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Biomedical subjects

A B Thomson

Publications and source records attributed to A B Thomson.

At least 145 records · Page 8Linked to original sources
PubMed1991

Effect of dietary fat on diabetes-induced changes in liver microsomal fatty acid composition and glucose-6-phosphatase activity in rats.

Experimental diabetes may manifest itself in a defect in liver microsomal fatty acid desaturation and increased activity of glucose-6-phosphatase (G-6-Pase). The present study was designed to determine whether these changes could be normalized by a change in the dietary fat consumed. Control and streptozotocin-induced diabetic rats were fed nutritionally adequate diets which varied in fatty acid composition. Fatty acid analysis of liver microsomal phospholipids revealed that non-diabetic control animals fed saturated fat (beef tallow) or a diet high in omega 3 fatty acids (fish oil) exhibited a significantly higher level of 18:2 omega 6 and a lower level of 20:4 omega 6 in the phosphatidylcholine and phosphatidylethanolamine fractions compared with diabetic animals. Control and diabetic animals fed the high linoleic acid diet had similar levels of 18:2 omega 6 in the microsomal phosphatidylcholine and phosphatidylserine fractions. Microsomal G-6-Pase activity was higher in diabetic than in control animals. Activity of G-6-Pase was lower in microsomes of control animals fed the soybean oil or the fish oil diet, but was not significantly reduced in diabetic animals fed high polyunsaturated fats. Blood glucose levels were similar in control groups fed the different diets, but the plasma hemoglobin Alc level was lower in diabetic animals fed the soybean oil diet. Cholesterol and triglyceride levels were lower in diabetic animals fed the fish oil-based diet. The results suggest that dietary fat manipulation has the potential to change at least some of the abnormalities in the microsomal membrane in experimental diabetes.

Animals↗
PubMed1991

Effect of nisoldipine on atherosclerosis in the cholesterol fed rabbit: endothelium dependent relaxation and aortic cholesterol content.

STUDY OBJECTIVE: The aim was to determine the effect of the calcium channel blocker nisoldipine on the loss of endothelium dependent relaxation and the accumulation of cholesterol in the aorta produced by feeding a diet enriched with cholesterol. DESIGN: 12 week old New Zealand white rabbits were assigned randomly to four groups with the following dietary and drug regimens: group A--standard diet + 2.5% cholesterol (n = 45); group B--standard diet + nisoldipine (n = 9); group C--standard diet + nisoldipine + 2.5% cholesterol (n = 9); group D--standard diet (n = 9). After 3 weeks the cholesterol supplements were stopped and all animals were given the standard rabbit diet. The animals in groups B and C were given nisoldipine (1 mg.kg-1.d-1) by mouth for the entire 7 week period. EXPERIMENTAL MATERIAL: Aortic tissue was removed for measurement of cholesterol content, endothelium dependent relaxation to acetylcholine, contractile responses to noradrenaline, relaxant responses to sodium nitrite, and sudan staining. Serum was obtained for measurement of cholesterol and triglyceride concentration. MEASUREMENTS AND MAIN RESULTS: At 7 weeks, endothelium dependent relaxation to acetylcholine was impaired in group A compared to group D, while that in group C was not. Aortic tissue cholesterol content in group A was significantly greater than in groups B, C, and D. At 15 weeks, ie, 12 weeks after reversal of the diet, endothelium dependent relaxation had recovered in the animals in group A. There was a significant reduction in the aortic cholesterol content at this stage. In two subgroups of A (groups A2 and A4) which were given nisoldipine immediately after and 4 weeks after cessation of cholesterol feeding respectively, the drug was found to have no influence upon restoration of endothelium dependent relaxation. However, the drug appeared to promote the retention of cholesterol within the aorta after cessation of cholesterol feeding. CONCLUSIONS: Nisoldipine protects against the accumulation of cholesterol and loss of endothelium dependent relaxation in the aorta of rabbits fed a diet supplemented with 2.5% cholesterol for three weeks. Administration of the drug after the lesions are established in the aorta also appears to retard the removal of cholesterol from the aorta.

Acetylcholine↗
PubMed1991

Lovastatin prevents the impairment of endothelium dependent relaxation and inhibits accumulation of cholesterol in the aorta in experimental atherosclerosis in rabbits.

