Elliot Weser

The metabolism of circulating disaccharides was studied in adult humans and rats. After iv infusions of 10 g of either lactose, sucrose, or maltose in four adults, no rise in blood glucose was noted. A mean of 8.7+/-1.89 g of the lactose and 6.3+/-1.39 g of the sucrose was excreted in the 24-hour urine sample. Only 0.11+/-0.03 g of the infused maltose was recovered in the urine, suggesting that the maltose was metabolized.After injection of (14)C-labeled lactose and sucrose in rats, 6.2+/-2.7 and 7.6+/-2.4%, respectively, was oxidized to (14)CO(2) in 24 hours; 62.1+/-13.5 and 68.4+/-10.8% of the respective disaccharides was excreted into the urine. Conversely, after injection of (14)C-labeled maltose 54.6+/-7.0% was oxidized to (14)CO(2) and 4.8+/-3.9% excreted in the urine. The per cent of maltose oxidized to CO(2) was similar to that of glucose. In addition to small intestinal mucosa, homogenates of rat kidney, brain, and liver as well as serum were found to have measurable maltase activities. The role of these tissue maltases in the metabolism of circulating maltose and maltosyloligosaccharides is discussed.

DURING the later months of normal pregnancy the serum activity of the enzymes nonspecific alkaline phosphatase, 5-nucleotidase and leucine aminopeptidase may exceed the serum levels in nonpregnant women.13 These changes in serum enzyme may be due in part to a release of enzymes from the placenta4 , 5 and in part to a decrease in the maternal hepatic excretory function, reflected also by a reduced clearance of bromsulfalein.6 , 7 Clinical manifestations of liver disease associated with more severe impairment of liver function have been described in a small percentage of pregnant women near term.1 , 8 , 12 In patients suffering from cholestatic jaundice of pregnancy generalized . . .

SEVERAL recent studies suggest that lactase deficiency is common in the adult. It may be present as an isolated enzyme defect1 2 3 4 5 or may accompany organic disease of the small bowel.6 7 8 The symptoms attributed to lactase deficiency —abdominal cramps, distention, flatulence and diarrhea — result from a failure to hydrolyze and absorb ingested lactose. Increased intestinal peristalsis, with passage of acid, watery stools, may be due both to an osmotic shift of fluid into the lumen and to the action of lactic and acetic acids resulting from bacterial fermentation of lactose.9 These symptoms disappear when lactose is eliminated from the diet. . . .