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Biomedical subjects

W Frølich

Publications and source records attributed to W Frølich.

10 recordsLinked to original sources

Calcium phosphate supplementation results in lower rat fecal bile acid concentrations and a more quiescent colonic cell proliferation pattern than does calcium lactate.

Although there is general agreement that dietary calcium is protective against colon carcinogenesis, considerable controversy exists on the relative efficacy of the counterion in calcium supplements. We therefore conducted a comparative study in rats of four forms of calcium supplementation (calcium phosphate, casein, lactate, and a 50:50 phosphate-carbonate combination). The relative effects of these supplements on measurements of colon physiology, in vivo pH, fecal fat, individual bile acids, and in vivo cell proliferation were measured in the same animals. In contrast to results when amounts of calcium are varied, there was no effect of form of supplement on total fecal output or output of fecal fat. Calcium phosphate resulted in the most acidified cecal contents. Calcium phosphate and calcium casein resulted in lower fecal concentrations of lithocholate and lower amounts of total fecal bile acids than supplementation with the calcium lactate or combination diets. In addition, rats fed calcium phosphate had lower concentrations of fecal beta-muricholate than rats provided with the calcium combination supplement. In the proximal colon, calcium phosphate resulted in a significantly lower number of cells per crypt column and a lower labeling index than the calcium lactate diet. The position of the highest labeled cell was lower with calcium phosphate supplementation than with supplementation from the calcium combination or the calcium lactate diet. There was a highly significant correlation between the pH of cecal contents and labeling index in the proximal colon (r = 0.98, p = 0.003). The results suggest that calcium phosphate may inhibit colon tumor incidence more effectively than calcium lactate, because the calcium phosphate group had a lower colonic proliferative status than the calcium lactate group. Changes in the proliferative status of colonocytes are known to precede and accompany neoplasia.

Animals

A very low intake of fat is required to decrease fecal bile acid concentrations in rats.

The purpose of this study was to determine the effect of different amounts of dietary fat on colonic cell proliferation and fecal bile acid concentrations. Thirty-nine male Sprague-Dawley rats were randomly assigned to three diets (13 rats per diet) containing 5, 10 and 20 g butter/100 g diet. Diets were fed for 3 wk. As fat intake increased, total fecal fat excretion remained constant. When dietary fat was decreased from 20 to 10 g/100 g diet, total fecal bile acid concentrations tended to increase 14.5%. However, a further reduction to 5 g butter/100 g diet significantly decreased fecal total bile acid concentration by 48% from the concentration in feces of rats fed 10 g butter/100 g diet. The concentration of deoxycholate (considered a highly promotive bile acid) was not reduced unless the amount of fat in the diet was reduced to 5 g/100 g. Labeling index was used as an intermediate marker for colon carcinogenesis. For deoxycholate, a decrease of fat intake to 5 g/100 g diet decreased the cecal labeling index relative to those of rats fed 10 or 20 g butter/100 g diet. These data indicate that decreasing the dietary fat from 20 to 10 g/100 g does not decrease fecal bile acid concentration or colonic cell proliferation, but some effects are seen in rats fed 5 g butter/100 g diet.

Animals

Rats fed high fat diets with increased calcium levels have fecal bile acid concentrations similar to those of rats fed a low fat diet.

The mechanism by which calcium may protect against colon carcinogenesis was studied in rats fed three levels of calcium (0.5, 1.0 and 1.5 g/100 g diet) and a high butter diet (20 g/100 g). Results were compared with values obtained using a low butter diet (5 g/100 g) supplemented with 0.5 g Ca/100 g diet. Concentration and relative proportions of individual fecal bile acids were determined by gas chromatography, and in vivo colonic cell proliferation was assessed using [3H]thymidine. Total fecal output and total fecal lipids increased as dietary calcium increased. When calcium supplementation remained at 0.5%, raising the level of fat in the diet increased the fecal concentrations of deoxycholate, omega-muricholate and total bile acids. However, when the level of fat supplementation remained constant at 20 g/100 g diet, but dietary calcium was 1.0 or 1.5 g/100 g, the concentration of these bile acids returned to the level found in feces of rats fed the low fat diet. Despite the significant decrease in the concentrations of certain fecal bile acids with increasing calcium supplementation, these differences were not reflected in substantive changes in epithelial cytokinetics. These data show that in rats fed high butter diets, 1.0% calcium is sufficient to lower total bile acid concentration and the concentrations of certain individual bile acids to those found in feces of rats fed low fat diets. Despite the significant effects of calcium on bile acid concentrations, minimal effects were observed on indices of colonic cell proliferation.