STUDY OBJECTIVE: The aim was to determine the effect of the HMG CoA reductase inhibitor, lovastatin, on the loss of endothelium dependent relaxation and the accumulation of cholesterol in the aorta produced by feeding a diet enriched with cholesterol. DESIGN: The study was conducted in two stages. In stage 1, New Zealand white rabbits were randomised into four groups. Group 1 (n = 15) was fed standard rabbit diet for 6 weeks. Groups 2 (n = 15), 3 (n = 12), and 4 (n = 12) were fed standard rabbit diet supplemented with 2% cholesterol for 2 weeks followed by standard rabbit diet only for the next 4 weeks. In addition, lovastatin (4 mg.kg-1.d-1) was given for the entire 6 weeks in group 3 and for the first 2 weeks only in group 4. In stage 2 a second group of animals was fed a diet supplemented with 0.5% cholesterol for 2 weeks in order to match the serum cholesterol levels in groups 3 and 4 of stage 1. EXPERIMENTAL MATERIAL: Aortic tissue was removed for measurement of cholesterol content, endothelium dependent relaxation (to acetylcholine), contractile responses (to noradrenaline), relaxant responses (to sodium nitrite), and sudan staining. Serum was obtained for measurement of cholesterol and triglyceride concentrations. MEASUREMENTS AND MAIN RESULTS: In stage 1, at the end of 2 weeks, the serum cholesterol was significantly lower in groups 3 and 4 than in group 2. At 6 weeks, endothelium dependent relaxation to acetylcholine (-6.0 log mol.litre-1) was impaired in group 2 compared to the other groups: group 1 78.5(SEM 5.0); group 2 43.5(7.8)%; group 3 79.4(4.6)%; group 4 84.7(3.4)%. The relaxant response to sodium nitrite was not impaired in group 2. Further, the aortic tissue cholesterol concentration in group 2 was significantly greater than that in group 1, at 355(65) v 105(10) nmol.mg-1 protein. In groups 3 and 4, the aortic cholesterol concentrations were significantly lower than those in group 2, at 74(4) and 94(17) nmol.mg-1 protein respectively. In stage 2, the serum cholesterol values were matched to those in groups 3 and 4 of stage 1. In these animals, after a further 4 weeks the aortic cholesterol was significantly greater than in group 3. CONCLUSIONS: Lovastatin attenuates the accumulation of cholesterol and preserves endothelium dependent relaxation in this model of experimental atherosclerosis. It is likely that the latter is a secondary phenomenon.

Acetylcholine↗
PubMed1991

Review article: new developments in the use of 5-aminosalicylic acid in patients with inflammatory bowel disease.

Sulphasalazine is composed of sulphapyridine and mesalazine (5-aminosalicylic acid, 5-ASA or mesalazine) joined by an azo bond. Sulphasalazine has been used clinically for 40 years but less than 10 years ago it was recognized that the active moiety is 5-ASA. Sulphapyridine appears to act only as a carrier molecule to deliver mesalazine to the bowel, yet it is the sulphapyridine which appears to be responsible for many of the adverse effects observed with sulphasalazine. Normally, mesalazine is rapidly absorbed from the upper gastrointestinal tract. Since the action of mesalazine is thought to be locally at the site of disease in the intestine, the 5-ASA must be 'protected' to ensure its release in the terminal ileum and colon, the site of bowel inflammation in patients with Crohn's disease or ulcerative colitis. Recent clinical studies have confirmed the efficacy of topical (suppositories and enemas) therapy for ulcerative proctitis and left-sided colitis; oral mesalazine has been proven to be useful for the treatment of acute ulcerative colitis and for the maintenance of remission. There is preliminary evidence for the clinical usefulness of mesalazine in acute Crohn's disease as well as for the maintenance of remission.

Aminosalicylic Acids↗
PubMed1991

Fish oil-enriched diet is mucosal protective against acetic acid-induced colitis in rats.

Products of arachidonic acid metabolism are elevated in patients with inflammatory bowel disease and this elevation is correlated with disease activity. Eicosapentaenoic acid competes with arachidonic acid and alters eicosanoid biosynthesis. In this experiment, the possibility that eicosapentaenoic acid could be used in the treatment of inflammatory bowel disease was investigated by determining the effect of 6 weeks of a fish oil-supplemented diet, enriched in eicosapentaenoic acid, on colonic and ileal morphology, histology, and in vivo fluid absorption in rats with 4% acetic acid-induced colitis. The results of an eicosapentaenoic acid-enriched diet were compared with results of saturated and polyunsaturated fatty acid-enriched diets. In rats with misoprostol pretreated acetic acid-induced colitis, an eicosapentaenoic acid-enriched diet reversed net colonic fluid secretion to absorption and prevented macroscopic and histologic injury, compared with saturated and poly-unsaturated fatty acid-enriched diets, which did not. The fish oil mucosal protective effect occurred in the presence of a 30-fold enhancement of PGE2 synthesis. In rats with non-misoprostol pretreated acetic acid-induced colitis, an eicosapentaenoic acid-enriched diet returned ileal fluid absorption to control levels, as compared with saturated and polyunsaturated fatty acid-enriched diets, which did not. In conclusion, a fish oil (eicosapentaenoic acid)-enriched diet, but not a saturated- or a polyunsaturated-enriched diet, protected colonic and ileal net fluid absorption in an experimental model of inflammatory bowel disease.

