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Cats Absorb β-Carotene, but It Is Not Converted to Vitamin A

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... Some early studies were unable to detect absorption of orally administered BC into blood or the liver of domestic cats [47,185]. However, more recent studies and our own experiments have found absorption of BC supplements into plasma to be quite substantial in cats, though these studies use relatively high doses [177,186,187]. Domestic cats consuming commercial diets seem to have very low to no circulating BC [18,187]. ...
... However, more recent studies and our own experiments have found absorption of BC supplements into plasma to be quite substantial in cats, though these studies use relatively high doses [177,186,187]. Domestic cats consuming commercial diets seem to have very low to no circulating BC [18,187]. However, Crissey et al. [27] found relatively high concentrations of serum BC in 11 captive wild felid species kept in zoos. ...
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Vitamin A is essential for life in all vertebrate animals. Vitamin A requirement can be met from dietary preformed vitamin A or provitamin A carotenoids, the most important of which is β -carotene. The metabolism of β -carotene, including its intestinal absorption, accumulation in tissues, and conversion to vitamin A, varies widely across animal species and determines the role that β -carotene plays in meeting vitamin A requirement. This review begins with a brief discussion of vitamin A, with an emphasis on species differences in metabolism. A more detailed discussion of β -carotene follows, with a focus on factors impacting bioavailability and its conversion to vitamin A. Finally, the literature on how animals utilize β -carotene is reviewed individually for several species and classes of animals. We conclude that β -carotene conversion to vitamin A is variable and dependent on a number of factors, which are important to consider in the formulation and assessment of diets. Omnivores and herbivores are more efficient at converting β -carotene to vitamin A than carnivores. Absorption and accumulation of β -carotene in tissues vary with species and are poorly understood. More comparative and mechanistic studies are required in this area to improve the understanding of β -carotene metabolism.
... A thyroxin deficit in rats prevents them from transforming β-carotenes into vitamin A (Hagemann and Schmidt, 2018, p. 213). Some carnivores like cats and minks rely on their diet containing sufficient amounts of vitamin A and are not affected by blocking this synthesis (McDowell and Cunha, 2014;Schweigert et al., 2002). Furthermore, dependence on prey is the reason that these animals are better suited to having varying vitamin A concentrations in the blood stream and means to store vitamin A in their body, which makes them less prone for hypervitaminosis A (Green and Fascetti, 2016;Schweigert et al., 1991). ...
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The field of chemical rodent control has seen no major developments in the last decades, even though anticoagulant rodenticides (AR), the mainly used substances to manage mice and rats, are known environmental pollutants and candidates for substitution under the European Biocidal Products Regulation 528/2012. Moreover, recent political developments in Europe and the USA demand more safety and sustainability in the management of chemicals, reinforcing the need for environmentally friendly substances. In this concept study, we present a step-by-step approach to improve the environmental properties of rodenticides. Repurposing of existing pharmaceuticals, the use of enantiomerically pure rodenticides, or the improvement of the formulation by microencapsulation can help to alleviate environmental problems caused by AR in the short term. Modification of the chemical structures or the development of prodrugs as medium-term strategies can further improve environmental properties of existing compounds. Ultimately, the development of new substances from scratch enables the utilisation of so far ignored modes of actions and the application of modern safe and sustainable-by-design principles to improve target specificity and reduce the negative impact on non-target organisms and the environment. Overall, our concept study illustrates the great potential for improvement in the field of chemical rodent control when applying available techniques of green and sustainable chemistry to known or potential rodenticides. Most promising in the medium term is microencapsulation that would allow for the use of acutely acting substances as it could circumvent bait shyness. On a longer timescale the de novo design of new rodenticides, which is the only method that can combine a high target specificity with good environmental properties, is the most promising approach.
... While most animals are able to synthesize vitamin A from some precursors, of which betacarotene is the most important, cats lack the dioxygenase enzyme that starts the conversion of carotenoids to retinal and need a dietary source of pre-formed vitamin A (Schweigert et al., 2002). Since the body of prey contains adequate amounts of vitamin A and only traces of carotenoids, the maintenance of the enzymes for the conversion of carotenoids into vitamin A would represent in cats only an energetic cost. ...
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Cats have become the most popular companion animal in Western Europe. Unlike other domestic animals, cats are strict carnivores and this influences both their nutritional requirements and food preferences. Cats have very high protein requirements and their diet must contain some nutrients, such as arginine, taurine, niacin, vitamin A and arachidonic acid. Besides its nutritional value, a diet for cats must also be highly palatable. This paper offers a quick overview of feline nutritional peculiarities and the factors that influence food palatability in cats.
... Fat-soluble vitamins work synergistically as well as antagonistically, particularly if imbalanced [19]. Felines also lack the ability to convert provitamin carotenoids, including ß-carotene, into active vitamin A [20]. Vitamin A is important to the integrity of the epithelium of the respiratory and digestive tracts. ...
