Early postnatal nutrition is involved in metabolic programming, an excess of protein being suspected to enhance early growth and the propensity to later develop insulin resistance and type 2 diabetes mellitus. The aim of the present study was to test the hypothesis that excessive protein intake during the suckling period would overstimulate the endocrine pancreas in the short term and alter durably its maturation, contributing to the later disruption of glucose homeostasis. Normal-birth-weight and low-birth-weight piglets were fed isoenergetic formulae providing an adequate-protein (AP, equivalent to sow milk) or a high-protein (HP, +48 %) supply between 7 and 28 d of age and were fed a standard diet until 70 d of age. During the formula-feeding period, the HP formula did not modify postprandial insulin secretion but transiently increased fasting insulin and the homeostasis model assessment-insulin resistance index (HOMA-IR, P < 0·05). Fasting insulin and HOMA-IR were restored to AP piglets' values 1 month after weaning. The structure of the endocrine pancreas was not affected by the protein content of the formula. The weight at birth had no major effect on the studied parameters. We concluded that a high-protein supply during the suckling period does not interfere with insulin secretion and endocrine pancreas maturation in the short term. It has no consequences either on glucose tolerance 1 month after weaning. The present study demonstrated that up-regulation of postprandial insulin secretion is not involved in higher growth observed in piglets fed a HP formula.

The health benefits of breast-feeding have been recognised for a long time. In particular, breast-feeding is associated with lower incidence of necrotising enterocolitis and diarrhoea during the early period of life and with lower incidence of inflammatory bowel diseases, type 2 diabetes and obesity later in life. The higher nutritional and protective degree of human milk is related to its nutritional composition that changes over the lactation period and to the biological activities of specific components while lower growth rate of breast-fed infants may be attributed to their self-regulation of milk intake at a lower level than formula-fed infants. Many results now suggest that the developmental changes in intestinal and pancreatic function that occur postnatally are modulated by the diet. Indeed, formula-feeding induces intestinal hypertrophy and accelerates maturation of hydrolysis capacities; it increases intestinal permeability and bacterial translocation, but does not induce evident differences in microbiota composition. Whether these changes would be beneficial for enhancing absorptive capacities and for educating the gut-associated immune system remains to be further studied. Moreover, it is evident that formula-feeding increases basal blood glucose and decreases plasma ketone body concentrations, while discrepancies on postprandial glycaemia, insulin and incretin responses in both human studies and experimental studies are inconclusive. Manipulating the composition of formula, by reducing protein content, adding prebiotics, growth factors or secretory IgA can modulate intestinal and pancreatic function development, and thereby may reduce the differential responses between breast-fed and formula-fed neonates. However, the developmental responses of the digestive tract to different feeding strategies must be elucidated in terms of sensitivity to developing diseases, taking into account the major role of the intestinal microbiota.

Nuclear microscopy is a suite of techniques based on a focused beam of MeV protons. These techniques have the unique ability to image density and structural variations in relatively thick tissue sections, map trace elements at the cellular level to the microgram per gram (dry weight) level, and extract quantitative information on these elements. The trace elemental studies can be carried out on unstained freeze-dried tissue sections, thereby minimizing any problems of contamination or redistribution of elements during conventional staining and fixing procedures. The pancreas is a gland with different specialized cells and a complex hormonal activity where trace elements play an important role. For example, zinc has an active role in insulin production, and calcium ions participate in the stimulation and secretion process of insulin. Using nuclear microscopy with a spatial resolution of 1 μm, we have located, using zinc mapping, the islets of Langerhans in freeze-dried normal rabbit tissue sections. The islets of Langerhans contain β-cells responsible for insulin production. Subsequent quantitative analyses have indicated elevations in most elements within the islets of Langerhans, and significantly so for the concentrations of Zn [3,300 compared to 90 μg/g (dry weight)] and Ca [1,100 compared to 390 μg/g (dry weight)].

High-fat feeding reduces the expression of GLUT-2 and the glycolytic enzyme glucokinase (GK). The transcription factor, pancreatic duodenal homeobox-1 (Pdx-1), is important for β-cell maintenance. The aim of the present study was to determine, in weanling Wistar rats, the effect of a maternal high-fat diet (HFD) during defined periods of gestation and lactation, on body weight, circulating glucose and insulin concentrations, and the expression of GLUT-2, GK and Pdx-1. At postnatal day 21, weights were recorded and glucose and insulin concentrations were measured. The expression levels for mRNA were quantified by LightCycler PCR. Pancreatic sections, immunostained for GLUT-2, GK or Pdx-1, were assessed by image analysis. Weanlings from dams fed an HFD throughout gestation were lighter, with heavier weanlings produced from dams fed an HFD throughout gestation and lactation. Both these groups of weanlings were normoglycaemic, all the others being hyperglycaemic. Hypoinsulinaemia was evident in weanlings from dams fed an HFD throughout gestation only and also for either the first week of lactation or throughout lactation. GLUT-2 mRNA expression was reduced and GLUT-2 immunoreactivity was increased in most of the weanlings. GK mRNA expression and immunoreactivity was reduced in most of the offspring. Pdx-1 mRNA expression was increased in weanlings from dams fed an HFD throughout both gestation and lactation and reduced in those from dams only fed a lactational HFD. Normal Pdx-1 immunoreactivity was found in all of the weanlings. A maternal HFD induces hyperglycaemia in weanlings concomitant with reduced GK expression which may compromise β-cell function.