Acetates↗
PubMed1991

Feeding diets containing 2% cheno- or urso-deoxycholic acid or cholestyramine to rats for two weeks alters intestinal morphology and bile acid absorption.

This study was undertaken to examine the effect of supplementing chow for 2 weeks with 2% cheno- (CDC) or ursodeoxycholic (UDC) acid or cholestyramine (CHOL) on the intestinal morphology and in vitro uptake of bile acids in adult rats. Food intake was higher in UDC and CHOL as compared with animals fed chow or CDC, or in animals pair-fed a chow-restricted diet (CRD). Body weight gain was lower in CDC and CRD but was unchanged by feeding UDC or CHOL. Jejunal mucosal surface area was similar in the five groups, although the ileal mucosal surface area was lower in UDC than in the other animals. Feeding UDC reduced the ileal uptake of cholic acid (C), taurocholic acid (TC), and glycocholic acid (GC). Feeding CDC had no effect on bile acid uptake except when compared with animals fed a chow-restricted diet. Feeding CHOL reduced the active ileal uptake of C, had no effect on the uptake of TC or GC or CDC, and was associated with increased uptake of stearic, linoleic, and linolenic acids. These effects were likely related to a direct effect of changes in the luminal bile acids rather than due to an indirect effect of the reduced food intake, since the ileal uptake of CDC and GC was greater in animals fed CDC than in those fed a chow-restricted diet with comparable weight gain. Thus, 2 weeks of feeding bile acids or bile acid binding agents may alter the form and function of the rat intestine, and as well may lead to changes in food intake and body weight gain.

Animals↗
PubMed1991

Adaptation of intestinal glucose transport in rats with diabetes mellitus occurs independent of hyperphagia.

Chronic diabetes enhances intestinal absorption of glucose and induces hyperphagia. We examined the enhanced intestinal absorption of glucose in ad libitum-fed rats with streptozocin-induced diabetes mellitus and compared these results with those obtained from pair-fed diabetic animals. Maximal transport capacity (Vmax) and carrier affinity (K0.5) were determined by measuring jejunal and ileal short circuit current (Isc) responses to varying concentrations of 3-O-methyl-D-glucopyranose and D-glucose. Pair-fed diabetic animals maintained the same body weight as animals fed ad libitum, although ad libitum-fed diabetic rats had an increased oral chow intake. Age-matched control rats maintained a constant jejunal and ileal Vmax and K0.5 throughout the study. Diabetic rats fed ad libitum demonstrated an enhanced Vmax and K0.5 in both jejunum and ileum. Pair feeding diabetic animals further enhanced jejunal Vmax while lowering jejunal K0.5 levels. In contrast, pair feeding diabetic animals delayed and blunted changes in ileal Vmax and prevented changes in ileal K0.5. In conclusion, signals other than those of hyperphagia regulate kinetic changes in glucose absorption during diabetes mellitus. Furthermore, these changes have differing effects on jejunum and ileum.

Adaptation, Biological↗
PubMed1991

Altered glucose carrier expression: mechanism of intestinal adaptation during streptozocin-induced diabetes in rats.

Intestinal adaptation of glucose transport during streptozocin-induced diabetes in rats was examined using microdensitometric analysis of [3H]phlorizin binding. Results of specific phlorizin binding were correlated with measurements of maximal transport capacity, carrier affinity, villus height, and enterocyte birth rate determined by the metaphase arrest technique. Animals diabetic for 14 days (acute) and 60 days (chronic) were compared with age-matched controls. In the jejunum, adaptation occurred only in chronically diabetic rats and consisted of a 10-fold increase in the density of phlorizin binding sites in the upper villus region (i.e., that portion normally transporting glucose), while in the ileum, adaptation occurred both in acute and chronically diabetic rats and consisted of 1) a 3-fold increase in density of phlorizin binding sites in the upper villus region of acutely diabetic rats and 2) an increased density in the upper villus region as well as the recruitment of phlorizin binding sites in the mid to lower villus region (i.e., that portion not normally transporting glucose) of chronically diabetic rats. Enhancement of glucose Vmax and villus length accompanied changes in binding, whereas enterocyte birth rates were similar in each group.

