Metabolism of circulating disaccharides in man and the rat.

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.

The metabolism of circulating maltose in man.

The utilization of circulating maltose was compared to that of glucose in six normal fasting subjects after intravenous injection of 25 g of either sugar. Blood samples were obtained over a 2 hr period and were assayed for free fatty acids (FFA), insulin, glucose, and total reducing substances. Urine was collected for 2 hr after maltose administration and assayed enzymatically for glucose and maltose. Blood glucose concentrations did not increase after maltose infusion, although a significant rise in total reducing substances was noted, indicating the presence of this disaccharide in the blood. Less than 3% of the administered maltose was excreted in the urine either as maltose or glucose. Initially, there was a fourfold increase in serum insulin concentration after glucose and a threefold increase after maltose infusion. Therefore, serum insulin concentrations gradually declined in a similar manner for both sugars. The plasma FFA at 15 min decreased 371 uEq/liter after glucose and 338 uEq/liter after maltose infusion. In other studies, 10 g maltose containing 5 muCi maltose-U-(14)C were injected into five human subjects and expired CO(2) collected for 6 hr. Maximal (14)CO(2) specific activity was noted at 170 min and a mean of 61.1% of the injected radioactivity was recovered as (14)CO(2). Less than 8% of the injected (14)C was excreted in the urine. These results indicate that maltose administered intravenously has similar metabolic effects when compared to glucose, and may be efficiently utilized as a carbohydrate substrate. The oxidation of intravenously administered maltose-U(14)C to (14)CO(2) demonstrates that circulating maltose is readily metabolized. A solution of maltose could provide twice the mass of sugar (and of calories) per milliliter as an equimolar solution of glucose. Parenterally administered maltose may be of clinical value and should be further studied.

Lactose malabsorption in Mexican-American adults.

Lactose malabsorption was determined in 277 Mexican-American (MA) and 142 Anglo-American (AA) adults aged 18 to 94 years old, and correlated with nutrient intake assessed from 24-hr dietary recalls, as well as with milk and dairy product consumption. Lactose malabsorption occurred in 144 of 277 (53%) MA and 21 of 142 (15%) AA. Analysis of dietary questionnaires revealed no differences between lactose absorbers and malabsorbers within each ethnic group in their consumption of protein, calories, riboflavin, vitamin A, or calcium. Vitamin A, calcium, and riboflavin intake was greater in AA than in MA subjects. Milk and dairy product consumption was the same in lactose absorbers and malabsorbers in both ethnic groups. Nearly 60% of MA malabsorbers and 24% of AA malabsorbers recognized experiencing symptoms after milk ingestion. Although group differences in milk consumption on the basis of lactose absorption status are not apparent, individual lactose malabsorbers may alter milk ingestion in response to lactose-induced symptoms. Lactose malabsorption occurs in over half of MA adults and may in some individuals present a clinically relevant problem.

Lactose malabsorption in Mexican-American children.

Inability to absorb lactose due to low intestinal lactase is common in many population groups. This study is the first to compare lactose tolerance in 282 Mexican-American (MA) children and 51 Anglo-American (AA) children 2 to 14 years of age with the dietary intake of selected nutrients found in milk. A lactose tolerance test and a 24-hr dietary recall were obtained for each child. Gastrointestinal symptoms were carefully recorded for a 24-hr period following the lactose load. Overall prevalence of lactose malabsorption was 37% in MA children and 8% in AA children, and it increased with age. Number of symptoms occurring in lactose malabsorbers of both ethnic groups also increased with age. Mean protein intake exceeded Recommended Dietary Allowances at all ages for both ethnic groups. Mean consumption of vitamin A, calcium, and energy was below the Recommended Dietary Allowance for MA children. There were no differences in calories, nutrient, or milk intakes between lactose absorbers and malabsorbers, but AA children drank more milk than MA children. Fifteen percent of lactose-absorbing MA, 23% of malabsorbing MA, but no AA children reported having symptoms after drinking milk. There was a significantly greater incidence of lactose intolerance in MA as compared to AA children. This suggests that Mexican-Americans share in the high incidence of primary lactose intolerance characteristic of the majority of the orld's peoples.

