Dietary tocotrienol reduces UVB-induced skin damage and sesamin enhances tocotrienol effects in hairless mice

We have previously reported that substantial amounts of tocotrienols were present in the skin of animals fed a diet containing a tocopherols and tocotrienols rich fraction (T-mix) extracted from palm oil, and further, that sesame lignans enhanced tocotrienol levels in the skin. The present studies were undertaken to determine whether dietary tocotrienols and those with sesamin could protect the skin from damage induced by UVB irradiation in hairless mice fed four diets: a vitamin E-free diet, a 50 mg/kg alpha-tocopherol diet, a 229 mg/kg T-mix (with 50 mg alpha-tocopherol) diet and a 229 mg/kg T-mix with 2 g/kg sesamin diet. In Experiment 1, mice were fed the diets for 6 wk, and half of the mice were exposed to 180 mJ/cm(2 )of UVB light once daily for 7 d. After the intensity of sunburn was scored, vitamin E and thiobarbituric acid reactive substances (TBARS) concentrations in the skin and liver were determined. In Experiment 2, hairless mice were initiated with a single application of 7, 12-dimethylbenz[a]anthracene (DMBA), then 1 wk later mice were fed the experimental diets and subjected to 180 mJ/cm(2) UVB irradiation twice weekly for 20 wk. Tumor incidences were counted once a week. Tocotrienols were detected in the skin of mice fed T-mix, but their concentrations were significantly lower than for alpha-tocopherol. Sesamin elevated tocotrienol contents in the skin. In spite of the high alpha-tocopherol contents, the effects of alpha-tocopherol on sunburn and incidence of tumor were slight. T-mix fed groups reduced the extent of sunburn and incidence of tumor, and further reduction of sunburn and incidence of tumor were observed in the T-mix with sesamin group. These results suggest that dietary tocotrienols protect the skin more strongly than alpha-tocopherol against damage induced by UVB and sesamin enhances tocotrienol effects.     

Nutritional Therapy in Persons Suffering from Psoriasis

Psoriasis is a chronic inflammatory skin disease. Immunological, genetic, and environmental factors, including diet, play a part in the pathogenesis of psoriasis. Metabolic syndrome or its components are frequent co-morbidities in persons with psoriasis. A change of eating habits can improve the quality of life of patients by relieving skin lesions and by reducing the risk of other diseases. A low-energy diet is recommended for patients with excess body weight. Persons suffering from psoriasis should limit the intake of saturated fatty acids and replace them with polyunsaturated fatty acids from the omega-3 family, which have an anti-inflammatory effect. In diet therapy for persons with psoriasis, the introduction of antioxidants such as vitamin A, vitamin C, vitamin E, carotenoids, flavonoids, and selenium is extremely important. Vitamin D supplementation is also recommended. Some authors suggest that alternative diets have a positive effect on the course of psoriasis. These diets include: a gluten-free diet, a vegetarian diet, and a Mediterranean diet. Diet therapy for patients with psoriasis should also be tailored to pharmacological treatment. For instance, folic acid supplementation is introduced in persons taking methotrexate. The purpose of this paper is to discuss in detail the nutritional recommendations for persons with psoriasis.     

Potential Role of Probiotics in Ameliorating Psoriasis by Modulating Gut Microbiota in Imiquimod-Induced Psoriasis-Like Mice

Psoriasis is an immune-mediated systemic disease that may be treated with probiotics. In this study, probiotic strains that could or could not decrease interleukin (IL)-17 levels were applied to imiquimod (IMQ)-induced psoriasis-like mice via oral administration. Bifidobacterium adolescentis CCFM667, B. breve CCFM1078, Lacticaseibacillus paracasei CCFM1074, and Limosilactobacillus reuteri CCFM1132 ameliorated psoriasis-like pathological characteristics and suppressed the release of IL-23/T helper cell 17 (Th17) axis-related inflammatory cytokines, whereas B. animalis CCFM1148, L. paracasei CCFM1147, and L. reuteri CCFM1040 neither alleviated the pathological characteristics nor reduced the levels of inflammatory cytokines. All effective strains increased the contents of short-chain fatty acids, which were negatively correlated with the levels of inflammatory cytokines. By performing 16S rRNA gene sequencing, the diversity of gut microbiota in psoriasis-like mice was found to decrease, but all effective strains made some specific changes to the composition of gut microbiota compared to the ineffective strains. Furthermore, except for B. breve CCFM1078, all other effective strains decreased the abundance of the family Rikenellaceae, which was positively correlated with psoriasis-like pathological characteristics and was negatively correlated with propionate levels. These findings demonstrated effects of strain-specificity, and how probiotics ameliorated psoriasis and provide new possibilities for the treatment of psoriasis.     

