Dietary Putrescine Research Articles

Non-Linear Association of Dietary Polyamines with the Risk of Incident Dementia: Results from Population-Based Cohort of the UK Biobank.

Natural polyamines, including spermidine (SPD), spermine (SPM) and putrescine (PUT), are evolutionarily conserved endogenous molecules crucially involved in central cellular processes. Their physiological importance may extend to the maintenance of cognitive function during aging. However, limited population-based epidemiological studies have explored the link between dietary polyamines and dementia risk. This study was a prospective analysis of 77,092 UK Biobank participants aged ≥ 60 years without dementia at baseline. We used Cox proportional hazard regression models to explore the associations between dietary polyamines and the risk of dementia, and restricted cubic splines to test the non-linear relationships. During a median follow-up of 12 years, 1087 incidents of all-cause dementia cases occurred, including 450 Alzheimer's disease (AD) cases and 206 vascular dementia (VD) cases. The fully adjusted hazard ratios (HRs) for the upper fourth quintile of dietary SPD, in comparison with the lowest quintile of intake, were 0.68 (95% confidence interval [95% CI]: 0.66-0.83) for the risk of all-cause dementia, 0.62 (95% CI: 0.45-0.85) for AD and 0.56 (95% CI: 0.36-0.88) for VD, respectively. A 26% reduction in dementia risk [HR: 0.74, (95% CI: 0.61-0.89)] and a 47% reduction in AD [HR: 0.53, (95%CI: 0.39-0.72)] were observed comparing the third with the lowest quintiles of dietary SPM. Dietary PUT was only associated with a reduced risk of all-cause dementia in the fourth quintile [HR (95% CI): 0.82 (0.68-0.99)]. Reduced risk was not found to be significant across all quintiles. There were 'U'-shaped relationships found between dietary polyamines and all-cause dementia, AD and VD. Stratification by genetic predisposition showed no significant effect modification. Optimal intake of polyamines was linked to a decreased risk of dementia, with no modification by genetic risk. This potentially suggests cognitive benefits of dietary natural polyamines in humans.

Putrescine mitigates intestinal atrophy through suppressing inflammatory response in weanling piglets

BackgroundPolyamines are essential for cell growth and beneficial for intestinal maturation. To evaluate the effects of putrescine on alleviating intestinal atrophy and underlying molecular mechanisms, both in vivo feeding trial and in vitro cell culture were conducted. Weanling pigs were fed a diet supplemented with 0, 0.1%, 0.2% or 0.3% putrescine dihydrochloride, whereas porcine intestinal epithelial cells (IPEC-J2) were challenged with lipopolysaccharide (LPS) in the presence of 200 μmol/L putrescine.ResultsDietary supplementation with 0.2% putrescine dihydrochloride decreased the incidence of diarrhea with an improvement in intestinal integrity. Inhibition of ornithine decarboxylase activity decreased the proliferation and migration of IPEC-J2 cells, and this effect was alleviated by the supplementation with putrescine. The phosphorylation of extracellular signal regulated kinase and focal adhesion kinase was enhanced by putrescine. LPS increased the expression of inflammatory cytokines [tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and IL-8], and inhibited cell proliferation and migration in IPEC-J2 cells. Adding exogenous putrescine suppressed the expression of TNF-α, IL-6 and IL-8, and recovered cell migration and proliferation in LPS-treated IPEC-J2 cells. Dietary putrescine supplementation also reduced the mRNA levels of TNF-α, IL-6 and IL-8 and their upstream regulator nuclear receptor kappa B p65 subunit in the jejunal mucosa of piglets.ConclusionsDietary supplementation with putrescine mitigated mucosal atrophy in weanling piglets through improving anti-inflammatory function and suppressing inflammatory response. Our results have important implications for nutritional management of intestinal integrity and health in weanling piglets and other neonates.

Dietary putrescine effects on performance parameters, nutrient digestibility, intestinal morphology and tissue polyamine content of broilers fed low protein diet.