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In 1889 Dr. John Bland-Sutton, a prominent London surgeon, was consulted about fatal rickets in over 20 successive litters of lion cubs born at the London Zoo. He evaluated the diet and found the cause of rickets to be nutritional in origin. He recommended that goat meat with crushed bones and cod-liver oil be added to the lean horsemeat diet of the cubs and their mothers. Rickets were reversed, the cubs survived, and subsequent litters thrived. Thirty years later, in classic controlled studies conducted in puppies and young rats, the definitive role of calcium, phosphate and vitamin D in prevention and therapy of rickets was elucidated. Further studies led to identifying the structural features of vitamin D. Although the Bland-Sutton diet provided calcium and phosphate from bones and vitamins A and D from cod-liver oil, some other benefits of this diet were not recognized. Taurine-conjugated bile salts, necessary for intestinal absorption of fat-soluble vitamins, were provided in the oil cold-pressed from cod liver. Unlike canine and rodent species, felines are unable to synthesize taurine, yet conjugate bile acids exclusively with taurine; hence, it must be provided in the diet. The now famous Bland-Sutton “experiment of nature,” fatal rickets in lion cubs, was cured by addition of minerals and vitamin D. Taurine-conjugated bile salts undoubtedly permitted absorption of vitamins A and D, thus preventing the occurrence of metabolic bone disease and rickets.
... While the extant data suggests that amphibians do not cleave dietary β-carotene, it is interesting to note that amphibian species harbor copies of the carotenoid cleavage enzymes in their genome. This scenario is similar to observations in carnivores; for example, the domestic cat (Felis catus) genome contains a predicted copy of beta-carotene 15,15′-monooxygenase 1, but these animals have been reported to absorb β-carotene without cleaving it [Schweigert et al., 2002]. ...
Article
Vitamin A status is an important consideration in the health of both wild and captive amphibians. Data concerning whole body vitamin A homeostasis in amphibians are scarce, although these animals have been used as experimental models to study the actions of vitamin A in vision, limb regeneration and embryogenesis. The available data suggest that many aspects of vitamin A biology in amphibians are similar to the canonical characteristics of vitamin A metabolism and actions established in mammals. This is consistent with the evolutionary conservation of these important biological processes. Amphibians must obtain vitamin A in their diet, with captive animals being prone to vitamin A deficiency. There is still much to be learned about vitamin A biology in amphibians that can only be achieved through rigorous scientific research. Improved understanding of amphibian vitamin A biology will aid the conservation of endangered amphibians in the wild, as well as the successful maintenance of ex situ populations. Zoo Biol. XX:XX-XX, 2014. © 2014 Wiley Periodicals, Inc.
... A similar phenomenon has been described in lions where skull malformations have been found as a cause for neurological signs, possibly caused by hypovitaminosis A [14] [15] [31]. Felids require preformed VA in their diet due to the lack of ability to convert β-carotene into retinol [32]. In captivity, a meat diet which is not supplemented and does not contain bones, viscera, fur or feathers may lead to these deficiencies. ...
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Neurological signs like ataxia and hind limb paresis have often been reported in cheetahs (Aci-nonyx jubatus), lions (Panthera leo) and snow leopards (Panthera unica). As a cause, copper and Vitamin A deficiencies have been discussed. Many cases were seen in cheetahs and lions in the United Arab Emirates (UAE) within the last years. The aim of this study was to find correlations between nutrition, serum, and tissue levels, focusing on copper and Vitamin A. Blood and tissue samples of affected and unaffected animals were analyzed at the Central Veterinary Research La-boratory in Dubai, UAE. Animals were split into three different groups (A, B and C) according to their diets. Minerals were determined in serum, tissue, food and water samples, and serum was additionally analyzed for Vitamin A and E. Liver, kidney and spinal cord samples were taken for histopathological investigations. Mean serum copper and liver copper levels of animals fed pure chicken muscle meat without supplements were significantly lower (0.41 ± 0.71 µM/L; 2.16 ± 0.95 ppm wet weight) than in animals fed a whole carcass prey diet (12.16 ± 3.42 µM/L; 16.01 ± 17.51 ppm wet weight) (p < 0.05). Serum Vitamin A and E levels were highest in animals fed whole car-cass prey diets (1.85 ± 0.68; 27.31 ± 5.69 µM/L). Liver zinc concentrations were highest in animals fed pure chicken meat only (43.75 ± 16.48 ppm wet weight). In histopathology, demyelination of the spinal cord was found in all of the affected animals and most commonly when fed a diet based on poultry without supplements. C. Kaiser et al.
... A similar phenomenon has been described in lions where skull malformations have been found as a cause for neurological signs, possibly caused by hypovitaminosis A [14] [15] [31]. Felids require preformed VA in their diet due to the lack of ability to convert β-carotene into retinol [32]. In captivity, a meat diet which is not supplemented and does not contain bones, viscera, fur or feathers may lead to these deficiencies. ...
Article
Neurological signs like ataxia and hind limb paresis have often been reported in cheetahs (Acinonyx jubatus), lions (Panthera leo) and snow leopards (Panthera unica). As a cause, copper and Vitamin A deficiencies have been discussed. Many cases were seen in cheetahs and lions in the United Arab Emirates (UAE) within the last years. The aim of this study was to find correlations between nutrition, serum, and tissue levels, focusing on copper and Vitamin A. Blood and tissue samples of affected and unaffected animals were analyzed at the Central Veterinary Research Laboratory in Dubai, UAE. Animals were split into three different groups (A, B and C) according to their diets. Minerals were determined in serum, tissue, food and water samples, and serum was additionally analyzed for Vitamin A and E. Liver, kidney and spinal cord samples were taken for histopathological investigations. Mean serum copper and liver copper levels of animals fed pure chicken muscle meat without supplements were significantly lower (0.41 ± 0.71 μM/L; 2.16 ± 0.95 ppm wet weight) than in animals fed a whole carcass prey diet (12.16 ± 3.42 μM/L; 16.01 ± 17.51 ppm wet weight) (p < 0.05). Serum Vitamin A and E levels were highest in animals fed whole carcass prey diets (1.85 ± 0.68; 27.31 ± 5.69 μM/L). Liver zinc concentrations were highest in animals fed pure chicken meat only (43.75 ± 16.48 ppm wet weight). In histopathology, demyelination of the spinal cord was found in all of the affected animals and most commonly when fed a diet based on poultry without supplements.
