PubMed Health⌕ Search

Biomedical subjects

S K Clinton

Publications and source records attributed to S K Clinton.

63 records · Page 4Linked to original sources
PubMed1985

The combined effects of dietary protein and fat on prolactin in female rats.

A 3 X 3 factorial experiment was conducted to examine how protein content (8, 16 and 32% of kcals from casein) and fat content (12, 24 and 48% of kcals from corn oil) interact to influence prolactin homeostasis in female rats. Weanling Sprague-Dawley rats were assigned to each of nine diets fed ad libitum. Dietary fat had no effect on the time of vaginal opening although first estrus occurred slightly earlier with high fat diets (P less than 0.05). Rats fed diets with protein at 8% of kcal showed a 2-wk delay in vaginal opening and first estrus. After 18-20 wk of feeding, serum and pituitary prolactin concentrations were determined after decapitation during the afternoon of proestrus or diestrus. Although serum prolactin was elevated at proestrus, there were no effects of fat or protein on the serum or pituitary prolactin. Another group of rats were fitted with jugular cannulae and treated with perphenazine, a potent prolactin-stimulating drug. Dietary fat or protein had no effect on prolactin secretion after perphenazine treatment. In the final experiment, rats fed each diet were treated with either i.p. saline or perphenazine followed by decapitation. The pituitary was removed 3 h later for determination of the amount of prolactin depleted from the pituitary. There was no effect of diet on the amount of pituitary prolactin depleted by perphenazine. No evidence was obtained that changes in dietary fat or protein concentration influence serum prolactin or its secretion in response to a provocative stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Plasma amino acids and excretion of protein end products by mice fed 10 or 40% soybean protein diets with or without dietary 2-acetylaminofluorene or N,N-dinitrosopiperazine.

Studies were conducted with 5- to 8-week-old male and female B6C3F1 mice to determine the influence of two carcinogens, 2-acetylaminofluorene (AAF) and N,N-dinitrosopiperazine (DNP), on plasma amino acid concentrations and on the excretion of lipids and nitrogenous metabolites. The carcinogens, AAF and DNP, were fed at concentrations of 0.25 and 0.05 g/kg of purified diet, respectively. Soybean protein constituted either 10 or 40% of the diet. Nutritional balances were measured over a 7-day period, after 7 days of acclimatization. Females ate less feed, gained less weight during acclimatization and excreted less fecal lipid as a percentage of intake than males. On the average, animals fed 40% protein consumed less total feed than those fed 10% protein. During acclimatization, DNP-fed animals ate and gained significantly less than controls. During week 2 DNP-fed animals gained significantly less than controls, although their feed intake was not significantly different. Fecal lipid excretion as a percentage of intake was significantly lower with carcinogens in the diet. The 40% protein diets increased lipid excretion in total and as a percentage of intake. With the exception of decreasing fecal lipid, AAF caused no consistent changes in feed intake, body weight, nitrogen (N) retention or N excretion. Neither carcinogen significantly influenced total fecal or urinary N, or the relative concentrations of the different forms of urinary N, when expressed as a percentage of N intake. Plasma ammonia rose with AAF feeding and plasma histidine rose with DNP feeding. Plasma concentrations of other amino acids were not changed consistently by either carcinogen. Feeding 40% protein caused a significant rise in plasma branched-chain amino acids, glycine and phenylalanine, and a significant decline in aspartate, threonine, serine, proline, citrulline, lysine and arginine.

2-Acetylaminofluorene↗
PubMed1984

The combined effects of dietary protein and fat on 7,12-dimethylbenz(a)anthracene-induced breast cancer in rats.