This study was carried out to investigate the effects of dietary putrescine (PUT) on broiler's response fed low crude protein (CP) diets. A total of 192 male day old chicks were fed with four dietary treatments including two levels of PUT (0 and 0.03%) and two levels of CP (normal and low) with factorial combinations. Weekly growth performance, nutrient digestibility and intestinal morphology (at the age of 21 days) and liver and intestinal tissue polyamines content were measured. As a result of this study lower dietary CP had a significant (P<0.05) lower body weight gain (BWG) and improved protein efficiency ratio (PER). PUT improved energy efficiency ratio (EER) significantly (P<0.05). Dry matter (DM) digestibility was decreased by lower dietary CP whereas 0.03% PUT significantly (P<0.05) increased it. Low CP caused significant (P<0.05) greater calcium digestibility, while this effect was not found when PUT was added. PUT had no effect on intestine villous height and crypt depth. Polyamine content of intestine and liver was influenced by the age of the birds, while PUT had no effects on them. In conclusion, dietary PUT has beneficial effects on EER in chicks fed CP-deficient diet, indicating possible involvement of PUT in energy metabolism. PUT supplementation did not moderate the reduced BWG of the chicks fed low protein. Intestinal and liver polyamine concentration was mainly affected by dietary CP and age of the birds rather than dietary PUT.

Role of dietary polyamines in a phase III clinical trial of difluoromethylornithine (DFMO) and sulindac for prevention of sporadic colorectal adenomas

Background:The polyamine-inhibitory regimen difluoromethylornithine (DFMO)+sulindac has marked efficacy in preventing metachronous colorectal adenomas. Polyamines are synthesised endogenously and obtained from dietary sources. Here we investigate dietary polyamine intake and outcomes in the DFMO+sulindac colorectal adenoma prevention trial.Methods:Dietary polyamine data were available for 188 of 267 patients completing the study. Total dietary polyamine content was derived by the sum of dietary putrescine, spermine and spermidine values and categorised into two groups: highest (>75–100%) vs the lower three quartiles (0–25, 25–50 and 50–75%). Baseline tissue polyamine concentration and ODC1 genotype were determined. Logistic regression models were used for risk estimation.Results:A significant interaction was detected between dietary polyamine group and treatment with regard to adenoma recurrence (P=0.012). Significant metachronous adenoma risk reduction was observed after DFMO+sulindac treatment in dietary polyamine quartiles 1–3 (risk ratio (RR) 0.19; 95% confidence interval (CI) 0.08–0.42; P<0.0001) but not in quartile 4 (RR 1.51; 95% CI 0.53–4.29; P=0.44). However, a lower number of events in the placebo group within dietary quartile 4 confound the aforementioned risk estimates.Conclusion:These preliminary findings reveal complex relationships between diet and therapeutic prevention, and they support further clinical trial-based investigations where the dietary intervention itself is controlled.

Polyamine transport is mediated by both endocytic and solute carrier transport mechanisms in the gastrointestinal tract.

The polyamines spermidine and spermine, and their precursor putrescine, are required for cell growth and cellular functions. The high levels of tissue polyamines are implicated in carcinogenesis. The major sources of exogenous polyamines are diet and intestinal luminal bacteria in gastrointestinal (GI) tissues. Both endocytic and solute carrier-dependent mechanisms have been described for polyamine uptake. Knocking down of caveolin-1 protein increased polyamine uptake in colon cancer-derived HCT116 cells. Dietary supplied putrescine was accumulated in GI tissues and liver in caveolin-1 knockout mice more than wild-type mice. Knocking out of nitric oxide synthase (NOS2), which has been implicated in the release of exogenous polyamines from internalized vesicles, abolished the accumulation of dietary putrescine in GI tissues. Under conditions of reduced endogenous tissue putrescine contents, caused by treatment with the polyamine synthesis inhibitor difluoromethylornithine (DFMO), small intestinal and colonic mucosal polyamine contents increased with dietary putrescine levels, even in mice lacking NOS2. Knocking down the solute carrier transporter SLC3A2 in HCT116-derived Hkh2 cells reduced the accumulation of exogenous putrescine and total polyamine contents in DFMO treated cells, relative to non-DFMO-treated cells. These data demonstrate that exogenous putrescine is transported into GI tissues by caveolin-1- and NOS2-dependent mechanisms, but that the solute carrier transporter SLC3A2 can function bidirectionally to import putrescine under conditions of low tissue polyamines.

