[Frontiers in Bioscience 2, e108-115, November 1, 1997]

	[Frontiers in Bioscience 2, e108-115, November 1, 1997] Reprints PubMed CAVEAT LECTOR
	EFFECT OF AGING AND CALORIC RESTRICTION ON INTESTINAL SUGAR AND AMINO ACID TRANSPORT Ronaldo P. Ferraris Dept of Pharmacology and Physiology, UMDNJ-New Jersey Medical School, 185 South Orange Ave., Newark, NJ 07103 Received 7/17/97 Accepted 10/2/97 3. EFFECT OF AGING ON SUGAR TRANSPORT There are conflicting reports on the effect of aging on intestinal sugar transport. Intestinal glucose brushborder transport per mg measured in vitro changed little with age (< 24 months old) until measured in senescent (30 months old) mice whose glucose uptake was greater than those in younger mice (20). Wallis et al (21) also found no age-related change in glucose transport rate per mg protein across the brush border membrane of human enterocytes. Both studies measured initial uptake rate under incubation conditions with minimal unstirred layers, suggesting that the transport function of intestinal cells remain largely unaffected by age. Transepithelial glucose and fructose transport was found to increase in old (24 months old) compared to those in young (4 months old) rats (22). Since these transepithelial measurements expressed uptake in terms of mucosal surface area, transport may have increased because intestinal mucosa from old mice may have more absorptive cells, or because each cell transported more sugar. In contrast to these findings, most studies find intestinal sugar transport to decrease with age. Esposito et al (23, 24) found net transintestinal glucose transport per mg in vivo and in vitro to decrease significantly with age and demonstrated the absence of an overshoot when measuring brushborder membrane uptake of glucose in aged rats. Age-related reductions in glucose transport and this absence of an overshoot, which is indicative of Na⁺-independence, were each confirmed by Vincenzini et al (25) in brushborder membrane vesicles from aged humans, and by Lindi et al (26) and Treves et al (27) in aged rats. The ability to concentrate glucose in the intestinal cell or in the serosal medium also diminished with age (23). Hirata et al (28) used two independent methods (glucose transport in brushborder membrane vesicles, and glucose-induced changes in transepithelial electrical potentials) to demonstrate age-related reductions in glucose transport by rat small intestine. Active, but not passive, absorption of 3-O-methylglucose per mg also decreased with age by about two fold in vivo (29) as well as in vitro using everted sacs and brushborder membrane vesicles in rats (30). Chen et al (31) found age-dependent decreases in 3-O-methylglucose transepithelial transport and Ferraris et al (32) found age-dependent decreases in transmembrane transport per mg in mice. These studies concluded that a decrease in number of glucose transporters is the probable mechanism underlying the decrease in active glucose transport.

[Frontiers in Bioscience 2, e108-115, November 1, 1997]
Reprints
PubMed
CAVEAT LECTOR

EFFECT OF AGING AND CALORIC RESTRICTION ON INTESTINAL SUGAR AND AMINO ACID TRANSPORT

Ronaldo P. Ferraris

Dept of Pharmacology and Physiology, UMDNJ-New Jersey Medical School, 185 South Orange Ave., Newark, NJ 07103

Received 7/17/97 Accepted 10/2/97

3. EFFECT OF AGING ON SUGAR TRANSPORT

There are conflicting reports on the effect of aging on intestinal sugar transport. Intestinal glucose brushborder transport per mg measured in vitro changed little with age (< 24 months old) until measured in senescent (30 months old) mice whose glucose uptake was greater than those in younger mice (20). Wallis et al (21) also found no age-related change in glucose transport rate per mg protein across the brush border membrane of human enterocytes. Both studies measured initial uptake rate under incubation conditions with minimal unstirred layers, suggesting that the transport function of intestinal cells remain largely unaffected by age. Transepithelial glucose and fructose transport was found to increase in old (24 months old) compared to those in young (4 months old) rats (22). Since these transepithelial measurements expressed uptake in terms of mucosal surface area, transport may have increased because intestinal mucosa from old mice may have more absorptive cells, or because each cell transported more sugar.

In contrast to these findings, most studies find intestinal sugar transport to decrease with age. Esposito et al (23, 24) found net transintestinal glucose transport per mg in vivo and in vitro to decrease significantly with age and demonstrated the absence of an overshoot when measuring brushborder membrane uptake of glucose in aged rats. Age-related reductions in glucose transport and this absence of an overshoot, which is indicative of Na⁺-independence, were each confirmed by Vincenzini et al (25) in brushborder membrane vesicles from aged humans, and by Lindi et al (26) and Treves et al (27) in aged rats. The ability to concentrate glucose in the intestinal cell or in the serosal medium also diminished with age (23). Hirata et al (28) used two independent methods (glucose transport in brushborder membrane vesicles, and glucose-induced changes in transepithelial electrical potentials) to demonstrate age-related reductions in glucose transport by rat small intestine. Active, but not passive, absorption of 3-O-methylglucose per mg also decreased with age by about two fold in vivo (29) as well as in vitro using everted sacs and brushborder membrane vesicles in rats (30). Chen et al (31) found age-dependent decreases in 3-O-methylglucose transepithelial transport and Ferraris et al (32) found age-dependent decreases in transmembrane transport per mg in mice. These studies concluded that a decrease in number of glucose transporters is the probable mechanism underlying the decrease in active glucose transport.