Disease relevance of Diet1

• The Diet1 locus confers protection against hypercholesterolemia through enhanced bile acid metabolism [1].
• PURPOSE: Diet composition is an important etiologic factor in prostate cancer (PCA) growth and has significant impact on clinical PCA appearance [2].
• Mice fed Diets B, C, and D exhibited lower body weights and elevated amounts of extractable total lipid in livers compared with mice fed diets without CLA (Diet A) [3].
• Three strains of mice and two rat strains commonly used in laboratory work and maintained on either ad libitum (AL) or calorically restricted (CR) diets in the National Institutes of Aging and Diet Restriction colony were examined by slit lamp for age-related cataracts at four or more time points during their life spans [4].
• Energy balance studies suggest that the overall efficiency of energy utilization does not increase during pregnancy in rodents, other than as a consequence of "hyperphagia". Diet-induced thermogenesis is not stimulated in response to the increased energy intake of the pregnant animal, the extra intake being retained at the maximum efficiency [5].

High impact information on Diet1

• We previously identified a genetic locus, Diet1, which is responsible for the resistant phenotype in B6By mice [1].
• Diet or hormonal manipulations as demonstrated here by treatments with high-fat diet or gonad removal and hormone replacement do not influence this low activation [6].
• SUMMARY BACKGROUND DATA: Diet influences the ability of gut-associated lymphoid tissue (GALT) to maintain mucosal immunity [7].
• Both diets had a reductive effect in plasma; however Diet I had relatively little effect on the glutathione redox status in tissue homogenates or mitochondria [8].
• In separate and independent studies, two different dietary mixtures, one enriched with vitamin E, vitamin C, L-carnitine, and lipoic acid (Diet I) and another diet including vitamins E and C and 13 additional ingredients containing micronutrients with bioflavonoids, polyphenols, and carotenoids (Diet II), were fed for 8 and 10 months, respectively [8].

Chemical compound and disease context of Diet1

• Male C57Bl/6J mice were fed Control or Trans Diets that were similar, except that 50% of the 18:1, which was all cis in the Control Diet, was replaced by tFA in the Trans Diet. At selected ages, body weight, epididymal fat pad weight, perirenal fat yield, adipose tissue cellularity and fatty acid composition were examined [9].
• We have studied three different types of weight-loss stress caused by Diet restriction, Activity or Separation, for their effects on the hypothalamic-pituitary axis in young female mice and their responses to tyrosine 100 mg/kg/day [10].
• Effect of Genistein with Carnitine Administration on Lipid Parameters and Obesity in C57Bl/6J Mice Fed a High-Fat Diet [11].

Biological context of Diet1

• A genome-wide scan revealed a locus, designated Diet1, on chromosome 2 near marker D2Mit117 showing highly significant linkage (lod = 9.6) between B6By alleles and hypo-response to diet [12].
• Body weights at 16 and 24 mon of age and epididymal fat pad weights at 8-24 mon of age were lower in mice fed the Trans Diet as compared to those fed the Control Diet. At the ages studied, the Trans Diet also resulted in lower values for perirenal fat weights, triacylglycerol to polar lipid ratios, and adipose cell size [9].
• Additionally, the distribution of S-phase cells in crypts of AOM-treated mice fed Diet 3 most closely resembled that of the saline controls [13].
• The age at the birth of the first litter for Diet 2 F(1) male (76.8 +/- 2.2 d) and female (58.4 +/- 2.1 d) was significantly greater (P<0.05) than the age at parturition for Diet 1 male and female F(1) test mice (64.1 +/- 1.8 and 51.9 +/- 1.2 d, respectively) [14].
• This diet (Regional Basic Diet - RBD) has negative effects on the growth, food intake and protein utilization in infected mice (acute phase of murine schistosomiasis) [15].

Anatomical context of Diet1

• Compared to the Control Diet, the Trans Diet resulted in adipose tissue lipids with higher percentages of 14:0 and 18:2n-6 and lower percentages of cis-18:1 and 20:4n-6 [9].
• Ova recovery rate and fertilization rate were significantly reduced in mice maintained on Diet 1 [16].
• METHODS: To examine the effect of AICAR on adipocyte differentiation in 3T3L1 cells and in a mouse Diet induced obesity (DIO) model, 3T3L1 cells were differentiatied in the presence or absence of different concentration of AICAR and neutral lipid content and expression of various adipocyte-specific transcription factors were examined [17].
• Blastocyst hatching in vitro was not observed in embryos from females maintained on Diet 1, and was greater in embryos from females fed Diets 4, 5, and 7 (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)[16]
• Cadmium-109 metabolism in mice. IV. Diet versus maternal stores as a source of cadmium transfer to mouse fetuses and pups during gestation and lactation [18].

Associations of Diet1 with chemical compounds

• Powdered AIN-76A diets (Harlan Teklad Research Diet, Madison, USA) containing 100 or 300 ppm I3C (group 1 or 2) or the same pellet diets without supplement (group 3) were fed to 6-week-old male C57BL/6J-Apc(Min)(/+) (Min/+) mice (The Jackson Laboratory, Bar Harbor, ME, USA) for 10 weeks [19].
• METHODS: Female Balb/c mice were fed over a period of 10 days either with an isocaloric and isonitrogenous control diet (Control), a glutamine enriched diet (Diet I) or a diet containing glutamine, arginine, glycine, and n-3 fatty acids (Diet II) [20].
• Analyses of women in the Malmö Diet and Cancer Study showed a mean niacin number of 60.4 with a range of 44 to 75 [21].
• The basal diet was the American Institute of Nutrition Diet 76A, to which was added 120 IU of retinyl palmitate per g diet, 1% canthaxanthin, or the combination of both [22].
• Sensitivity to adriamycin of BL6 from mice fed Low Tyr and Phe Diet is increased and is not altered by change in metastatic potential [23].

Analytical, diagnostic and therapeutic context of Diet1

• To investigate the function of Diet1, we compared mRNA expression profiles in the liver of B6By and B6J mice fed an atherogenic diet using a DNA microarray [1].
• The disease in this patient was precipitated by carbohydrate restriction as outlined in the "Scarsdale Gourmet Diet". Our mutation detection and confirmation strategy included PCR, automated sequencing, and restriction enzyme digestion [24].
• Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-6:omega-3 Ratio in Diet: Athymic Mouse Xenograft Model Simulating Radical Prostatectomy [25].

References