Role of dietary polyamines in a phase III clinical trial of DFMO and sulindac for prevention of metachronous colorectal adenomas.

1523 Background: Our group has previously demonstrated that polyamine-inhibitory regimen difluoromethylornithine (DFMO) plus sulindac vs. placebo has marked efficacy in preventing metachronous colorectal adenomas in a phase-III trial. Polyamines are synthesized endogenously but also obtained from diet. Here we investigate the role of dietary polyamines in the phase III placebo controlled colorectal adenoma prevention trial with DMFO + sulindac. Methods: Dietary polyamine data were available for 222 of 375 baseline study patients, and for 188 of 267 patients completing the study. A dietary questionnaire completed by each patient was collected at the initiation of the study. Total dietary polyamine content was derived by the sum of dietary putrescine, spermine and spermidine values and further categorized into highest (75%-100%) quartile group vs. a group with lower three quartiles (0-25, 25-50 and 50%-75%). Baseline tissue polyamine concentration was determined using HPLC methodology. Linear and logistic regression analyses were used for risk estimation. Results: A significant direct association was observed between dietary polyamine intake and tissue spermidine (p = 0.02) and spermine concentrations (p = 0.04) at baseline. Higher dietary polyamine group at baseline was associated with adenomas > 1 cm (43.6 % vs. 26.4 %; p = 0.01),high grade adenomas (32.7% vs. 20.4 %; p = 0.06) and advanced adenomas (52.7% vs. 35.9 %; p = 0.02). Among all patients, a significant interaction was observed between treatment, dietary polyamines and the risk of metachronous adenomas (p = 0.01). Therefore we stratified the final analyses (n = 188) by polyamine intake groups. We observed a significant risk reduction of metachronous adenomas from treatment with DFMO+sulindac in the lower dietary polyamine group (RR = 0.19 [0.09-0.40] p < 0.0001) and no benefit in the higher dietary polyamine group (RR = 1.04 [0.32-3.36] p = 0.94). Conclusions: Controlling dietary polyamines may be an effective strategy for preventing the occurrence of colorectal adenomas and colorectal cancer. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Cancer Prevention Pharmaceuticals Cancer Prevention Pharmaceuticals

Effects of early feeding and exogenous putrescine on growth and small intestinal development in posthatch ducks

1. Effects of early feeding with a diet containing added putrescine on duck intestinal development and growth performance were examined by a 2 × 2 factorial arrangement with two different feeding times (6 and 48 h) and two levels of putrescine (0 and 0⋅25%). 2. A significant main effect of early feeding on increasing body weight (BW) was observed from hatch to 35 d, whereas dietary putrescine had no significant effect on BW. 3. In the first week posthatch, enhanced small intestinal weight and intestinal density (weight of intestinal tissue/unit length of intestine), increased villus length and reduced crypt depth were observed in the early feeding group, while no effect was observed when putrescine was added to the diet. 4. Maltase and sucrase activity and protein/DNA ratio in jejunum were increased by early feeding in the first week, while decreased by putrescine supplementation. 5. In conclusion, early feeding methods have great potential for small intestine development and thereafter enhanced the growth performance of ducks, but dietary putrescine used during this period should be used cautiously to avoid toxicity.

Is putrescine an essential nutrient for avians?

Putrescine addition to a complete crystalline amino acid diet elicited a growth response in young chicks, suggesting that putrescine may be an essential nutrient in avians. However, high dietary putrescine levels can depress weight gain.