Dietary fatty acids temporarily alter liver very long-chain fatty acid composition in mice.

To determine the influence of dietary fatty acids on tissue very long-chain fatty acid (VLFA) composition, mice were fed four diets containing 15 g fat/100 g diet derived largely from either safflower oil, peanut oil, olive oil or glycerol trioleate oil. The diets varied widely in the composition of VLFA and other fatty acids. Digestibility of total dietary VLFA ranged from 84.6% in mice fed the glycerol trioleate diet to 96.7% in those fed the safflower oil diet. After 3 mo, the saturated VLFA composition of liver total lipids and sphingomyelin was lower in animals fed the glycerol trioleate oil diet than in mice fed most other diets. Although the saturated VLFA content of the peanut oil diet was more than 15-fold greater than that of the other diets, animals fed the peanut oil diet showed little or no selective increase in liver saturated VLFA. The VLFA composition of brain was comparable in all dietary groups. After 8 mo of feeding, the liver saturated VLFA composition tended to increase and differences between groups disappeared. Liver peroxisomal beta-oxidation of lignocerate (24:0) was similar among all dietary groups. These results demonstrate that dietary fatty acids shorter than VLFA temporarily influence the saturated VLFA composition of liver.     

Examination of host immune resistance against Listeria monocytogenes infection in cyclophosphamide-treated mice after dietary lipid administration

BACKGROUND & AIMS: Despite the beneficial effects in the resolution of inflammatory disorders due to their immunosuppressive properties, n-3 polyunsaturated fatty acids are associated with a reduction of immune resistance to some microorganisms. Here, we examine the influence of different dietary lipids on host immune resistance against Listeria monocytogenes in mice treated with cyclophosphamide (CPA). METHODS: Balb/c mice were fed one of four diets, which contained either olive oil (OO), fish oil (FO), hydrogenated coconut oil (HCO) or low fat (LF) for 4 weeks. Subsequently, mice were treated with CPA or PBS, prior to L. monocytogenes infection. Splenocyte proliferation, survival analysis, counts of viable bacteria from spleens and livers, and measurement of pro-inflammatory cytokine levels were determined. RESULTS: The FO-rich diet reduced survival, particularly in CPA-treated mice. CPA was responsible for a significant increase of viable bacteria recovery from spleens and livers within each group fed high fat diets, which was aggravated in mice fed an FO diet. In addition, a significant increase of both TNF-alpha and IL-12p70 levels was detected in this group. These results may acquire a crucial relevance in clinical nutrition, particularly when FO diets are administered to immunocompromised patients. CONCLUSIONS: The mechanism(s) that impair(s) the elimination of L. monocytogenes could be associated with a low mitogen-stimulated splenocyte proliferation, and with an alteration of pro-inflammatory cytokine production. The application of the neutropenic agent CPA moderately aggravates the immunosuppressive state mainly in FO-fed animals.     

Dietary eicosapentaenoic acid and docosahexaenoic acid equally incorporate as decosahexaenoic acid but differ in inflammatory effects

OBJECTIVE: The omega-3 polyunsaturated fatty acids are involved in the modulation of the immune response. Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) produced from dietary precursors may not be sufficient to match nutritional requirements and thus should be included in our diet. In this sense, the administration of higher amounts of DHA than of EPA in infant formulations is recommended. The aims of this work were to demonstrate that dietary administration of EPA or DHA to mice allows reaching similar tissue DHA levels and to compare their anti-inflammatory effects and mechanisms of action. METHODS: Balb/c mice were fed diets enriched with EPA or DHA for 3 wk. Twelve hours before sacrifice, a contact dermatitis was induced in the ears of the animals. Tissue fatty acid contents were determined. Cytokine and immunoglobulin concentrations were measured by enzyme-linked immunosorbent assay, and ears were collected to analyze local inflammatory effects. RESULTS: The DHA concentrations attained in tissues were similar to the two diets, whereas the EPA concentration increased only when the diet was enriched with this polyunsaturated fatty acid. Although EPA and DHA reduced ear inflammation, EPA reduced neutrophil infiltration in the ears more efficiently. EPA was associated with a greater reduction in the systemic macrophage inflammatory response and T-helper type 2 response and with increased interleukin-10 production. CONCLUSION: Similar levels of DHA in tissues are reached in mice fed an EPA- or a DHA-enriched diet. Dietary EPA and DHA show anti-inflammatory properties, but EPA appears to be more potent.     

