Heat stress increases apical glucose transport in the chicken jejunum.

In chickens, elevated environmental temperature reduces food intake. We have previously reported that, during heat stress, the intestinal mucosa has an increased capacity to take up sugars. To investigate whether the effects of warm environment on sugar uptake are an intestinal adaptation to lower energy intake or a response attributable to heat stress, we examined the glucose transport kinetics of apical and basolateral membranes of the jejunum and the mucosal morphology of broiler chickens maintained in climatic chambers for 2 wk. Experimental groups were 1) control ad libitum (CAL), fed ad libitum and in thermoneutral conditions (20 degrees C); 2) heat stress ad libitum (HSAL), fed ad libitum and kept in a heated environment (30 degrees C); and 3) control pair-fed (CPF), maintained in thermoneutral conditions and fed the same amount of food as that consumed by the HSAL group. Both the CPF and the HSAL groups showed reduced body weight gain, but only the HSAL chickens had lower plasma thyroid hormones and higher corticosterone than CAL and CPF groups. The fresh weight and length of the jejunum were only reduced in the HSAL group. The activity and expression of apical sodium-dependent glucose transporter 1 (SGLT-1) were increased by approximately 50% in the HSAL chickens, without effects in the CPF group. No changes in K(d) or in SGLT-1 and glucose transporter-2 K(m) were observed in the pair-fed and heated birds. These results support the view that increased intestinal hexose transport capacity is entirely dependent on adaptations of apical SGLT-1 expression to heat stress and is not due to reduced food intake.

Spray-dried porcine plasma reduces the effects of staphylococcal enterotoxin B on glucose transport in rat intestine.

We investigated the intestinal transport of D-glucose (D-Glc) and 3 essential amino acids in a model of intestinal inflammation, and the effects of dietary supplementation with animal plasma proteins on this function. Wistar Lewis rats were fed a diet containing an isonitrogenous amount of milk protein (control group) or a diet supplemented with either spray-dried animal plasma (SDAP) or immunoglobulin concentrate (IC) from porcine plasma, from d 21 of life (weaning) until d 35. On d 30 and 33, rats were challenged intraperitoneally with Staphylococcus aureus enterotoxin B (SEB; groups SEB, SEB-SDAP, and SEB-IC) and on d 35, brush border membrane vesicles (BBMVs) were prepared and used for transport and binding studies. Administration of SEB reduced D-Glc transport across sodium glucose transporter 1 [SGLT1; 20% reduction in maximal transport rate (Vmax); P < 0.05], without affecting the Michaelis constant (Km). The results from specific phlorizin binding, Western blot, and immunohistochemistry supported the view that the effects of SEB are due to reduced expression of D-Glc transporters in the apical membrane. SEB increased the passive diffusion constant (Kd) for D-Glc 3-fold (P < 0.05). SEB did not affect mediated or passive amino acid fluxes of L-leucine, L-methionine, or L-lysine. Dietary SDAP increased the D-Glc Vmax in the SEB group without affecting the passive component. Changes in d-Glc Vmax due to SEB and to the dietary treatments were correlated with changes in the number of SGLT1 transporters present in the BBMVs (r = 0.9468; P < 0.05). Dietary IC had no observed effect. We estimate that, in rats challenged with SEB, SDAP supplementation can increase glucose absorption by 8-9% during the interdigestive periods.

Ontogenetic expression and regulation of Na(+)-D-glucose cotransporter in jejunum of domestic chicken.

To evaluate the effect of age on sugar transport, we determined the uptake of methyl alpha-D-glucopyranoside and the abundance of the Na(+)-D-glucose cotransporter (SGLT1) in jejunal brush-border membrane (BBM) vesicles of 2-day- and 5-wk-old chickens. Methyl alpha-D-glucopyranoside transport per BBM protein was 40% lower in adults than in newly hatched chickens. This finding was matched by parallel declines in site density of SGLT1, which were detected by Western blot. The immunohistochemical study showed that SGLT1 was exclusively located in the BBM of enterocytes along the entire villus and was absent in the crypt in both age groups, and there was an 11-fold increase in the total absorptive area during development. Northern blot studies of the abundance of SGLT1 mRNA showed similar levels for the groups studied. We conclude that the age-related decline in Na(+)-dependent hexose transport per unit of BBM protein in the chicken jejunum is due to a reduction in the density of SGLT1 cotransporter and is regulated by a posttranscriptional mechanism.

Regulation of SGLT1 expression in response to Na(+) intake.

In the chicken intestine, the reduction in Na(+) intake led to a decrease in the transport of alpha-methyl-D-glucoside in the ileum (reduction of 42%) and in the rectum (51%). These reductions were reversed within 24 h after resalination and were inversely correlated to the changes in aldosterone plasma concentration. The reduction in intestinal hexose transport in the low Na(+)-fed animals was due to a decrease in the number of Na(+)-dependent D-glucose cotransporters (SGLT1) in the rectum (46%) and in the ileum (38%). Northern blot analysis showed that specific SGLT1 mRNA was expressed in the jejunum, ileum, and rectum. The amount of SGLT1 mRNA was the same in all intestinal regions and was not affected by Na(+) intake, supporting the view that the effects of dietary Na(+) on intestinal hexose transport involve posttranscriptional regulation of SGLT1. This study suggests that changes in SGLT1 expression may be involved in the homeostasis of Na(+).