... Een voeder zonder vitamine A, maar rijk aan beta-caroteen kon bij katten de ontwikkeling van deficiëntiesymptomen niet voorkómen (2). De kat kan beta-caroteen uit de voeding opnemen en ook splitsen in twee retinolmolekulen (8)(9)(10), maar in onvoldoende mate om de retinolbehoefte te dekken. ...
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De kat en vitamine A Vitamine A is een essentiële voedingsstof voor de kat. Zowel een tekort als overmaat, gedurende langere tijd, veroorzaakt ernstige aandoeningen. Als zuivere stof is vitamine A zeer oxidatiegevoelig. Derhalve worden bij de productie van kattenvoeders gestabiliseerde preparaten gebruikt. In 1957, 35 jaar na de ontdekking van vitamine A in onderzoek bij ratten (1), werd door Gerschoff et al. (2) gepubliceerd dat het vitamine ook voor de kat een essentiële voedingsstof is. Twee tot drie maanden na verstrekking van een semisynthetisch voeder (Noot 1) zonder vitamine A, hadden jonge katten gewichtsverlies, licht roze tot rode uitvloeiing rond de oogleden en spierzwakte in de achterpoten. Tijdens een congres in 1964 sprak Sumner-Smith, dierenarts te Bristol, over voedingsgerelateerde problemen bij katten (3). Hij zei onder meer dat zijn voedingsadvies voor een kat vaak werd weggewuifd door de eigenaar met de reactie dat haar/zijn kat niets anders wil eten dan lever. In 1965 lieten Seawright et al. (4) zien dat een destijds bekende botaandoening bij katten, die veel runderlever aten, werd veroorzaakt door intoxicatie met vitamine A. Vitamines A en D Na een periode van 10 tot 17 weken op een voeder met varkensvet als enige vetbron stopte de groei van jonge ratten (5, Noot 2). De publicatie uit 1913 toont dat vervanging van varkensvet door een etherextract van boter, eieren of eidooier de groei herstelde, terwijl een etherextract van olijfolie dat niet deed. De groeifactor in boter en eieren werd later vetoplosbaar A genoemd, ter onderscheiding van wateroplosbaar B (cf. 6). Bij ratten beschermde groeifactor A behalve tegen groeivertraging ook tegen gebrekkige calciumafzetting in het bot (rachitis) en uitdroging van het oogbindvlies (xeroftalmie). In 1922 bleek dat de groeifactor uit twee vitamines bestaat (1, Noot 3). Na doorborrelen van groeifactor A met lucht trad groeivertraging en xeroftalmie op, maar geen rachitis. De oxidatiegevoelige en-ongevoelige component zouden als vitamines A en D bekend worden. Vitamine A en caroteen In 1932 werd de structuur van vitamine A opgehelderd (7). Retinol, de belangrijkste vorm van vitamine A in de voeding, bestaat uit 20 koolstofatomen met een ringstructuur aan één uiteinde en een hydroxylgroep aan het andere. Het retinolmolekuul bevat vijf onverzadigde bindingen waardoor het zeer oxidatiegevoelig is. Dit verklaart dat de retinolcomponent van groeifactor A werd geïnactiveerd door lucht. De opname van vitamine A bij de kat leek efficiënter op een vetrijk in plaats van vetarm voeder (2). Deze bevinding wordt verteringsfysiologisch ondersteund. De opname van het vetoplosbare retinol door de darm lift mee met de vertering en absorptie van voedingsvetten.
... However, early investigations indicated that the domestic cat lacks the ability to convert β-carotene to vitamin A. The recent interest in carotenoids in pet nutrition as potential antioxidants demands additional studies to clarify the assumptions that dietary β-carotene cannot be used as a source for vitamin A in domestic cats [78] (Table 7). ...
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Specific clinical trials are needed to design helpful therapeutic interventions in CDS cats. However, the first step is to obtain a reliable tool enabling early diagnosis of the disease. Hitherto, the evaluation of oxidative stress may be considered more as a preventative assessment than a diagnostic tool. Even so, the evaluation of oxidative stress and its factors of variation with age allow us to monitor the success - or failure - of the many nutritional and pharmacological strategies that exist in Feline Medicine today.
... Dogs can meet their entire vitamin A requirement through -carotene [5]. And although cats require preformed vitamin A, they can efficiently absorbcarotene, as evidenced by elevated plasma concentrations after supplementation [6]. Furthermore, -carotene may play additional roles in health, including immune response, gap junction communication, and other cellular functions [7], but more research is needed to further elucidate these effects. ...