Anti-oxidant properties of N-acetyl-L-cysteine do not improve the immune resistance of mice fed dietary lipids to Listeria monocytogenes infection

BACKGROUND & AIMS: Current knowledge of the potential effects that several dietary lipids exert on immune functions indicates that these substances participate actively in the modulation of immune system by which they contribute to the improvement of the conditions of patients suffering from inflammatory disorders. However, long-chain n-3 polyunsaturated fatty acids induce an immunosuppressive status that leads to a reduction of the host natural resistance to infectious agents as well as to an enhancement of oxidative damage. Hence, the present study has been designed to evaluate the effects on the immune system of the antioxidant N-acetyl-L-cysteine (NAC) in mice fed dietary lipids and infected with Listeria monocytogenes. METHODS: Balb/c mice were fed for 4 weeks with diets containing either olive oil (OO, 20% by weight), fish oil (FO, 20% by weight) or hydrogenated coconut oil (HCO, 20% by weight). After dietary lipid administration mice were experimentally infected with L. monocytogenes or treated with NAC (25mg/ml intraperitoneally). RESULTS: NAC at a concentration of 1mM promoted a loss of cell viability, although no differences were observed among the four groups. After injection of NAC in combination with L. monocytogenes, 25% of mice fed a low-fat (LF) diet survived. However, in the groups fed dietary lipids no effect on survival of mice was found. NAC participated in the reduction of superoxide anion generation measured with nitroblue tetrazolium (NBT) in the group fed a FO diet. Finally, NAC reduced the recovery of L. monocytogenes from spleen of mice fed diets containing LF or HCO. CONCLUSIONS: On the basis of these results, we can confirm that the administration of NAC improves survival in mice fed LF diet, whereas a reduction in the generation of superoxide radicals was measured in mice fed a FO diet and infected with L. monocytogenes. Similarly, bacterial recovery was diminished in mice fed diets containing LF or HCO. Hence, these data reveal a beneficial effect of NAC in mice fed LF or HCO and a detrimental action of this antioxidant in mice fed diets containing FO or OO.     

Lipid profile of rats fed high-fat diets based on flaxseed, peanut, trout, or chicken skin

OBJECTIVE: Dietary saturated fatty acids are associated with coronary disease. Conversely, dietary monounsaturated polyunsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs) seem to exert a protective effect. This study evaluated the lipid profile of rats fed high-fat (HF) diets, with fat added as different sources of PUFA (flaxseed and trout), MUFA (peanut), and saturated fatty acid (chicken skin). METHODS: Adult male Wistar rats were placed into six dietary groups (n = 10): control (normal); high fat, with 1% cholesterol, 10% soy oil, and 5% lard; and four groups fed similar HF diets, with 10% lipid as trout, flaxseed, peanut, or chicken skin. After 28 d the animals were killed. Blood, livers, and adipose tissue samples were collected. RESULTS: A higher level (P < 0.05) of total serum cholesterol was observed in rats fed the normal diet (93.57 +/- 14.95 mg/dL) compared with those fed the HF diet (67.57 +/- 12.54 mg/dL). Total cholesterol levels in rats fed the flaxseed diet were lower (P < 0.05) than in rats fed the other fats. No difference was observed in cholesterol levels between groups fed the peanut and chicken skin diets (P > 0.05). Animals fed the peanut diet showed decreased body weight gain than did animals in the other treatment groups. There were large lipid and cholesterol depositions in livers of rats fed the HF diet. Lipid deposition in adipose tissue followed the same dietary fatty acid profile, i.e., high levels of omega-3 PUFA in the flaxseed group, high levels of MUFA in the peanut and chicken skin groups and high levels of omega-6 PUFA in the trout group. CONCLUSIONS: These data indicate that flaxseed is promising for dietary manipulation of hyperlipidemia.     