Impact of dietary amino acids and polyamines on intestinal carcinogenesis and chemoprevention in mouse models

Colon cancer in humans is influenced by both genetic and dietary risk factors. The majority of colon cancers have somatic mutations in the APC (adenomatous polyposis coli) tumour-suppressor gene. Dietary arginine enhances the risk of APC-dependent colon carcinogenesis in mouse models by a mechanism involving NOS2 (nitric oxide synthase 2), as elimination of NOS2 alleles suppresses this phenotype. DFMO (difluoromethylornithine), a specific inhibitor of polyamine synthesis, also inhibits dietary arginine-induced colon carcinogenesis in C57BL/6J-Apc(Min)/J mice. The primary consequence of dietary arginine is to increase the adenoma grade in these mice. Either loss of NOS2 alleles or inhibition of polyamine synthesis suppresses the arginine-induced increase in adenoma grade. In addition to promoting intestinal carcinogenesis, polyamines can also reduce the efficacy of certain intestinal cancer chemopreventive agents. The NSAID (non-steroidal anti-inflammatory drug) sulindac is a potent inhibitor of intestinal carcinogenesis in the C57BL/6J-Apc(Min)/J mouse model and is used to treat humans with FAP (familial adenomatous polyposis). Dietary putrescine reduces the ability of sulindac to suppress intestinal tumorigenesis in the mouse model. These data suggest that reducing polyamine metabolism and dietary polyamine levels may enhance strategies for colon cancer chemoprevention.

Polyamines in tea processing

The distribution of dietary polyamines, putrescine, spermidine and spermine, was determined during processing of Camellia sinensis. Black tea manufacture is carried by a series of processes on fresh tea leaves involving withering, rolling, fermentation, drying and sieving. The aim of this research was to determine the effect of tea processing on the polyamine content in relation with antioxidant enzymes, superoxide dismutase, lipid peroxidase and glutathione peroxidase. Before processing, the spermine content was much higher than the putrescine and spermidine content in green tea leaves. Spermine was significantly decreased during processing while the putrescine and spermine contents increased during withered and rolling and decreased in the following stages. The superoxide dismutase activity increased at the withering stage and declined during processing. The transcript level of the polyamine biosynthesis-responsible enzyme ornithine decarboxylase was reduced during each processing step. This study reveals the importance of protection of nutritional compounds that are essential for health during the manufacturing process.

Dietary Putrescine Reduces the Intestinal Anticarcinogenic Activity of Sulindac in a Murine Model of Familial Adenomatous Polyposis

: The nonsteroidal antiinflammatory drug sulindac displays chemopreventive activity in patients with familial adenomatous polyposis (FAP). Sulindac metabolites induce apoptosis in colon tumor cells, in part, by a polyamine-dependent mechanism that can be suppressed with exogenous putrescine. To determine the relevance of this mechanism in animals, we treated ApcMin/+ mice, a model of human FAP, with sulindac alone or in combination with dietary putrescine. Sulindac increased steady-state RNA levels and enzymatic activity of the polyamine catabolic enzyme spermidine/spermine N1-acetyltransferase and intestinal levels of monoacetylspermidine, spermidine, and spermine in the small intestine of mice. Sulindac also decreased the activity of the biosynthetic enzyme ornithine decarboxylase but not adenosylmethionine decarboxylase (AMD). Dietary putrescine increased intestinal putrescine contents, whereas the combination of dietary putrescine and sulindac yielded the highest levels of intestinal putrescine and correlated with a statistically significant reduction in AMD enzyme activity. Dietary putrescine did not statistically significantly increase tumorigenesis, although it significantly increased the grade of adenoma dysplasia (P < 0.05). The effectiveness of sulindac to suppress intestinal carcinogenesis was partially abrogated by dietary putrescine. These data suggest that sulindac exerts at least some of its anticarcinogenic effects in mice via a polyamine-dependent mechanism. Because high concentrations of putrescine can be found in certain dietary components, it may be advantageous to restrict dietary putrescine consumption in patients undergoing treatment with sulindac.