3-O-Methylglucose↗
PubMed1991

Isocaloric modification of dietary lipids influences intestinal brush border membrane composition in diabetic rats.

Variations in the dietary fatty acid composition and cholesterol content are associated with alterations in the intestinal uptake of hexoses and lipids in control and diabetic rats. Changes in the composition of the brush membrane (BBM) lipids may provide a possible mechanism for the observed alterations in transport properties. Accordingly, control and streptozotocin diabetic animals were fed one of four isocaloric semisynthetic diets for two weeks: beef tallow with low cholesterol, beef tallow with high cholesterol, fish oil with low cholesterol or fish oil with high cholesterol. BBM were prepared and assessed for marker enzyme activity and lipid composition. Fish oil feeding was associated with a reduction in total phospholipid content in control and diabetic jejunal and ileal BBM; this fall in total phospholipids was due to a reduction in BBM sphingomyelin. Cholesterol supplementation increased control jejunal BBM sucrase activity in animals fed beef tallow but reduced sucrase activity in animals fed fish oil. In fish oil fed diabetic animals, jejunal and ileal BBM alkaline phosphatase activity was increased with cholesterol supplementation. The elevation in BBM total phospholipids (phosphatidylethanolamine) associated with diabetes in beef tallow fed animals was not observed in the jejunal BBM of animals fed fish oil or in the ileal BBM of animals fed fish oil with high cholesterol. Thus, (a) feeding an omega-3 polyunsaturated fatty acid diet (fish oil) reduced total phospholipid content in BBM of control and diabetic animals, primarily due to a reduction in sphingomyelin; and (b) feeding an omega-3 polyunsaturated fatty acid diet or dietary cholesterol supplementation alter the activity of BBM enzymes. These results suggest that variations in dietary fat composition and the associated changes in BBM composition and enzyme activity contribute to altered intestinal function in diabetes.

Animals↗
PubMed1991

The irradiation-associated decline in the in vivo uptake of glucose observed in rats fed fish oil is prevented by feeding a diet enriched in saturated fatty acids.

Previous in vitro studies have shown that abdominal irradiation diminishes the uptake of many nutrients and that the extent of this effect can be modified by varying the type of dietary fatty acid. This study was undertaken to determine (1) the effect of dietary fish oil fatty acids (FO) on the in vivo absorption of D-glucose and (2) the effect of feeding isocaloric diets containing FO or beef tallow (BT) on the in vivo uptake of glucose 2 weeks after a single 600 cGy exposure to abdominal irradiation from a 137Cs source. Feeding FO reduced the jejunal and ileal maximal transport rate (Vmax) and Michaelis constant (Km) for glucose uptake in nonirradiated control animals. In irradiated rats the Vmax was higher and the Km was lower in animals fed BT than in those fed FO. The passive component of glucose uptake was higher in control rats fed FO than in those fed BT yet was lower in irradiated animals fed FO compared with those fed BT. Although the value of the Km fell with FO, the effective resistance of the intestinal unstirred water layer rose so that the uptake of lower concentrations of glucose was undisturbed. However, FO reduces the uptake of higher concentrations of glucose as a result of a decline in the value of the Vmax that is sufficiently large to override the enhanced passive permeability of the intestine to glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1990

Diet fat composition alters membrane phospholipid composition, insulin binding, and glucose metabolism in adipocytes from control and diabetic animals.