... Felids have higher demands for vitamin A when compared with other species due to their inability to convert B carotene to vitamin A. 19 As such, it is suspected that they might be more susceptible to retinol dietary deficiency. 17 In our case, we suspect the origin of the hypovitaminosis A was due to poor dietary intake as retinol concentration is limited in chicken muscle. ...
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An adult, male, domestic longhair cat was evaluated for chronic progressive visual impairment and lethargy. Neurological abnormalities localised to the cerebellum/central vestibular system, and optic chiasm/retinas and/or optic nerves were present on clinical examination. MRI and CT studies showed diffuse hyperostosis with thickening of the calvarium and tentorium cerebelli causing compression and distortion of the brain. Biochemical testing showed low plasma retinol levels at 0.1 μmol/l (0.86–2.2). Postmortem examination showed reduction in volume of the frontal lobes secondary to diffuse skull hyperostosis. Microscopically, there were mild white matter spongiosis affecting the corona radiata and optic nerves and multiple small plaque-like thickening of the meninges. This is the first case report to provide a comprehensive clinical, diagnostic imaging and pathological details of hypovitaminosis A in a cat.
... It is essential for healthy cell division and differentiation. 64 Many plants contain precursor provitamin A carotenoids that omnivorous animals such as dogs can metabolize to form active vitamin A. 65 On the other hand, obligate carnivores such as cats cannot use carotenoids and require dietary provision of preformed vitamin A. 66,67 Inclusion of vegetables rich in β-carotene can be used to formulate canine diets that contain adequate precursors for vitamin A metabolism. Furthermore, synthetic vitamin A analogs, in the form of retinyl esters, can also be added to plant-based diets. ...
... Although early studies were unable to detect significant amounts of β -carotene in the blood of cats given oral doses, more recent studies have found β -carotene absorption to be relatively efficient in cats, which brings into question issues regarding the limits of detection and specificity of earlier methods used for retinoid and carotenoid detection. For example, Schweigert et al. (2002) have reported that cats are able to absorb β -carotene from the diet, but it is not efficiently converted to vitamin A. Unlike most mammals, cats have little capacity to convert carotenoids to vitamin A, because of low levels of β -carotene 15,15'-monooxygenase, an enzyme essential for the conversion of carotenoids to retinol (Figure 24.4). Cats and ferrets should be fed animal sources rich in retinyl ester or vitamin A as retinyl palmitate or acetate in supplements (Lederman et al., 1998;White et al., 1993). ...
Chapter
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Overview of selected functions of vitamins and their assessments in laboratory animals
... In dogs, part of the provitamin A carotenoids, such as ß-carotene, may first undergo dioxygenasemediated cleavage into retinal, but cats lack this enzyme (30,37). In contrast to passive absorption, the mucosal transporter and convertor of ß-carotene are under negative feedback by the liver's vitamin A reserve (38,39). ...
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Carotenoids in petfood Carotenoids pertain to pigments synthesized by plants. They participate in capturing sunlight energy and furnish the variety of yellow to red colors in fruits and vegetables. Highlighted carotenoids in petfood are mostly linked with immunity support and high antioxidant value. The four health carotenoids concern beta-carotene, lycopene, lutein and astaxanthin. Prototypical ingredients, rather than concentrated additives, serve as carotenoid carriers. Beta-carotene is named after carrots and provides their yellowish-orange color. The intestinal wall of dogs takes up beta-carotene and can convert it into vitamin A. In contrast, cats require preformed vitamin A as they cannot synthesize it. "Carrots as natural source of beta-carotene" is a phrase used in some petfood promotional texts. Immune-health claims for dietary beta-carotene are not substantiated by published research in dogs and cats. Lycopene is responsible for the red color in tomatoes, lutein is so for the yellow-colored marigold flowers and astaxanthin for the red of krill shells and specific microalgae. Those natural sources function as carotenoid delivery vehicles in petfood. After feeding purified forms of lutein and astaxanthin to dogs and cats, indicators of the animals' immune responses were measured. The results do not provide solid evidence that lutein and astaxanthin enhance immunity. Data on lycopene are lacking. Antioxidants may neutralize unstable, reactive molecules (free radicals) and prevent them from doing damage to various chemical, bodily structures. There is no proof that the four carotenoids have antioxidant activity within the canine and feline body. And furthermore, it has not been demonstrated that added carotenoids in complete petfood improve immune and visible health of dogs and cats. Carotenoid structures Plant carotenoids are located in chloro-and chromoplasts. They give colors to non-green (parts of) plants, while being masked by the presence of green chlorophyll. Lycopene and ß-carotene are ranked among the carotenes. Lutein and astaxanthin belong to the oxycarotenoids/xanthophylls. All-trans lycopene (C 40 H 56) is a linear tetraterpene assembled from 8 isoprene units. ß-Carotene is formed by enzymatic conversion of lycopene's ends into six-carbon rings. Lutein results from end cyclization of lycopene and hydroxylation of each ring. Astaxanthin's rings have both a keto and hydroxyl group. Carotenoid carriers Carotenoid contents in plant materials are highly variable as they depend on many factors, including cultivar, growing conditions, harvest time and ripening stage. For the carotenoid carriers in petfood, the average amounts per kg dry matter are as follows: 0.7 g ß-carotene in carrots (1-3, Note 1), 2.0 g
... Amylase is not present in cat's saliva and their gastrointestinal tract is relatively short compared to omnivores so they can digest meat much faster than vegetables (NRC 2006). Cats lack the enzyme called 'β-carotene 15,15dioxygenase' and therefore, they cannot convert beta carotene to vitamin A and need to get vitamin A directly from the food of animal sources (Schweigert et al. 2002). Taurine, an amino acid, is essential for cats and they need to get it through dietary animal sources (Knopf et al. 1978). ...