Dietary Putrescine (1,4-Diaminobutane) Influences Recovery of Turkey Poults Challenged with a Mixed Coccidial Infection

Exogenous dietary putrescine (1,4-diaminobutane) can increase growth rates of neonatal animals, including calves, chicks, and piglets, under nutritional stress. Turkey poults often have a high mortality rate and this may be due to poor initial feeding behavior and inadequate development of the intestinal tract. We conducted an experiment to determine the effect of dietary putrescine supplementation on growth performance and the role of dietary putrescine in prevention and recovery from a coccidial challenge. A total of 160 1-d-old turkey poults were fed a corn and soybean meal–based starter diet supplemented with 0.0 (control), 0.1, 0.2, and 0.3 g/100 g purified putrescine (8 birds/pen, 5 pens/diet). At 14 d of age, half the birds were infected with ∼43,000 sporulated oocysts. The experiment lasted 24 d. Fecal samples were gathered from d 3 to d 5 postinfection by total collection. Ten control and 10 infected birds fed each diet were sampled on d 6 and d 10 postinfection. The induced infection produced significant depressions in growth and feed intake and detrimental morphological changes in the small intestine of poults in the absence of mortality. Weight gains, protein content of jejunum, and morphometric indices of duodenum, jejunum, and ileum were greater in challenged poults fed 0.3 g/100 g putrescine than in controls. We conclude that dietary putrescine supplementation may be beneficial to poult growth, mucosal development of the small intestine, and to recovery from subclinical coccidiosis.

Dietary Interaction of 1,4-Diaminobutane (Putrescine) and Calcium on Eggshell Quality and Performance in Laying Hens

An experiment was conducted to evaluate the potential dietary interaction between 1,4-diaminobutane (putrescine) and calcium on eggshell quality and overall laying performance. One hundred ninety-two 30-wk-old White Leghorn hens were fed a corn-and soybean-meal-based diet supplemented with 0.00, 0.05, 0.10, or 0.15% putrescine and 2.5, 3.0, 3.5, or 4.0% calcium in a factorial design (12 birds per diet) for 4 wk. The percentage of egg production increased linearly (P < 0.05) with increasing levels of dietary calcium. Significant interactions (P < 0.05) were observed between dietary putrescine and calcium for eggshell thickness, eggshell deformation, percentage of eggshell, calcium intake, total calcium retention, total eggshell calcium, and percentage of eggshell calcium. Interactions were due to quadratic effects of putrescine or calcium on these parameters. Eggshell thickness and percent eggshell increased when hens were fed 3.5% calcium in combination with 0.1% putrescine; however, calcium intake and calcium retention were significantly lower (P < 0.05). Eggshell quality improved with increasing dietary levels of calcium due to increased calcium retention and calcium balance. Increasing levels of dietary putrescine did not have a negative effect on eggshell quality; however, calcium intake was lower at higher-supplemented levels of putrescine. It was observed that dietary calcium in excess of requirements resulted in increased egg production and eggshell quality. Eggshell quality improved when hens were fed 3.5% calcium diet in combination with 0.10% putrescine. It was concluded that small supplements of dietary putrescine may improve eggshell quality, depending on dietary calcium concentration.

Effects of Dietary 1,4-Diaminobutane (Putrescine) on Eggshell Quality and Laying Performance of Hens Laying Thin-Shelled Eggs

Experiments were conducted to evaluate the potential for dietary 1,4-diaminobutane (putrescine) to influence eggshell quality and overall laying performance in hens. Forty-eight, 60-wk-old White Leghorn hens laying thin-shelled eggs were fed a corn and soybean meal-based diet supplemented with 0.00 (control), 0.05, 0.10, or 0.15% putrescine for 4 wk. Twelve hens that laid thick-shelled eggs were also fed the control diet. The feeding of supplemental putrescine decreased feed consumption; however, egg weight decreased only at higher levels of supplementation. Increasing dietary levels of putrescine responded quadratically in eggshell deformation, eggshell weight, and eggshell weight as a percentage of egg weight (P < 0.05). There were no significant differences in shell deformation, shell thickness, or shell weight when comparing hens laying thick-shelled eggs and those laying thin-shelled eggs that were fed 0.05% supplemental putrescine. Calcium intake, calcium retention, and calcium balance decreased linearly (P < 0.05) with increasing levels of dietary putrescine. Pancreatic putrescine concentrations were significantly higher (P < 0.05) in hens laying thick-shelled eggs compared with hens laying thin-shelled eggs. It appeared that pancreatic cells synthesized more polyamines in hens laying thick-shelled eggs. This increase in polyamines might have caused improved eggshell quality by increasing calcium transport. It was concluded that 0.05% supplemental putrescine improved eggshell quality; however, higher levels proved to be toxic.

