Dietary Β-carotene Research Articles

Association between dietary β-carotene intake with Parkinson's disease and all-cause mortality among American adults aged 40 and older (NHANES 2001-2018).

The existing evidence concerning the correlation between dietary β-carotene intake and Parkinson's disease (PD) is currently deemed insufficient. Thus, this research aims to investigate the relationship between dietary β-carotene intake and both the prevalence of PD and all-cause mortality within the US (United States) population. The research employed cross-sectional analysis and cohort studies utilizing data from 16,852 participants in the National Health and Nutrition Examination Survey (NHANES) spanning from 2001 to 2018. Weighted logistic regression, weighted cox regression, restricted cubic splines (RCS), subgroup analysis, and sensitivity analyses were employed to validate the research objectives. Among all eligible subjects, the mean age was 59.62 ± 11.77 years, with a prevalence of PD at 1.82% overall, with 43.88% in males. In the fully adjusted model, dietary β-carotene intake exhibited a negative association with PD prevalence [odds ratio (OR) = 0.95; 95% confidence interval (CI): 0.90 ~ 0.997; p = 0.040]. Utilizing RCS analysis, a negative linear correlation between dietary β-carotene intake and PD prevalence was observed (non-linear p = 0.857). Furthermore, after controlling for multiple variables, dietary β-carotene intake was inversely associated with all-cause mortality [Hazard ratios (HR) = 0.98; 95% CI: 0.97 ~ 0.99; p = 0.002], with RCS curves indicating a negative linear relationship (nonlinear: p = 0.082). Comparable patterns of association were noted in subgroup analyses, and consistent findings were derived from additional sensitivity analyses. The cross-sectional and cohort study reveals a significant negative correlation between dietary β-carotene intake and both the prevalence of PD and all-cause mortality in the general population. This suggested that supplementing with dietary β-carotene might have certain benefits for reducing the prevalence of PD and all-cause mortality. However, further rigorously designed expected studies are needed to establish the causal relationship between them.

Could alternative pathways for carotenoid transformation affect colour production efficiency? A correlative study in wild common crossbills (Loxia curvirostra)

In many vertebrates, dietary yellow carotenoids are enzymatically transformed into 4C-ketocarotenoid pigments, leading to conspicuous red colourations. These colourations may evolve as signals of individual quality under sexual selection. To evolve as signals, they must transmit reliable information benefiting both the receiver and the signaler. Some argue that the reliability of 4C-ketocarotenoid-based colourations is ensured by the tight link between individual quality and mitochondrial metabolism, which is supposedly involved in transforming yellow carotenoids. We studied how a range of carotenoids covary in the feathers and blood plasma of a large number (n > 140) of wild male common crossbills (Loxia curvirostra). Plumage redness was mainly due to 3-hydroxy-echinenone (3HOE). Two other, less abundant, red 4C-ketocarotenoids (astaxanthin and canthaxanthin) could have contributed to feather colour as they are redder pigments. This was demonstrated for astaxanthin but not canthaxanthin, whose feather levels were clearly uncorrelated to colouration. Moreover, moulting crossbills carried more 3HOE and astaxanthin in blood than non-moulting ones, whereas canthaxanthin did not differ. Canthaxanthin and 3HOE can be formed from echinenone, a probable product of dietary β-carotene ketolation. Echinenone could thus be ketolated or hydroxylated to produce canthaxanthin or 3HOE, respectively. In moulting birds, 3HOE blood levels positively correlated to astaxanthin, its product, but negatively to canthaxanthin levels. Redder crossbills also had lower plasma canthaxanthin values. A decrease in hydroxylation relative to ketolation could explain canthaxanthin production. We hypothesize that red colouration could indicate birds' ability to avoid inefficient deviations within the complex enzymatic pathways.

Maternal genetics and diet modulate vitamin A homeostasis of the offspring and affect the susceptibility to obesity in adulthood in mice.