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The taste of food is an essential characteristic for cats and has been shown to affect food selection. However, understanding of food selection by cats using taste characteristics is far from complete. Therefore, the aim of the present review was to summarize the current knowledge on food preference and the role of taste on this selection in domestic cats. Appetite regulation is one of the determinants of palatability in cats and involves a highly complex interplay between hypothalamus, adipose tissue, and digestive tract. However, knowledge on this interplay is scarce in cats. When evaluating different foods for cats, behavioural responses such as facial expressions involving the movements and positions of ears, tongue, and head can provide increased insight into the effectiveness of formulating a more palatable diet. This paper also reviews food additives currently used in industry for enhancing the palatability of cat foods. In summary, a better understanding of the factors that affect the food preference in cats is essential to produce high-quality foods because cats will not eat a food with a flavour they dislike even though it is complete and nutritionally balanced.
... Both ingested forms of vitamin A must be converted to retinal and retinoic acid after absorption to support biologic processes [2]. But, interestingly, most carnivores (entirely meat-eating animals) are poor converters of beta-carotene, and they cannot create any vitamin A from beta-carotene [3]. ...
Article
Vitamin A is an essential fat-soluble micronutrient. It is necessary for the normal functioning of epithelial tissues, replication of genetic materials, perception of light or for smoothly running the immune system. Provitamins A (carotenoids) are powerful antioxidants. They can also be precursors for not only retinol but also for the most active forms of vitamin A - retinal and retinoic acid. However, the reverse transformation doesn`t take place, it is impossible to endoge-nously obtain carotenoids from retinol or its oxidized forms. The efficiency of converting carotenoids to retinol depends mainly on two factors. The first one is the type of carotenoid. β-carotene is converted to vitamin A twice as efficiently as other carotenoids, and the second factor is the bioavailability of the provitamin A. As fat-soluble substances, carotenoids are better ab-sorbed in the presence of enough fats. Vitamin A deficiency is associated with the malfunction of visual system as a result of xerophthalmia or night blindness. In addition, the lack of vitamin A can cause deterioration of the skin and mucous membranes and may lead to a high infant mortality rate. At the same time, hypervitaminosis A is a serious tera-togenic factor. An insufficient supply of carotenoids impairs the antioxidant defence mechanism of the body, which increases the risks of oxidative damage of cellular struc-tures, and probably leads to cancerous diseases. Vitamin A is not synthesized by plants. Herbivorous and fruit-eating animals synthesize it from carotenoids obtained from plant foods but carnivores have al-most lost this ability. Thus, only animal tissues are sources of vitamin A for them. As a result, vegetarians consume substantially less vitamin A than omnivores, and vegans don’t consume vitamin A at all. However, they get much more ca-rotenoids from their diet, and as a result, the total intake of retinol equivalent does not differ much among the groups. Serum β-carotene concentrations are generally higher in vegans. However, there is a disparity regarding the level of retinol. Thus, there is little evidence to date to conclude that any of the three groups has an increased risk of vitamin A deficiency compared to the others.
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In the prevention of diseases with increasing frequency in aged animals - such as tumors and of arteriosclerosis - as well as of age induced immunosuppression a good supply with antioxidants - especially with vitamin E - is of importance. At diseases combined with pain, at infectious diseases and at tumor patients the content of ascorbic acid in the blood plasma is lowered and an application of ascorbic acid recommendable. The functions of the ascorbic acid are described. For the stimulation of the activity of the immune system and for the improvement of the supply at diseases with anorexia a combination with vitamin A, D3 and E is applied. After operations and bone fractures it stimulates the regeneration. At continuous heavy muscular activity of sled dogs a supplementary application of ascorbic acid and of vitamin E is useful for the efficiency. For the feed of older animals a supplement of at least each 100 mg ascorbic acid and vitamin E per kg is recommended.
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In the period between 1880 and 1930, the role of nutrition and nutritional deficiency as a cause of rickets was established based upon the results from 6 animal models of rickets. This greatly prevalent condition (60%-90% in some locales) in children of the industrialized world was an important clinical research topic. What had to be reconciled was that rickets was associated with infections, crowding, and living in northern latitudes, and cod liver oil was observed to prevent or cure the disease. Several brilliant insights opened up a new pathway to discovery using animal models of rickets. Studies in lion cubs, dogs, and rats showed the importance of cod liver oil and an antirachitic substance later termed vitamin D. They showed that fats in the diet were required, that vitamin D had a secosteroid structure and was different from vitamin A, and that ultraviolet irradiation could prevent or cure rickets. Several of these experiments had elements of serendipity in that certain dietary components and the presence or absence of sunshine or ultraviolet irradiation could critically change the course of rickets. Nonetheless, at the end of these studies, a nutritional deficiency of vitamin D resulting from a poor diet or lack of adequate sunshine was firmly established as a cause of rickets.
