Submitted to: Journal of Animal Science
Publication Type: Abstract Only
Publication Acceptance Date: September 8, 2003
Publication Date: September 8, 2003
Citation: Baldwin, R.L., Rodriquez, S.M., Guimaraes, K.C., Mathews, J.C., Mcleod, K.R., Harmon, D.L., 2003. Influence of abomasal carbohydrates on small intestinal sodium-dependent glucose co-transporter activity and abundance in steers [abstract]. Journal of Dairy Science 86 (Suppl. 1):266.
There is conflicting data concerning the extent of up-regulation of SGLT1 in response to carbohydrate in the small intestinal lumen. An experiment was conducted to determine the effect of glucose and starch hydrolysate on activity and abundance of sodium-dependent glucose co-transporter 1 (SGLT1) in the small intestine of steers. In a randomized complete block design, forty crossbred beef steers (243 ± 2 kg BW) were fed 0.163 Mcal ME/(kg BW0.75·d) (1M) or 0.215 Mcal ME/(kg BW0.75·d) (2M) or they were fed 0.163 Mcal ME/(kg BW0.75·d) and infused for 35 d into the rumen (R) or abomasum (A) with starch hydrolysate (S) or into the abomasum with glucose (G). Steers were slaughtered, and brush-border membrane vesicles were prepared from the small intestinal samples obtained from five equidistant sites along the intestine. The maltase activity, Na+ dependent glucose transport capacity and SGLT1 protein abundance of the vesicles were determined. Maltase specific activity in vesicles and homogenates differed with intestinal sampling site (quadratic; P < 0.001). The AG treatment yielded a higher intestinal maltase specific activity (38 nmol glucose·mg protein-1 ·min-1) compared to the AS, RS, 1M or 2M treatment [34, 26, 23, and 23 nmol glucose·mg protein-1 ·min.-1, respectively (SEM=3; P = 0.02)]. Sodium dependent glucose uptake by the membrane vesicles was not affected by treatment, but decreased distally along the intestine (P < 0.001). There was no effect of treatment on SGLT1 protein abundance, but SGLT1 protein abundance increased from the duodenum to the ileum (linear; P = 0.05). The inverse relationship between glucose uptake and SGLT1 abundance suggests that regulation of glucose transport capacity is complex, involving factors other than SGLT1 abundance.