Development of core competencies in clinical nutrition.

A nationwide survey of core competencies of nutrition knowledge and skills that primary care physicians should know and/or be able to do has been completed. Nutrition competencies were synthesized from a review of clinical nutrition practices as reported in the medical literature and by medical school faculty group discussions. A nutrition competency questionnaire was sent to 445 practicing physicians and to 752 department chairpersons in every US medical school in the disciplines of family practice, medicine, obstetrics and gynecology, pediatrics, psychiatry, and surgery. The overall response rate for practitioners and faculty combined was 46.03%. Of the 55 nutrition competencies, 28 items received very strong support (greater than 90% of respondents marked agree or completely agree). Twenty-two competencies received strong support (80 to 89% of respondents marked agree or completely agree), and five items received mixed support (40 to 79% of respondents marked agree or completely agree). Statistical comparisons of the item responses between practitioners and faculty were significantly different (p less than 0.05) on 19 (35%) of the items. It is anticipated that the 50 nutrition competencies that have received strong or very strong agreement among the 551 physicians representing primary care disciplines across the US will serve as guidelines for continued development of medical school curriculum and continuing medical education in clinical nutrition.

Comparative study of nutritional adaptation to defined formula diets in rats.

Little is known about the specific effects of defined formula diets (DFD) on mucosal growth of the small intestine, pancreas, or liver. In the present study male Sprague Dawley rats weighing 220 to 250 g were fed isocaloric amounts of DFD (61 kcal/day) by continuous intragastric infusion. The diets fed were Vivonex, Vivonex-HN, Flexical, and Ensure. Oral chow-fed rats with intragastric water infusions served as reference. All groups gained weight: chow 50.50 g, Vivonex 21.17 g (P < 0.005), Vivonex-HN 25.40 g (P < 0.005), Flexical 30.5 g (P < 0.01), Ensure 39.29 g (NS). After 2 weeks rats were killed, the small bowel excised, rinsed, and divided into eight equal segments. Mucosal weight, DNA, and protein concentration per centimeter segment were measured. The pancreas was also removed, homogenized, and amylase activity assayed (units/g). Livers were excised, weighed, lipid content measured, and liver histology was examined by light microscopy. Mucosal weight, DNA, and protein concentrations per segment were decreased significantly in most bowel segments of DFD fed rats. Amylase activity per gram pancreas was significantly reduced in rats fed Vivonex, Flexical, and Ensure, Serum amylase activity was also lowered in animals on DFD. There was significant accumulation of lipid in the liver of Vivonex and Flexical animals (P < 0.01). Liver histology confirmed the striking increase in fat in the Vivonex and Flexical groups. These effects may result from differences in DFD absorption, mucosal metabolism, stimulation of enteric hormone release, and/or bile and pancreatic secretions.

Nutritional aspects of malabsorption. Short gut adaptation.

Adaptation of remaining small bowel after extensive intestinal resection plays an important part in maintaining adequate nutrition. The metabolic consequences of short bowel depend upon the anatomic extent of bowel removed, the functional condition of remaining digestive organs and the degree to which adaptive changes occur. The pathophysiology of short bowel results primarily from the abnormal absorption of nutrients and selective metabolites leading to malnutrition and other organ complications. Nutrients in the lumen of the small intestine are required to stimulate the process of intestinal adaptation (mucosal hyperplasia). This stimulation may be mediated via direct mucosal absorption or metabolism of nutrients, the presence of pancreaticobiliary secretions in the intestine, trophic effects of circulating enteric hormones, or neurovascular influences. Understanding the mechanisms by which mucosal growth may be stimulated could lead to important clinical applications.

Radiography of ileal adaptation in the rat following jejunectomy.