Animals

Diabetic control is improved by guar gum and wheat bran supplementation.

Twenty-eight insulin-dependent diabetics were treated with different dietary regimes for three periods of three months. Initially they used a white flour bread (run-in period), then their daily bread ration was enriched with guar gum (mean dose: 29 g), and then with wheat bran (mean dose: 33 g) in a randomized crossover pattern. Fasting and postprandial blood glucose levels were measured on filter paper spots collected once weekly at home, and other biochemical values were measured monthly. No improvement in diabetic control was seen during the run-in period. Mean postprandial blood glucose decreased from 12.0 +/- 3.8 mmol/l (mean +/- SD) in the run-in period to 9.7 +/- 2.8 mmol/l (p less than 0.01) in the guar period and to 9.7 +/- mmol/l (p less than 0.01) in the bran period. HbA1 decreased from 10.5 +/- 2.1% in the run-in period to 9.7 +/- 1.6% (less than 0.05) at the end of the guar period and 9.9 +/- 1.2% (not significant) at the end of the bran period. Only modest changes were seen in serum-lipids--total cholesterol decreased significantly in the guar period, but not in the bran period. In this study both guar gum and wheat bran were well tolerated and produced a substantial decrease in postprandial blood glucose.

Adolescent

Epidemiology of polyps in the rectum and sigmoid colon. Evaluation of nutritional factors.

Epidemiological studies have suggested an association between diet and colorectal cancer. Case/control studies, however, have been scarce, and studies based on interview with cancer patients who have symptoms from their cancer are inevitably prone to bias. An endoscopic population screening study for detection of colorectal adenomas enabled a double-blind registration of diet during 5 consecutive weekdays. Neither the participant nor the dietitian was informed of the findings at endoscopy. The estimation of 23 nutritional components was based on analysis of local commercial food and on the composition of foods in Norway. Results showed increasing consumption of fat and decreasing consumption of fiber and cruciferous vegetables in the presence of increasing neoplastic changes. The present material will form the basis for dietary-related follow-up studies.

Colonic Neoplasms

Bioavailability of iron from wheat bran in pigs.

Iron anemia was induced in pigs immediately after birth by feeding an iron depletion diet containing only 17 mg iron/kg feed. (The requirement for iron in this period is 50 mg iron/kg feed). When Hb concentrations were 5 g/100 ml the pigs were given iron repletion diets. One group received 7% bran in the diet, about 60% of the iron derived from the bran and 40% from ferrous sulfate. The other group received no bran and 80% of the iron from ferrous sulfate. There were no differences, either in the increase of Hb or in the increase of serum iron, in the two groups. In a second experiment, one group received all their iron from cereals, and an addition of 20% bran in the diet. The other group received no bran and 80% of the iron from ferrous sulfate. There was no significant difference in the bioavailability of the iron present in the diets. In our experiments bran seemed to have no inhibitory effect on iron absorption, even when 20% bran was included in the diet.

Anemia, Hypochromic

Effect of estrogen treatment on coagulation and fibrinolysis in postmenopausal women. With special reference to cold activation of factor VII.

Estriol (E3) and estradiol (E2) was given to 81 women with perimenopausal complaints. Venous blood was sampled before and after 2 weeks' treatment. In plasma coagulation and fibrinolysis the most marked estrogen effects were seen within the extrinsic coagulation system, with increased Thrombotest and Normotest activities. The incidence of cold activation of factor VII showed a marked increase after treatment with 6 mg of E2 or 8 mg of E3. The cold activation of factor VII was correlated to an activation of the plasma kallikrein system, as revealed by the peptidase activity of plasma kallikrein. The treatment with E2 and E3 induced changes also in the plasma proteolytic capacity, and in some proteinase inhibitors (antithrombin III, Cl inactivator). Like the effects within the plasma coagulation and kallikrein systems, these effects were similar to those reported after treatment with ethinyl estradiol, mestranol, and diethylstilbestrol, and in pregnancy. The conclusion is drawn, therefore, that the coagulation and fibrinolytic effects of E2 and E3 are basically similar to those of other estrogens, the differences between the various estrogens being more of a quantitative than of a qualitative nature. For the changes described, no absolute dose dependency could be found. Thus, treatment with E2 and E3 should be submitted to the same precautions as treatment with other estrogens.

Administration, Oral