Effects of Dietary 1, 4-Diaminobutane (Putrescine) on Eggshell Quality and Laying Performance of Older Hens

We conducted an experiment to evaluate the potential for dietary 1,4-diaminobutane (putrescine) to promote eggshell quality and overall laying hen performance. A total of 128, 60-wk-old Barred Rock hens were fed a corn and soybean meal-based layer diet supplemented with 0.0 (control), 0.2, 0.4, and 0.6% free base 1,4-diaminobutane for 4 wk. The feeding of supplemental putrescine decreased feed consumption (P ≤ 0.05) and egg mass (P ≤ 0.05) and tended to decrease egg production (P < 0.08). Albumen quality was not significantly affected (P < 0.09) by the end of the experiment, as determined by Haugh units. Eggshell thickness was not significantly improved with lower levels of dietary putrescine (P < 0.08). Although dietary putrescine did not have any effect on the relative weights of duodenum, jejunum + ileum, or pancreas, there was a linear increase in putrescine concentrations in tissues (P ≤ 0.05). Supplementation of dietary putrescine also resulted in increased putrescine and spermidine concentrations in egg (P ≤ 0.05). Egg weight and eggshell deformation increased over time; however, eggshell weight, eggshell weight as percentage of egg weight, and eggshell thickness decreased (P ≤ 0.05). It appeared that eggshell quality declined regardless of diet over the 4-wk experimental period. It was concluded that the lack of effect of dietary putrescine on egg parameters, with the exception of albumen quality and eggshell thickness, was due to putrescine toxicity. Hens transferred excess dietary putrescine and metabolites to eggs.

Uptake, inter-organ distribution and metabolism of dietary putrescine in the rat

The movement of a single dose of 14C-putrescine in the lumen of the rat gastrointestinal tract was followed for 3 hours after intragastric intubation. Putrescine progressed in the gut lumen in a wave-like fashion and was absorbed in the small bowel. Maximal uptake was observed at 2 hours; therefore, this time-point was selected to measure the concentration dependency of putrescine uptake by the small intestine and distribution between the vital organs in a wide concentration range (1/10 to 100 times the dietary input). Putrescine uptake by the small bowel was likely to be by passive diffusion, because the absorption was in proportion to input. The fate of putrescine was determined in the plasma, small bowel, liver, and skeletal muscle by measuring the radioactivity of the polyamines, their acetyl derivatives, and amino acids at physiologic concentrations. It appears that approximately 10% of the dietary input reaches the putrescine body pool.

Effect of feeding raw soybeans on polyamine metabolism in chicks and the therapeutic effect of exogenous putrescine.

The inclusion of isolated soy protein in milk replacer diets for calves and neonatal pigs inhibits development of intestinal mucosal cells. Simultaneous administration of putrescine partially overcomes this effect. We therefore conducted experiments to determine the potential for dietary putrescine to overcome the toxicity of raw soybeans in chicks. In the first experiment, week-old chicks were fed either an isolated soy protein-based control diet or an isoenergetic and isonitrogenous diet containing 52% raw, ground soybeans for 14 d. The feeding of raw soybeans depressed (P < .001) growth and feed consumption, caused enlargement (P < .001) of the duodenum and pancreas, depressed (P < .001) activities of polyamine synthetic enzymes in the duodenum, and reduced (P < .01) duodenal tissue concentrations of putrescine. In the second experiment, the diet containing raw soybeans was fed with and without .2, .3, and .4% supplemental putrescine. The feeding of supplemental putrescine largely overcame the inhibition of growth due to the feeding of raw soybeans and increased intestinal putrescine concentrations. Putrescine supplementation had no effect, however, on pancreatic and intestinal enlargement in birds fed raw soybeans and tended to depress the activity of polyamine synthetic enzymes. The beneficial effects of putrescine supplementation were confirmed in the third experiment when up to 1.0% supplemental putrescine was fed. We conclude that the toxicity of raw soybeans to chicks can be overcome by feeding putrescine. These effects are likely due to improved nutrient uptake by overcoming the adverse effects of lectins in the intestinal tract and are not likely due to alleviation of the pancreatic enlargement caused by protease inhibitors.