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Many animals convert β-carotene to retinol to meet their vitamin A (VA) requirement. However, this pathway is inefficient in many carnivores. This study quantified the plasma response to a single oral dose of [(2) H(8)]-β-carotene in adult domestic cats, including measurement of [(2) H(4)]-retinol derived from the dose. Cats were fed with either a control diet containing adequate VA (n = 5) or a VA-devoid diet (n = 5) for 28 days. An oral dose of either 5 mg/kg body weight (BW) (n = 4) or 10 mg/kg BW (n = 6) of [(2) H(8) ]-β-carotene was administered on day 28. Plasma samples were collected prior to dosing and at 6, 12, 24, 32, 48, 72, 120, 168 and 216 h post-dose. Plasma retinoids and β-carotene were measured using HPLC and [(2) H(4)]-retinol by GC-ECNCI-MS (gas chromatography/electron capture negative chemical ionization/mass spectrometry). β-carotene was undetectable in plasma prior to dosing. Post-dose, mean peak plasma β-carotene was 0.37 ± 0.06 nmol/ml at 9.0 ± 1.8 h following the dose, while [(2) H(4) ]-retinol peaked at 3.71 ± 0.69 pmol/ml at 55.2 ± 16.3 h. The ratio per cent of total area under the curve for [(2) H(4)]-retinol compared with the β-carotene response was 4.6 ± 2.6%. There was little effect of diet or dose on the β-carotene or [(2) H(4)]-retinol responses. The appearance of [(2) H(4)]-retinol in plasma indicates that cats are capable of converting β-carotene to active VA. Conversion efficiency was not calculated in this study, but it is likely inadequate to meet cats' VA requirement without the inclusion of preformed VA in the diet.
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To review our current understanding of vitamin A uptake from foods. There are advancements in understanding the molecular processes involved in vitamin A uptake and the regulation of these processes. A number of genes involved in vitamin A transport and metabolism have been recently identified. The identification of mutations in human genes and targeted disruption of mouse genes have provided further insight as to how these genes contribute to meeting nutritional needs. The rate limiting steps in the lymphatic absorption of vitamin A involve intracellular processing of vitamin A within the enterocyte. The key steps appear to be related to chylomicron formation and secretion and are closely coupled with fat absorption. The genes encoding serum retinol binding protein, cellular retinol binding protein I and cellular retinol binding protein II have been disrupted by homologous recombination in mice. Studies of these knockout mice indicate that extrahepatic uptake of postprandial vitamin A may play a particularly important role in the maternal-offspring transfer of vitamin A. Further studies of the transfer of maternal dietary vitamin A have important implications for assessing the upper limits of maternal vitamin A supplementation.
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The aim of this review was to summarise the available literature on the effects of consuming raw red meat diets on the gastrointestinal microbiome of the cat and dog. In recent years, feeding raw meat diets to cat and dogs has increased, in part associated with trends in human nutrition for “natural” and “species-appropriate” diets. These diets range from home-prepared unprocessed, nutritionally incomplete diets to complete and balanced diets with sterilisation steps in their manufacturing process. Feeding some formats of raw meat diets has been associated with nutritional inadequacies and zoonotic transfer of pathogens. The feeding of raw meat diets has been shown to alter the gastrointestinal microbiome of the cat and dog, increasing the relative abundances of bacteria associated with protein and fat utilisation, including members of the genera Fusobacterium and Clostridium. While in humans, these genera are more commonly known for members that are associated with disease, they are a diverse group that also contains harmless commensals that are a normal component of the gastrointestinal microbiota. Moreover, members of these genera are known to produce butyrate from protein and amino acid fermentation and contribute to intestinal homeostasis in raw meat-fed dogs and cats. Currently, only a limited number of studies have examined the impacts of raw meat diets on the cat and dog microbiota, with many of these being descriptive. Additional controlled and systems-based studies are required to functionally characterise the roles of key microbial groups in the metabolism of raw meat diets, and determine their impacts on the health and nutrition of the host.
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Oxidative stress may contribute to the progression of chronic renal failure. In this study, cats with spontaneous renal insufficiency were fed a dry cat food supplemented with the antioxidants vitamins E and C, and beta-carotene for 4 weeks. When compared with healthy cats, cats with renal insufficiency had a tendency to oxidative stress. The antioxidant supplements significantly reduced DNA damage in cats with renal insufficiency as evidenced by reduced serum 8-OHdG and comet assay parameters. Therefore, supplements of vitamins E and C and beta-carotene as antioxidants may be beneficial to cats with renal disease.
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Three experiments were conducted to study the uptake of oral beta-carotene by blood plasma and leukocytes in domestic cats. In Experiment 1, mature female Tabby cats (12 mo old) were given once orally 0, 10, 20 or 50 mg of beta-carotene and blood taken at 0, 12, 24, 30, 36, 42, 48 and 72 h after dosing. Concentrations of plasma beta-carotene increased in a dose-dependent manner. Peak concentrations were observed at 12-24 h and declined gradually thereafter. The half-life of plasma beta-carotene was 12-30 h. In Experiment 2, cats were dosed daily for six consecutive days with 0, 1, 2, 5 or 10 mg beta-carotene. Blood was sampled once daily at 12 h after each feeding. Daily dosing of cats with beta-carotene for 6 d resulted in a dose-dependent increase in circulating beta-carotene. Experiment 3 was designed to study the uptake of beta-carotene by blood leukocytes. Cats were fed 0, 5 or 10 mg of beta-carotene daily for 14 d. Blood leukocytes were obtained on d 7 and 14 to determine beta-carotene content in whole lymphocytes and in subcellular fractions. Blood lymphocytes took up large amounts of beta-carotene by d 7 of feeding. Furthermore, beta-carotene accumulated mainly in the mitochondria (40-52%), with lower amounts accumulating in the microsomes (20-35%), cytosol (15-34%), and nuclei (1.5-6%). Therefore, domestic cats readily absorb beta-carotene across the intestinal mucosa and transfer the beta-carotene into peripheral blood leukocytes and their subcellular organelles. beta-Carotene uptake kinetics show that some aspects of beta-carotene absorption and metabolism in cats are similar to those of humans.