Dietary calcium is a major factor in 1,25-dihydroxycholecalciferol suppression of experimental autoimmune encephalomyelitis in mice.

The active form of vitamin D (1,25-dihydroxycholecalciferol) is a potent immune system regulator. Treating mice with 1, 25-dihydroxycholecalciferol and feeding them diets high in calcium can completely suppress the induction of experimental autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE). Experiments described here were carried out on mice in which development of EAE was induced. Mice were fed diets containing various amounts of calcium and 1,25-dihydroxychole-calciferol. Variables measured were as follows: 1) incidence and severity of EAE; 2) serum calcium concentrations; 3) body weight; 4) total number of cells in the lymph nodes; and 5) interleukin-4 (IL-4) and transforming growth factor-beta1 (TGF-beta1) mRNA levels. When calcium was removed from the diet, the incidence of EAE was reduced 20% in both males and females. Further, the lower the dietary level of calcium, the higher was the dose of 1,25-dihydroxycholecalciferol required to prevent the symptoms. Thus, 1, 25-dihydroxycholecalciferol was found most effective in mice fed a diet adequate or high in calcium. 1,25-Dihydroxycholecalciferol treatment of mice fed high dietary calcium resulted in a decreased number of lymphocytes in the lymph nodes and increased IL-4 and TGF-beta1 mRNA levels. When calcium was omitted from the diet, 1, 25-dihydroxycholecalciferol supplementation increased TGF-beta1 mRNA. Increased IL-4 mRNA and decreased lymphocytes in the lymph nodes in response to 1,25-dihydroxycholecalciferol occurred only when dietary calcium was adequate or high. Our results suggest that dietary calcium and 1,25-dihydroxycholecalciferol are both involved in the prevention of symptomatic EAE.     

Dietary fatty acids affect the immune system in male mice sensitized to ovalbumin or vaccinated with influenza

PUFA are precursor molecules for eicosanoids such as leukotrienes and prostaglandins and may influence immune function through other mechanisms involving membranes, cell signaling, and gene expression. Immune-modulating properties of diets containing different oils [sunflower oil, rich in linoleic acid; linseed oil, rich in α-linolenic acid; salmon oil, rich in marine (n-3) PUFA; and beef tallow, rich in SFA] were investigated in an influenza-vaccination model, in which the delayed-type hypersensitivity (DTH) response was studied in C57BL/6 mice, and an ovalbumin (OVA)-sensitization model for experimental allergy in BALB/c mice. Six-week-old mice were fed the different diets for 7 wk. The first vaccination or OVA sensitization was given 2 wk after the start of the dietary intervention. In the mice vaccinated with influenza, the DTH response to the vaccine was significantly higher in mice fed the marine (n-3) PUFA diet compared to all other groups, indicating that these PUFA promote a T helper-1 response. In the OVA-sensitized mice, those fed the marine (n-3) PUFA diet had a less severe acute allergic skin response (ASR), suggesting that (n-3) PUFA lessen the T helper-2 response. Mice fed the SFA-rich diet had the most severe ASR, indicating that a diet with high levels of SFA may contribute to increased severity of allergic symptoms. Whereas significant differences in in vivo immune responses were measured, in vitro responses did not differ among the dietary groups. In conclusion, using 2 different models of immune responses demonstrates potential benefits from marine (n-3) PUFA.     

2,4-Dinitrofluorobenzene-induced contact hypersensitivity response in NC/Nga mice fed fructo-oligosaccharide

Strategies to manipulate gut microbiota in infancy have been considered to prevent the development of allergic diseases later in life. We previously demonstrated that maternal dietary supplementation with fructo-oligosaccharide (FOS) during pregnancy and lactation modulated the composition of gut microbiota and diminished the severity of spontaneously developing atopic dermatitis-like skin lesions in the offspring of NC/Nga mice. The present study tested whether dietary FOS affects contact hypersensitivity (CHS), another model for allergic skin disease, in NC/Nga mice. In experiment 1, 5-wk-old female NC/Nga mice were fed diets either with or without FOS supplementation for 3 wk and then received 2,4-dinitrofluorobenzene (DNFB) on the ear auricle 5 times at 7-d intervals. FOS supplementation reduced CHS response as demonstrated by ear swelling. Quantitative RT-PCR analysis showed that mRNA levels for interleukin (IL)-10, IL-12p40, and IL-17 in the lesional ear skin were significantly lower in mice fed FOS. In experiment 2, female NC/Nga mice were fed diets either with or without FOS during pregnancy and lactation. After weaning, offspring were fed the diets supplemented with or without FOS. Three weeks after weaning, offspring received DNFB on the ear auricle 4 times at 7-d intervals. Although FOS supplementation after weaning reduced ear swelling, maternal FOS consumption was ineffective in offspring. The present data suggest that dietary FOS reduces CHS while maternal FOS consumption is ineffective in offspring of DNFB-treated NC/Nga mice.     