The present study was designed to determine if diet fat-induced alteration in the fatty acid composition of the adipocyte plasma membrane alters insulin binding and the insulin responsiveness of glucose metabolism in control and diabetic states. Normal (control) and diabetic (streptozotocin-induced) rats were fed high fat semipurified diets providing a high or low polyunsaturated to saturated fatty acid (P/S) ratio. Feeding a high P/S diet increased the polyunsaturated fatty acid content of major membrane phospholipids of the adipocyte plasma membrane from both normal and diabetic animals. The diabetic state was associated with an elevated content of linoleic acid and a reduced level of arachidonic acid consistent with reduced delta 6-desaturation. Feeding the high P/S diet to diabetic animals increased membrane linoleic acid content and prevented the decrease observed in the arachidonic acid of membrane phospholipids. The high P/S diet was associated with increased insulin binding in nondiabetic animals but did not change the amount of insulin bound by cells from diabetic animals. Significantly (p less than 0.05) increased rates of insulin-stimulated glucose transport and lipogenesis (glucose incorporation into lipids) were observed in control animals fed the high as compared to the low P/S diet. The rates of insulin-stimulated glucose transport, oxidation, and lipogenesis were lower (p less than 0.05) for cells from diabetic as compared to control animals. However, feeding a high P/S diet significantly improved rates for all three of these functions (p less than 0.05). It is concluded that diet-induced alterations in membrane composition may provide a mechanism for improving the cellular response to insulin in cells from diabetic animals.

Adipose Tissue↗
PubMed1990

The physiology of adaptation to small bowel resection in the pig: an integrated study of morphological and functional changes.

This study examined the adaptive response to extensive small intestinal resection in the juvenile domestic pig. Control animals underwent an ileal transection with end-to-end anastomosis, whereas resected pigs had a resection of the mid-75% of the total small bowel length. Animals were followed for 16 weeks. Resected animals gained less weight than controls, with no significant difference in feed intake per unit animal weight. In vivo fat, protein, carbohydrate, and total energy absorption were reduced in resected animals. Resected pigs had increased in vitro passive ileal uptake of fatty acids, cholesterol, and L-glucose, but no change in active D-glucose uptake. Microscopic morphology was altered, with an increase in the size of villi, a decrease in villous density, and no net change in mucosal surface area per unit of serosal surface area. Gross bowel length and diameter increased proportionately more in the resected than the control groups. This study demonstrated that massive resection results in a significant change in nutritional status in the growing pig. Functional and morphological changes occur, demonstrating intestinal adaptation. These findings suggest that this model would be suitable for the study of therapeutic modalities for the short-bowel syndrome in humans.

Animals↗
PubMed1990

Alteration of the lipid composition of rat testicular plasma membranes by dietary (n-3) fatty acids changes the responsiveness of Leydig cells and testosterone synthesis.

Experiments were conducted to assess whether changing dietary fat composition altered phospholipid composition of rat testicular plasma membranes in a manner that altered receptor-mediated action of luteinizing hormone (LH)/human chorionic gonadotropin (hCG). Weanling rats were fed diets that provided high or low cholesterol intakes and that were enriched with linseed oil, fish oil or beef tallow for 4 wk. Feeding diets high in (n-3) fatty acids decreased plasma and testicular plasma membrane 20:4(n-6) content. A marked reduction of the 22:5(n-6) content and an increase in the 22:6(n-3) content of testicular plasma membrane was found only in animals fed fish oil. A decrease in binding capacity of the gonadotropin (LH/hCG) receptor in the plasma membrane, with no change in receptor affinity, was observed for animals fed either linseed oil or fish oil diets. Dietary treatments that raised plasma membrane cholesterol content and the cholesterol to phospholipid ratio in the membrane were associated with increased binding capacity of the gonadotropin receptor. Feeding diets high in 18:3(n-3) vs. those high in fish oil altered receptor-mediated adenylate cyclase activity in a manner that depended on the level of dietary cholesterol. Feeding diets high in cholesterol or fish oil increased basal and LH-stimulated testosterone synthesis relative to that in animals fed the low cholesterol diet containing linseed oil. It is concluded that changing the fat composition of the diet alters the phospholipid composition of rat testicular plasma membranes and that this change in composition influences membrane-mediated unmasking of gonadotropin receptor-mediated action in testicular tissue.

Adenylyl Cyclases↗
PubMed1990

Intestinal microsomes: polyunsaturated fatty acid metabolism and regulation of enterocyte transport properties.

Recent evidence has suggested that transport of nutrients from the lumen to the interior of the gastrointestinal epithelium and exit of nutrients from the enterocyte to the circulation is governed by physicochemical properties of brush border and basolateral membranes, respectively. The main determinants of membrane properties are phospholipid, cholesterol, and fatty acyl chain composition (chain length and degree of unsaturation). Lipid synthesis occurs in enterocyte microsomes and the fine tuning of lipid composition is done at other subcellular sites by deacylation-reacylation or by changing the polar head group (e.g., by phosphatidylethanolamine methyltransferase). The present paper will focus on the mechanisms by which enterocyte membranes adapt functional properties in response to external stimuli. It is proposed that under the influence of internal or external stress, the enzymes of lipid metabolism in microsomes are modulated. These changes in lipid synthesis are reflected in other subcellular membranes, changing their physicochemical status and thus transport phenomena. One of the initial events appears to be alteration in desaturase enzyme activity. Our results suggest that desaturase activity and the fatty acyl profiles of the intestinal mucosal phospholipid rapidly respond to physiological conditions such as fasting and dietary fat treatment.