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The contents of retinol and retinyl esters as well as retinol-binding protein (RBP) in the plasma, urine, liver and kidneys of dogs, raccoon dogs and silver foxes were investigated. In the plasma and urine of all three species, vitamin A was present as retinol and retinyl esters. Vitamin A levels (1376+/-669 microg x g(-1)) were significantly higher in the livers of dogs than in the kidneys (200+/-217 microg x g(-1), P < 0.001 ). However, vitamin A levels in the kidneys of raccoon dogs (291+/-146 microg x g(-1)) and silver foxes (474+/-200 microg x g(-1)) were significantly higher than in the liver (67+/-58 microg x g(-1) and 4.3+/-2.4 microg x g(-1), respectively, both P < 0.001). RBP was immunologically detected in the blood plasma of all species, but never in the urine. In the liver, immunoreactive RBP was found in hepatocytes. In the kidneys of all species, RBP was observed in the cells of the proximal convoluted tubules. The levels of vitamin A in the livers of raccoon dogs and silver foxes were extremely low, which would be interpreted as a sign of great deficiency in humans. This observation might indicate that the liver status cannot be used as an indicator of vitamin A deficiency in canines. The high levels of vitamin A in the kidneys in all three species may indicate a specific function of the kidney in the vitamin A metabolism of canines.
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Retinyl esters (RE) have been used extensively as markers to study chylomicron (CM) catabolism because they are secreted in the postprandial state with CM and do not exchange with other lipoproteins in the plasma. To understand the mechanism of secretion of RE by the intestine under the fasting and postprandial states, differentiated Caco-2 cells were supplemented with radiolabeled retinol under conditions that support or do not support CM secretion. We observed that these cells assimilate vitamin A by a rapid uptake mechanism. After uptake, cells store retinol in both esterified and unesterified forms. Under fasting conditions, cells do not secrete RE but secrete free retinol unassociated with lipoproteins. Under postprandial conditions, cells secrete significant amounts of RE only with CM. The secretion of RE with CM was independent of the rate of uptake of retinol and intracellular free and esterified retinol levels, and was absolutely dependent on the assembly and secretion of CM. The secretion of RE was correlated with the secretion of CM and not with the secretion of total apolipoprotein B. Inhibition of CM secretion by Pluronic L81 decreased the secretion of RE and did not result in their increased secretion with smaller lipoproteins. These data strongly suggest that RE secretion by the intestinal cells is a specific and regulated process that occurs in the postprandial state and is dependent on the assembly and secretion of CM. We propose that RE are added to CM during final stages of lipoprotein assembly and may serve as signposts for these steps.
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The immuno-modulatory role of dietary lutein in domestic cats is unknown. Female Tabby cats (10-month old; n=56) were supplemented daily for 12 weeks with 0, 1, 5 or 10 mg lutein. Blood was collected on Weeks 0, 2, 4, 8 and 12 to assess the following: (1) mitogen-induced peripheral blood mononuclear cells (PBMCs) proliferation, (2) changes in PBMC subpopulations, (3) interleukin-2 (IL-2) production and (4) plasma immunoglobulin (Ig)G production. In addition, delayed-type hypersensitivity (DTH) response to concanavalin A (Con A) or a polyvalent vaccine was performed on Weeks 0, 6 and 12. Dietary lutein increased plasma lutein concentrations in a dose-dependent manner (p<0.001) and concentrations had not reached steady state after 12 weeks of feeding in cats given 5 or 10 mg lutein. Concentrations of plasma retinol and α-tocopherol were not influenced by diet. The DTH response to vaccine but not to Con A increased (p<0.05) in a dose-dependent manner on Week 6. Compared to control, cats fed lutein also showed enhanced Con A- and pokeweed mitogen-stimulated PBMCs proliferation. Dietary lutein also increased the percentages of CD4+ and CD21+ lymphocytes on Week 12 but had no significant effect on pan T, CD8 and MHC class II markers. Plasma IgG was higher (p<0.05) in cats fed 10 mg lutein on Weeks 8 and 12. These results support the immuno-modulatory action of lutein in domestic cats.
1. In canines and mustelides total vitamin A was 10-50 times higher compared to other species due to a high amount of retinyl esters (40-99% of total vitamin A) in blood plasma. The dominant vitamin A ester was in most species retinyl stearate. 2. In Ursidae, Procyonidae, Viveridae and Felidae, total vitamin A was much lower. When present, however, retinyl esters also represented 10-65% of total vitamin A in plasma. 3. Only retinol was detected in plasma of the family, Hyaenidae, and the suborder, Pinnipedia. 4. In maned wolf cubs it was found that retinol, retinyl esters and alpha-tocopherol increased with the age of the animals, reaching values comparable to adult animals at the age of 5 months.