Perinatal nutrition exerts a profound influence on adult metabolic health. This study aimed to investigate whether increased maternal vitamin A (VA) supply can lead to beneficial metabolic phenotypes in the offspring. The researchers utilized mice deficient in the intestine-specific homeobox (ISX) transcription factor, which exhibits increased intestinal VA retinoid production from dietary β-carotene (BC). ISX-deficient dams were fed a VA-sufficient or a BC-enriched diet during the last week of gestation and the whole lactation period. Total retinol levels in milk and weanling livers were 2- to 2.5-fold higher in the offspring of BC-fed dams (BC offspring), indicating increased VA supplies during late gestation and lactation. The corresponding VA-sufficient and BC offspring (males and females) were compared at weaning and adulthood after being fed either a standard or high-fat diet (HFD) with regular VA content for 13 weeks from weaning. HFD-induced increases in adiposity metrics, such as fat depot mass and adipocyte diameter, were more pronounced in males than females and were attenuated or suppressed in the BC offspring. Notably, the BC offspring were protected from HFD-induced increases in circulating triacylglycerol levels and hepatic steatosis. These protective effects were associated with reduced food efficiency, enhanced capacity for thermogenesis and mitochondrial oxidative metabolism in adipose tissues, and increased adipocyte hyperplasia rather than hypertrophy in the BC offspring. In conclusion, maternal VA nutrition influenced by genetics may confer metabolic benefits to the offspring, with mild increases in late gestation and lactation protecting against obesity and metabolic dysregulation in adulthood.NEW & NOTEWORTHY A genetic mouse model, deficient in intestine-specific homeobox (ISX) transcription factor, is used to show that a mildly increased maternal vitamin A supply from β-carotene feeding during late gestation and lactation programs energy and lipid metabolism in tissues and protects the offspring from diet-induced hypertrophic obesity and hepatic steatosis. This knowledge may have implications for human populations where polymorphisms in ISX and ISX target genes involved in vitamin A homeostasis are prevalent.

Effect of dietary β-carotene supplementation on growth and antioxidant capability of pre-adult male Chinese mitten crab, Eriocheir sinensis

β-carotene has been shown to be beneficial for the color formulation, survival, antioxidation, immunity and stress resistance of many crustaceans. This study was conducted to investigate the effects of dietary supplementation of synthetic β-carotene on growth, antioxidant status, high pH resistance, color parameters, and carotenoids composition of pre-adult Chinese mitten crab Eriocheir sinensis. Three diets were formulated to contain 3.06, 52.40 and 103.59 mg/kg dry diets of synthetic β-carotene (defined as Diet 1 - 3). The results showed that: (1) There were no marked differences in body weights or feed utilization, suggesting that β-carotene was not particularly efficient in enhancing the growth of pre-adult E. sinensis. (2) Indicators of antioxidant capacity (T-AOC, MDA) and immunity (AKP, ACP) both got improved in the hepatopancreas and hemolymph with the supplementation of 50–100 mg/kg β-carotene in the diets. (3) The stress test with high pH indicated Diet 1 treatment had the highest mortality among all treatments, and the lowest mortality was found in Diet 3 treatment. (4) For color enhancement, the redness of the carapace and hepatopancreas increased significantly with the increase of dietary β-carotene supplementation at Day 30. Combined, the inclusion of β-carotene in the diet could enhance the antioxidative capability, non-specific immunity, stress resistance to high pH and tissue carotenoid contents, and the optimal level of dietary synthetic β-carotene supplementation was suggested to be around 50 mg/kg for pre-adult male E. sinensis.

β-Carotene accelerates the resolution of atherosclerosis in mice

β-Carotene oxygenase 1 (BCO1) catalyzes the cleavage of β-carotene to form vitamin A. Besides its role in vision, vitamin A regulates the expression of genes involved in lipid metabolism and immune cell differentiation. BCO1 activity is associated with the reduction of plasma cholesterol in humans and mice, while dietary β-carotene reduces hepatic lipid secretion and delays atherosclerosis progression in various experimental models. Here we show that β-carotene also accelerates atherosclerosis resolution in two independent murine models, independently of changes in body weight gain or plasma lipid profile. Experiments in Bco1-/- mice implicate vitamin A production in the effects of β-carotene on atherosclerosis resolution. To explore the direct implication of dietary β-carotene on regulatory T cells (Tregs) differentiation, we utilized anti-CD25 monoclonal antibody infusions. Our data show that β-carotene favors Treg expansion in the plaque, and that the partial inhibition of Tregs mitigates the effect of β-carotene on atherosclerosis resolution. Our data highlight the potential of β-carotene and BCO1 activity in the resolution of atherosclerotic cardiovascular disease.

β-Carotene accelerates the resolution of atherosclerosis in mice.