Six Sprague-Dawley rats were evaluated radiographically and histologically for adaptive changes in the ileum following total jejunal resection. Additionally, six rats were used as controls and six rats had sham operations. Marked hypertrophy of the ileum and hyperplasia of the mucosa with thickening of the ileal wall were documented in all six of the jejunectomized rats, compared with sham and unoperated controls. Radiographic changes were demonstrated in the bowel wall in three of six resected animals. These consisted of an irregular, serrated lumen that was normal to narrowed in caliber. No radiographic or histologic changes were seen in the control or sham rats. These results correlate radiographic changes with adaptive morphology of rat ileum after jejunal resection and resemble changes of adaptation seen in humans who have had jejunal-ileal bypass, jejunal resection, or nontropical sprue.

Effect of diverting bile and pancreatic secretions into the ileum on small bowel mucosa in rats fed a liquid formula diet.

The long-term effects of diverting bile and pancreatic secretions directly into the ileum on small bowel mucosa was determined in rats fed a hydrolyzed liquid formula diet. Male Sprague-Dawley rats were divided into four experimental groups: duodenal papilla transplant-sham operation, transplantation of the duodenal papilla into the ileum, bile duct sham operation, and transplantation of the bile duct into the ileum. After 28 days, animals were killed, the same bowel removed, rinsed with cold isotonic saline, and divided into six segments (two jejunal segments and four ileal segments). The mucosa of each segment was weighed and assayed for DNA and protein concentration, and specific activity of sucrase and maltase. Bile and particularly pancreatic secretions diverted into the ileum stimulated local mucosal growth compared with their respective controls. The absence of pancreatic secretions from the jejunum also was associated with an increase in jejunal mucosal mass. Diverting pancreatic secretions into the ileum decreased ileal sucrase and maltase specific activity while the absence of both bile and pancreatic secretions from the jejunum increased jejunal sucrase specific activity. The results suggest that bile and pancreatic secretions entering the ileum are important factors in stimulating ileal mucosal hyperplasia while the absence of these secretions from the proximal intestine is associated with greater jejunal mucosal growth. The mechanisms regulating jejunal mucosal growth appear to be different than those influencing the ileum.

Non-hormonal regulation of intestinal adaptation.

Infusion of simple sugars and some amino acids into the lumen of the small bowel stimulates local mucosal growth where these substrates come into direct contact with the mucosa. This stimulation does not require active absorption or mucosal metabolism of the substrate and in the case of glucose can be inhibited by phlorizin. Infusion of sugars and some amino acids into ileal lumen results in mucosal growth of proximal bowel distant from the site of infusion. Diverting pancreatico-biliary secretions from proximal to distal small bowel lumen markedly stimulates growth in distal small bowel, while the absence of these secretions from the duodenojejunum paradoxically results in growth of the mucosa at this site. Such regional differences in adaptation suggest that regulation of mucosal growth is different in proximal and distal small bowel.

Pyrimidine biosynthetic enzymes in rat intestine after small bowel resection.

After small bowel resection in the rat, mucosal hyperplasia and an increase in nucleic acid synthesis and cell proliferation occur in remaining small intestine. Male Sprague-Dawley rate underwent resection of 50 cm of proximal or distal intestine or sham operation. One month and 6 months after surgery, aspartate transcarbamylase, dihydroorotase, and uridine kinase were assayed in whole mucosa, and in some instances, in crypt mucosa ffrom the remaining intestinal segment. In control bowel, enzyme activity was significantly greater proximal compared with distal segments. One month after proximal or distal resection, mucosal enzyme activity per cm of gut was greater in the remnant bowel compared with controls. There was no such difference at 6 months. Specific enzyme activity of whole mucosa did not increase after resection because the assay was influenced by the disproportionately large contribution of villous protein. Specific enzyme activity (including thymidine kinase) of isolated crypt mucosa was significantly increased 1 month after distal resection. In addition, [3H]thymidine uptake into DNA of crypt mucosa from proximal remnants was also significantly increased. These results indicate that after small bowel resection, the enzymes of pryimidine biosynthesis increase in remaining bowel and parallel the accelerated rate of cell proliferation.