Failure of Dietary Putrescine to Enhance the Growth of Rainbow Trout (Oncorhynchus mykiss)

Reduction of herring meal (to 100 g∙kg−1) in rainbow trout (Oncorhynchus mykiss) diets and its replacement by soybean and corn gluten meals led to reduced feed intake and growth. The diamine putrescine, when included in calf diets, reduced the effects of antinutritional factors in soybean meal; it also enhanced the growth of chicks. Putrescine (1–4 g∙kg−1) added to practical trout diets did not increase feed intake or growth over a 12-wk period. Putrescine concentrations in the trout tissues were not increased by this treatment, nor were the activities of the putrescine and polyamine biosynthetic enzymes ornithine decarboxylase and adenosylmethionine decarboxylase significantly changed. When a higher putrescine concentration (13.3 g∙kg−1) was used, in line with the calf diets, it reduced weight gain, feed intake, and gain/feed ratio. Lack of effect of putrescine at the lower concentrations (where it was effective with chicks) was ascribed to the enzyme diamine oxidase, shown to be active in the pyloric ceca and the anterior intestine of the trout. Passage of food through the gastrointestinal tract of trout is about 10-fold longer than in chicks. This may explain the failure of dietary putrescine to elevate tissue putrescine levels in trout.

Effect of Dietary Putrescine on Whole Body Growth and Polyamine Metabolism

Putrescine (1,4-diaminobutane) is the simplest of the mammalian polyamines. These are small, positively charged molecules which are essential for cell growth and are thought to play a role in regulation of anabolic events such as synthesis of DNA, RNA, and protein. Recent reports have indicated the potential for dietary precursor amino acids of putrescine to alter tissue putrescine concentrations. The current study was conducted to determine the physiologic significance of these effects by feeding up to flooding doses of putrescine to determine any influence on whole body growth and polyamine metabolism. A total of 96 chicks were fed purified crystalline amino acid diets containing 0.0, 0.2, 0.4, 0.6, 0.8, or 1.0% purified putrescine (four birds per pen, four pens per diet) for 14 days. The feeding of 0.2% putrescine increased growth rate beyond that of controls while further supplements reduced growth and were toxic when 0.8 and 1.0% putrescine were fed. Hepatic and muscle concentrations of ornithine increased with dietary putrescine while the effect in kidney was much less. Putrescine concentrations in liver, kidney, and muscle rose when 0.4% putrescine or more was fed. This effect was particularly obvious in muscle in which there were also increases in the concentrations of spermidine and spermine. In a subsequent similar experiment, putrescine was fed at 0.0, 0.1, 0.2, 0.3, 0.4, or 0.5% to determine the effect on the activities of the key enzymes regulating polyamine synthesis. The feeding of putrescine at even 0.1% caused a rapid reduction in hepatic ornithine decarboxylase activity while S-adenosylmethionine decarboxylase and arginase activities were not influenced by diet. It was concluded that excess tissue putrescine can be toxic to whole organisms but small, orally administered doses of this metabolite can promote growth.

Putrescine and spermidine as growth-promoting substances for the saw-toothed grain bettle, Oryzaephilus surinamensis (L.) (coleoptera, silvanidae)

1. 1. Dietary putrescine increased survival of larvae of Oryzaephilus surinamensis (L.) at a concentration of 0·50 mg/g and of pupae at 0·20 mg and 0·50 mg/g. It increased rate of development, except at 0·10 mg and 1·00 mg/g. 2. 2. Dietary spermidine decreased survival of pupae at 0·02 mg, 0·10 mg and 0·20 mg/g. It increased rate of development at 0.05 mg/g only, and decreased it at 0·10 mg, 0·20 mg and 1·00 mg/g. 3. 3. Putrescine may have vitamin activity and spermidine, antimetabolite activity for this organism.