Influence of extremes of protein and energy intake on survival of B/W mice

Energy restriction increases longevity and life span of B/W mice as it does in mice of other long-lived or short-lived strains. Mice of autoimmune-prone strains that develop certain diseases of aging experience an increase in median longevity when energy intake is restricted early in life. The present experiments analyze the influence of restricting energy intake while feeding constant, adequate and greatly excessive amounts of protein, and constant amounts of minerals and vitamins. The experiments assess the influence of excess protein intake in mice fed ad libitum versus those restricted in energy intake. Ad libitum feeding of diets with protein composition ranging from 15 to 50% did not alter longevity or onset and manifestations of renal disease in B/W mice. In mice consuming a restricted energy intake of a diet providing identical amounts of protein to those consumed by ad libitum-fed mice, whether the protein intake was very high or normal, longevity was equally greatly prolonged. Ad libitum feeding of diets of greatly differing protein content is well tolerated by B/W mice. Both the 15 and 50% protein diets, when ad libitum fed, permitted expression of autoimmune disease and glomerulonephritis in B/W mice but did not adversely influence development or progression of disease. Restriction of energy intake of either the normal protein diet or the high protein diet greatly prolonged the life of mice of the autoimmune-prone, glomerulonephritis-prone B/W strain.     

Nutrition Intervention: A Strategy Against Systemic Inflammatory Syndrome

Background: Sepsis and septic shock syndrome are the leading causes of death in critically ill patients. Lipopolysaccharide (LPS) released by the colonic microorganisms may translocate across a compromised lumen, leading to upregulated reactive oxidative stress, inflammation, and sepsis. The authors examined an enteral formula high in cysteine (antioxidant precursor), ω‐3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and prebiotic fructooligosaccharides (FOS) against systemic inflammatory syndrome. Methods: Rats were allocated to (1) standard soy‐based diet high in cysteine and crude fiber and devoid of EPA‐DHA (CHOW); (2) whey‐peptide‐based liquid diet high in cysteine, EPA‐DHA, and FOS (CYSPUFA); or (3) casein‐based liquid isonitrogenous diet, low in cysteine and devoid of EPA‐DHA‐FOS (CASN). Liquid diets provided 25% and CHOW, 23% of calories as protein. After 6 days on diets, rats received an intraperitoneal injection of LPS or saline. Animals gained weight on their respective diets and lost weight after LPS administration. The CYSPUFA group lost considerably less weight (vs CASN or CHOW, P < .05). Inflammatory cytokines significantly increased by 4 hours and subsided 18 hours after assault. The CASN group showed elevated liver enzyme alanine aminotransferase release from damaged hepatocytes and developed severe hepatic pathology with low hematocrit. The CHOW group developed more severe hepatic lesions compared with those on liquid diets. Concentration of liver enzyme and pathology were improved in rats receiving CYSPUFA. Conclusions: Data indicate that CYSPUFA, a diet rich in EPA‐DHA‐FOS, protects against LPS‐induced systemic inflammatory responses and warrants clinical studies in critically ill patients.     

C-reactive protein and interleukin-6 are decreased in transgenic sickle cell mice fed a high protein diet

