was attributed to increases in b-cell mass, islet number, and number of extraislet b-cells. Pancreatic expression of insulin and glucagon was elevated, and cells expressing the glucagon-like peptide 1 receptor were more abundant in RYGB pigs. Our data from a pig model of RYGB emphasize the key role of improved b-cell function and b-cell mass to explain the improved glucose tolerance after RYGB as food intake and body weight remained identical.Roux-en-Y gastric bypass surgery (RYGB) leads to remission of type 2 diabetes (T2D) in most patients within days after surgery (1). Importantly, this occurs long before any substantial weight loss has occurred (2). The reason for this remains a controversy, as studies have shown that the beneficial effects of RYGB on T2D are weight loss independent (e.g., [3]), while others suggest that they result from reduced food intake (4). Clinical studies have shown that RYGB has greater effect on remission of T2D than, for example, vertical sleeve gastrectomy, despite similar weight loss (5). This is in support of weight-independent factors underlying the resolution of T2D upon RYGB. One factor, accounting for the beneficial metabolic effects of RYGB, may be changes in circulating levels of gut hormones and their effects on the islets. In particular, increased levels of the incretin hormone glucagon-like peptide 1 (GLP-1) have been implicated as a factor contributing to remission of T2D (2,6). The effect of RYGB on glucose-dependent insulinotropic peptide (GIP) is less clear (6,7). Other factors, including gut microbiota (8), intestinal glucose sensing (9), and bile acids (10), may also contribute. Nevertheless, it is of great clinical importance to resolve this issue, as it will have a strong impact on how treatment for a large group of patients is devised. In fact, if a specific mechanism were to be identified, it could be used as the basis for a new treatment modality.One problem in the dissection of effects of RYGB on glucose metabolism is that studies on b-cell mass in humans are lacking, and it is extremely difficult to generalize from data in rodents (11) because of huge differences in pancreatic anatomy and physiology between the species. To circumvent these problems, we devel...

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