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A method for the removal of serum chylomicrons before density gradient ultracentrifugation of the other serum lipoproteins using an SW 41 swinging bucket rotor is presented. In a preliminary spin, the chylomicrons with an Sf greater than 400 X 10(-13) s float to the top of the gradient, whereas the other lipoproteins are retained in the infranatant fraction. After removal of the chylomicrons, the other serum lipoproteins are subsequently fractionated by isopycnic density gradient ultracentrifugation. Analysis of the separated lipoprotein fractions suggested that this procedure permits isolation of a chylomicron fraction consisting solely of chylomicrons but that the very low density lipoprotein fraction subsequently isolated also contains chylomicrons or chylomicron remnants with an Sf less than 400 X 10(-13) s, and that there is considerable overlap in flotation rate and particle size of very low density lipoproteins and chylomicrons.
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The effects of lutein and lycopene on beta-carotene absorption and cleavage were investigated in 12 male subjects. Responses of carotenoids and retinyl palmitate in the triacylglycerol-rich lipoprotein (TRL) fraction after a separate 15-mg beta-carotene dose were compared with those after a dose of 15 mg beta-carotene combined with 15 mg lycopene or lutein (given as natural concentrates or extracts). After combined dosing with lutein, the areas under the curve (AUCs) of beta-carotene and retinyl palmitate in the TRL fraction, adjusted for the triacylglycerol response, were 66% (P = 0.019) and 74% (P < 0.059), respectively, compared with 100% after dosing with beta-carotene alone. After combined dosing with lycopene these percentages were 90% and 101%, respectively (NS). Beta-carotene conversion, estimated from the ratio between the AUC for retinyl esters and beta-carotene, assuming eccentric cleavage, was 69%, 71%, and 72% for treatment with only beta-carotene, beta-carotene combined with lycopene, and beta-carotene combined with lutein, respectively. In addition, a pilot study was performed to evaluate application of TRL response curves to measure absorption of carotenoids from vegetable sources (15 mg carotenoid as carrots, spinach, and tomato paste). As compared with the carotenoid concentrates, responses were considerably lower or hardly measurable (beta-carotene and retinyl palmitate after carrots, lutein after spinach), except for lycopene and retinyl palmitate after a single dose of tomato paste. In conclusion, this study showed that lutein, but not lycopene, negatively affected beta-carotene absorption when given simultaneously with beta-carotene but apparently had no effect on beta-carotene cleavage.
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Dogs differ from other species with respect to the occurrence of a high percentage of retinyl esters in blood plasma and the excretion of substantial amounts of vitamin A in the urine. Our investigation focussed on the effects of different concentrations of vitamin A in the diet, ranging from concentrations below NRC requirements of 25 IU/kg body weight (BW) to 2400 IU/kg BW, on the levels of retinol and retinyl esters (palmitate/oleate and stearate) in canine blood plasma and urine. The plasma levels of retinyl esters paralleled the levels of vitamin A in the feed (r = 0.91; p < 0.001). The highest plasma level (12.1 +/- 0.4 mg/l) was observed at the highest level in the diet. This observation may be explained by the fact that in dogs retinyl esters are associated with lipoproteins. Even under prolonged feeding on vitamin A levels below NRC requirements, retinyl esters were still present in the plasma (2.8 +/- 0.1 mg/l). Levels of retinol were not affected (1.2 +/- 0.03 vs. 1.0 +/- 0.03 mg/l, respectively). In the urine, the concentration of retinol and retinyl palmitate/oleate increased with the first increase of vitamin A in the diet to 1.2 +/- 0.4 mg/l of total vitamin A. Urinary levels were elevated and fluctuated with up to four peaks while dietary vitamin A levels were above NRC requirements. But the amount of retinol and retinyl esters excreted did not show any dependence on the amount of vitamin A in the diet. When the amount of vitamin A in the diet was at or below requirements, only traces of retinol and retinyl esters were detected in urine. Thus, contrary to current knowledge for most other mammals, retinyl ester levels in plasma and retinol and retinyl esters in the urine of dogs proved to be clearly but differently affected by the amount of vitamin A supplied with the diet. Contrary to retinol, plasma levels of retinyl esters closely reflect the actual supply of vitamin A with the feed. The occurrence of retinol and retinyl esters in urine may, however, be due to dietary supply of vitamin A in excess of standard requirements, thereby providing a useful indicator of a dietary supply of vitamin A above requirement. The mechanism involved in the possible regulation of urinary excretion of retinol and retinyl esters remains to be elucidated.
Effect of simultaneous, single oral doses of beta-carotene with lutein or lycopene on the beta-carotene and retinyl ester responses in the triacylglycerol-rich lipoprotein fraction of men
  • A H Terpstra
Terpstra, A. H. (1985) Isolation of serum chylomicrons prior to density gradient ultracentrifugation of other serum lipoprotein classes. Anal. Biochem. 150: 221-227. 8. van den Berg, H. & van Vliet, T. (1998) Effect of simultaneous, single oral doses of beta-carotene with lutein or lycopene on the beta-carotene and retinyl ester responses in the triacylglycerol-rich lipoprotein fraction of men. Am. J. Clin. Nutr. 68: 82-89.