Sickle cell disease is associated with hypermetabolism and a consequent shortage of substrates for normal growth and healthy immune response. The protein:energy ratio is a major determinant of dietary adequacy; the requirement for optimal growth of control mice is 20% of energy from dietary protein. This study investigated the efficacy of increased dietary protein for improving weight gain and reducing inflammation in the Berkeley sickle cell mouse model (S). The study examined the effect of diet on weight gain and circulating levels of 2 inflammatory proteins, C-reactive protein (CRP), and cytokine interleukin-6 (IL-6). Male C57BL/6 (C) control (n = 8) and S mice (n = 8) were randomized at weaning to 40 d of isoenergetic diets containing 20% (normal) and 35% (high) of energy from protein (C20, C35, S20, S35), replacing dextrin. Rate of weight gain was calculated and plasma CRP and IL-6 concentrations determined by ELISA. Liver mRNA expression of these proteins was measured by real-time PCR and L-arginase by colorimetric assay. S35 mice tended to gain weight more rapidly than S20 mice (P = 0.06) and more rapidly than C35 mice (P < 0.01). Circulating CRP and IL-6 levels were also lower in S35 mice than in S20 mice (P < 0.05), as was liver CRP mRNA expression (P < 0.01). These results demonstrate that introducing a high protein diet at weaning attenuates the steady-state inflammation in this S mouse model. Dietary L-arginine availability was investigated as a possible mechanism for increased nitric oxide production and consequent reduced inflammation.     

The effect of various dietary fats on skin tumor initiation.

The type of dietary fat has been shown to modulate the initiation stage of mammary tumorigenesis, with saturated fat fed before and/or during carcinogen treatment resulting in increased tumor incidence. This study was designed to determine whether different types of dietary fat alter the initiation stage of skin carcinogenesis by use of the initiation-promotion mouse skin carcinogenesis model. Sencar mice were divided into three groups and maintained on one of the experimental diets. The AIN-76-based diets consisted of 10% total fat with various types of fat: 8.5% menhaden oil plus 1.5% corn oil, 8.5% coconut oil plus 1.5% corn oil, and 10% corn oil. After three weeks mice were initiated with 10 nmol dimethylbenz[a]anthracene (DMBA). Two weeks later, all mice were switched to a diet containing 5% corn oil. Promotion began four weeks after initiation with twice-weekly application of 1 microgram 12-O-tetradecanoylphorbol-13-acetate and continued for 12 weeks. No statistically significant differences in kilocalories of food consumed or body weights were observed between diet groups during the study. The final papilloma incidence, yield, and size were not significantly different among the diet groups. In a parallel study, [3H]DMBA binding to epidermal DNA showed no dietary differences. Unlike the mammary carcinogenesis model, these data suggest that the type of fat fed during DMBA initiation had minimal effects on this stage of skin carcinogenesis.     

The Role of Nutrition in Immune-Mediated,Inflammatory Skin Disease: A Narrative Review

Immune-mediated inflammatory skin diseases are characterized by a complex multifactorial etiology, in which genetic and environmental factors interact both in genesis and development of the disease. Nutrition is a complex and fascinating scenario, whose pivotal role in induction, exacerbation, or amelioration of several human diseases has already been well documented. However, owing to the complexity of immune-mediated skin disease clinical course and breadth and variability of human nutrition, their correlation still remains an open debate in literature. It is therefore important for dermatologists to be aware about the scientific basis linking nutrition to inflammatory skin diseases such as psoriasis, atopic dermatitis, hidradenitis suppurativa, bullous diseases, vitiligo, and alopecia areata, and whether changes in diet can influence the clinical course of these diseases. The purpose of this narrative review is to address the role of nutrition in immune-mediated inflammatory skin diseases, in light of the most recent and validate knowledge on this topic. Moreover, whether specific dietary modifications could provide meaningful implementation in planning a therapeutic strategy for patients is evaluated, in accordance with regenerative medicine precepts, a healing-oriented medicine that considers the whole person, including all aspects of the lifestyle.     

Macronutrient selection in rats: effect of fat type and level

The effect of type and level of dietary fat on subsequent diet selection was examined in young Sprague-Dawley rats. Isoenergetic, isonitrogenous diets composed of corn oil or tallow (commercial grade), each at 5 or 34%, were fed to rats for 2 wk, and their preference for diets covarying in carbohydrate and protein was subsequently tested. When compared to either of the corn oil groups or the 5% tallow group, rats previously fed the high tallow diet selected more protein and less carbohydrate. Subsequent experiments testing the effects of 5, 20 or 34% tallow indicated that this preference for protein was induced by exposure to the tallow diets for only 18 h. In addition, the 34% tallow group selected more protein than did rats fed 5 or 20% tallow. Tests of diet selection with 5 or 34% corn oil, tallow or hydrogenated coconut oil indicated that rats fed 34% tallow ate significantly more protein than the 34% corn oil group. Furthermore, animals fed a 34% pure, additive-free tallow diet exhibited a preference for protein. These studies suggest that the type and level of dietary fat interact to influence dietary selection.     