A 3 X 3 factorial experiment was conducted to examine how protein content (8, 16, 32% of kilocalories from casein) and fat content (12, 24, 48% of kilocalories from corn oil) interact to influence 7,12-dimethylbenz(a)anthracene (DMBA)-induced breast carcinogenesis in rats. Forty weanling Sprague-Dawley rats were assigned to each of 9 diets fed ad libitum. After 4 weeks each rat received DMBA (20 mg/kg) via gastric intubation. No substantial statistical interactions of protein and fat were observed on tumor incidence. Increasing dietary corn oil increased the percentage of rats with palpable tumors. Rats fed diets containing 12, 24 and 48% of kilocalories from corn oil showed 35, 49 and 70% tumor prevalence at necropsy, and the total number of tumors per fat level was 65, 81 and 182, respectively. Each doubling of dietary fat concentration approximately doubled the odds of a rat developing a tumor. Multiple tumors were more common with the highest corn oil intake. The odds of finding a second tumor in rats with one tumor increased by a factor of 7.5 when fat kilocalories were increased from 24 to 48% compared to a decrease of one-third when fat kilocalories were increased from 12 to 24%. Dietary corn oil significantly increased the prevalence of adenocarcinomas and adenomas but not fibroadenomas. Dietary protein did not significantly affect tumor prevalence. However, tumors palpated in rats fed 16% of kilocalories as protein regressed more frequently than in rats fed low or high protein diets. Multiple logistic-regression results indicate that, in addition to the response to dietary corn oil, tumorigenesis was increased in rats with greater ad libitum food consumption. This conclusion is supported by reanalysis that used direct rate adjustment and average partial association tests.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Effects of dietary lipid saturation on prolactin secretion, carcinogen metabolism and mammary carcinogenesis in rats.

Isoenergetic diets containing 20% corn oil, 20% beef tallow, or an equal mixture of 10% corn oil and 10% beef tallow (mixed fat) were fed to 30 rats per diet for 28 weeks following weaning. DMBA [7,12-dimethylbenz(a)anthracene] was administered (1.75 mg/100 g body weight) in a single oral dose after 4 weeks of feeding. After 28 weeks, 70% of the rats fed corn oil had mammary tumors versus 47% for mixed fat and 30% for tallow. Diet had no effect on the number of tumors per tumor-bearing rat or the proportion of tumors that were adenocarcinomas. Other rats assigned to each of the three diets were killed at the time corresponding to DMBA administration for examination of hepatic mixed-function oxidase activity. NADPH cytochrome c reductase activity and cytochrome P-450 content were higher in rats fed corn oil or mixed fat rather than tallow. However, no significant differences in aryl hydrocarbon hydroxylase, glutathione transferase, and uridine-diphosphoglucuronide transferase activities were observed. The effects of dietary fat saturation on enzyme activity failed to show a clear association with DMBA carcinogenesis. In other rats assigned to the three dietary treatments for 4 or 16 weeks, lipid saturation did not change serum prolactin (PRL) concentrations during diestrus or proestrus. PRL secretion was examined following a provocative stimulus (perphenazine) in rats fed the experimental diets for 4 or 10-22 weeks. Although perphenazine increased serum PRL and depleted the pituitary of PRL, differences in dietary lipid saturation caused no significant changes in these indices. These data show that the incidence of mammary tumors in rats fed high fat diets (20% by weight) was greater in those fed corn oil compared to beef tallow. The effect of dietary lipid source on tumorigenesis was not associated with changes in carcinogen-metabolizing enzyme activity or PRL secretion.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Omega-3 fatty acids and endothelial leukocyte adhesion molecules.

Although dietary fatty acids can modulate atherogenesis and inflammation, the mechanisms by which this occurs are poorly understood. Induction in endothelial cells of adhesion molecules for circulating leukocytes and of inflammatory mediators by cytokines likely contributes to early phases of atherogenesis and inflammation. We report here that incorporation into cellular lipids of one specific fatty acid of the omega-3 family, docosahexaenoic acid (DHA), decreases cytokine-induced expression of endothelial leukocyte adhesion molecules, secretion of inflammatory mediators, and leukocyte adhesion to endothelial cells. These properties of DHA may contribute to antiatherogenic and antiinflammatory effects of omega-3 fatty acids.

Adult↗