Animals↗
PubMed1990

Critical period programming of intestinal glucose transport via alterations in dietary fatty acid composition.

Intestinal adaptation occurs in response to physiological or pathological processes that include resection, aging, diabetes, radiation, lactation, chronic alcohol feeding, and feeding diets of varying lipid, protein, or carbohydrate composition. The mechanisms involved in the adaptive response include alterations in morphology, cell kinetics, digestive enzyme activity, transport, membrane lipid composition, and enzymes involved in lipid metabolism. This discussion will review the effect of aging and alterations in dietary fatty acid composition on the small intestine. In addition, it may be possible to program the intestinal response to aging by feeding diets of differing fatty acid composition during the critical period of weaning. Alterations in the ratio of polyunsaturated to saturated fatty acids in the diet modifies the age-associated changes in the intestinal uptake of glucose. The changes occur rapidly, progressively, and irreversibly, suggesting that the intestinal uptake of glucose is subject to critical period programming. The mechanism by which diet may modify the ability of the intestine to up- or down-regulate glucose transport requires further investigation.

Animals↗
PubMed1990

A model for demonstration of reversal of impairment of endothelium-dependent relaxation in the cholesterol-fed rabbit.

This investigation was undertaken to determine whether it was possible to restore endothelium-dependent relaxation (EDR) in the cholesterol-fed rabbit model of atherosclerosis following discontinuation of the cholesterol. New Zealand white rabbits, approximately 8 weeks of age, were randomized into (i) control group (9 animals fed a standard rabbit diet) and (ii) experimental group (27 animals: fed the same diet supplemented with 2.5% cholesterol). The experimental animals were restored to the standard diet after 3 weeks. EDR to acetylcholine (-9.0 to -5.0 log mol/L) was examined in the experimental animals at 3, 7, and 15 weeks after commencement of the study (n = 9 at each stage) and the nine control animals examined after 7 weeks. At the end of 7 weeks, EDR to acetylcholine (-6.0 log mol/L) was significantly (p less than 0.05) impaired in the experimental group (34.3 +/- 3.8%) compared with that in the control group (79.8 +/- 3.0%). The loss of EDR was not apparent in the experimental group at 3 weeks (relaxation: 81.7 +/- 4.7%). At the end of 15 weeks, the EDR was significantly restored in the experimental group (relaxation: 63.6 +/- 5.1%). These findings demonstrate that it is possible to reverse the loss of EDR that occurs with cholesterol feeding in the rabbit by limiting the period of exposure to a high cholesterol diet.

Acetylcholine↗
PubMed1990

Radiation and the small intestine. Future perspectives for preventive therapy.

Radiotherapy continues to enjoy a prominent role in the treatment of certain human tumors. Unfortunately, the undesired effect of radiation upon normal intestinal tissue often limits its therapeutic potential. While there is abundant information on the effects of radiation on the morphology of the intestine and on the proliferative process which occurs in the intestinal crypts, there is a paucity of information on the early and late effects of sublethal doses of radiation upon the absorptive functions of the intestine. The intestinal epithelium has a rapid turnover rate and is highly radiosensitive. Radiotherapy for malignant human neoplasms is a relatively safe and effective form of treatment, but it may become limited by its undesired side effects upon the gastrointestinal tract. A variety of clinical tests have been suggested as potential indicators of impending intestinal damage, but there is little information on the time course of radiation damage and the associated impairment of intestinal function. Such basic information is essential to assess early functional changes and to thereby allow for the development of suitable clinical tests to allow for the prediction of impending intestinal damage. Provision of this information to the radiotherapist would permit alterations to the timing or dose schedules of radiotherapy and would allow continued treatment, while avoiding or reducing unwanted side effects. In recent years, there has been extensive research on radiation injury to small intestine. This article will review some of the progress in this field, and will focus on potential future therapy to prevent or treat radiation damage to the intestine. These agents include WR-2721, enprostil, vasopressin, defined-formula diets and alterations in the ratio of dietary polyunsaturated-saturated fatty acids.

Forecasting↗