The effect of various dietary fats on skin tumor initiation

The type of dietary fat has been shown to modulate the initiation stage of mammary tumorigenesis, with saturated fat fed before and/or during carcinogen treatment resulting in increased tumor incidence. This study was designed to determine whether different types of dietary fat alter the initiation stage of skin carcinogenesis by use of the initiation‐promotion mouse skin carcinogenesis model. Sencar mice were divided into three groups and maintained on one of the experimental diets. The AIN‐76‐based diets consisted of 10% total fat with various types of fat: 8.5% menhaden oil plus 1.5% corn oil, 8.5% coconut oil plus 1.5% corn oil, and 10% corn oil. After three weeks mice were initiated with 10 nmol dimethyl‐benz[a]anthracene (DMBA). Two weeks later, all mice were switched to a diet containing 5% corn oil. Promotion began four weeks after initiation with twice‐weekly application of 1 μg 12‐O‐tetradecanoylphorbol‐13‐acetate and continued for 12 weeks. No statistically significant differences in kilocalories of food consumed or body weights were observed between diet groups during the study. The final papilloma incidence, yield, and size were not significantly different among the diet groups. In a parallel study, [³H]DMBA binding to epidermal DNA showed no dietary differences. Unlike the mammary carcinogenesis model, these data suggest that the type of fat fed during DMBA initiation had minimal effects on this stage of skin carcinogenesis.     

The influence of dietary lactose on phosphorus-induced nephrocalcinosis in female rats.

The effect of dietary lactose, when compared with glucose, on phosphorus-induced nephrocalcinosis was studied in young, female rats. Nephrocalcinogenic diets containing either 0.4 or 0.6% (w/w) phosphorus were used, and lactose was added up to concentrations of 30%. The diets were fed for 28 days. The 0.4 and 0.6% phosphorus diets, when compared with a diet containing 0.2% phosphorus, caused mild and severe kidney calcification, respectively; kidney calcification was demonstrated chemically by the analysis of kidney calcium, and histologically by staining kidney slides for calcium deposits. Dietary lactose caused calciuria, decreased urinary pH and increased cecum weights. The addition of lactose to the diet partly counteracted nephrocalcinogenesis induced by diets containing 0.4% phosphorus, but it did not influence the severity of nephrocalcinosis seen in rats fed diets containing 0.6% phosphorus. It is suggested that high amounts of lactose in the diet have only weak anti-nephrocalcinogenic activity.     

Metabolism of cholesterol is altered in the liver of C3H mice fed fats enriched with different C-18 fatty acids.

We examined whether the degree of saturation of C-18 fatty acids influenced hepatic cholesterol metabolism in C3H mice. The mice were fed diets containing 20 g/100 g fat, enriched in stearic (18:0), oleic (18:1) or linoleic acid (18:2) with or without 1 g/100 g cholesterol. Plasma total cholesterol concentration was lower in mice fed the 18:0 diet relative to those fed the 18:1- or 18:2-enriched diets (P < 0.05) regardless of dietary cholesterol supplementation. Dietary cholesterol significantly raised hepatic total cholesterol concentration (P < 0.05) in those fed the 18:1- and 18:2-enriched diets, but not in mice fed the 18:0-enriched diet. Dietary cholesterol raised biliary cholesterol concentration (P < 0. 05) in mice fed the 18:1- and 18:2-enriched diets, but not in mice fed the 18:0-enriched diet. The cholesterol saturation index was variably affected by the fat diets. Feeding diets containing cholesterol suppressed the hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity and induced acyl coenzyme A:cholesterol acyl transferase (ACAT) activity compared with feeding diets without cholesterol (P < 0.05), indicating that the liver was exposed to dietary cholesterol. Hepatic ACAT activity was lower in mice fed the 18:0-enriched diet compared with those fed the 18:1- or 18:2-enriched diets (P < 0.05). Addition of cholesterol to the 18:1 diet induced the largest increase of hepatic ACAT activity, and this was associated with the enrichment of VLDL with cholesterol. Varying the degree of saturation of C-18 fatty acids influences the metabolism and disposition of hepatic cholesterol.