β-Carotene oxygenase 1 (BCO1) catalyzes the cleavage of β-carotene to form vitamin A. Besides its role in vision, vitamin A regulates the expression of genes involved in lipid metabolism and immune cell differentiation. BCO1 activity is associated with the reduction of plasma cholesterol in humans and mice, while dietary β-carotene reduces hepatic lipid secretion and delays atherosclerosis progression in various experimental models. Here we show that β-carotene also accelerates atherosclerosis resolution in two independent murine models, independently of changes in body weight gain or plasma lipid profile. Experiments in Bco1-/- mice implicate vitamin A production in the effects of β-carotene on atherosclerosis resolution. To explore the direct implication of dietary β-carotene on regulatory T cells (Tregs) differentiation, we utilized anti-CD25 monoclonal antibody infusions. Our data show that β-carotene favors Treg expansion in the plaque, and that the partial inhibition of Tregs mitigates the effect of β-carotene on atherosclerosis resolution. Our data highlight the potential of β-carotene and BCO1 activity in the resolution of atherosclerotic cardiovascular disease.

Deposition and bioconversion law of β-carotene in laying hens after long-term supplementation under adequate vitamin A status in the diet

β-Carotene, because it is the precursor of vitamin A and has versatile biological roles, has been applied as a feed additive in the poultry industry for a long time. In this study, we investigated the deposition and bioconversion of β-carotene in laying hens. A total of 600 Hy-line brown laying hens at 40 wk of age were randomly divided into 5 dietary treatments, each group's dietary supplemental levels of β-carotene were 0, 15, 30, 60, 120 mg/kg feed, and the vitamin A levels were all 8,000 IU/kg. After 14-wk trial, samples were collected, then carotenoids and different forms of vitamin A were detected using the novel method developed by our laboratory. We found that dietary β-carotene treatment had no significant effects on laying hens' production performance and egg quality (P > 0.05), except the yolk color. The deposition of β-carotene in the body gradually increased (P < 0.01) with the supplemental dose, whereas the contents of lutein and zeaxanthin decreased (P < 0.05). When the β-carotene supplemental level was above 30 mg/kg in the diet, the different forms of vitamin A in in serum, liver, ovary, and yolks were increased compared to the control group (P < 0.05). However, these indicators decreased when the additional dose was 120 mg/kg. Moreover, the mRNA levels of the genes involved in β-carotene absorption, bioconversion, and negative feedback regulation in duodenal mucosa and liver were upregulated after long-term feeding (P < 0.05). Histological staining of the ovaries indicated that the deposition of β-carotene led to a lower rate of follicle atresia (P < 0.05), and this positive effects may be related to the antioxidant function of β-carotene, which caused a reduction of oxidation products in the ovary (P < 0.05). Altogether, β-carotene could accumulate in laying hens intactly and exert its biological functions in tissue. Meanwhile, a part of β-carotene could also be converted into vitamin A but this bioconversion has an upper limit and negative feedback regulation.

Abstract 305: Dietary β-carotene Accelerates Atherosclerotic Resolution By Promoting Treg Expansion In The Atherosclerosis Lesion

Forkhead box P3 ( FoxP3 ) + regulatory T cells (Tregs) mediate atherosclerosis resolution and regression by promoting an anti-inflammatory environment in the lesion. FoxP3 is upregulated by retinoic acid, the active form of vitamin A, but whether vitamin A status influences atherosclerosis resolution remains unexplored. We hypothesized that β-carotene, the main vitamin A precursor in human diet, accelerates atherosclerosis resolution by upregulating FoxP3 expression to promote Treg expansion. We induced atherosclerosis in FoxP3 EGFP mice fed Western diet control (WD-Control) and injected with an anti-sense oligonucleotide targeting the LDLR (ASO-LDLR) for 16 weeks. After this period, we harvested a subset of mice as Baseline, while the remaining mice underwent atherosclerosis resolution upon the interruption of ASO-LDLR infusions to recover LDLR expression and normalize plasma lipids for a period of three weeks. During this time, mice either continued on the same WD-Control or were switched to a Western diet supplemented with 50 mg of β-carotene/kg of diet (WD- β-carotene). To examine the implication of Tregs, we injected a subset of WD-β-carotene with anti-CD25 (WD-β-carotene + anti-CD25), while WD-Control and a second subset of WD- β-carotene mice were injected with IgG control. We estimated atherosclerosis resolution by quantifying macrophage and collagen contents in the lesions present at the level of the aortic root. WD-β-carotene-fed mice injected with IgG showed a reduction in macrophage content accompanied by an increase in collagen in comparison to all the remaining groups, while WD-β-carotene + anti-CD25 lesions resembled those present in WD-Control mice. We examined Treg the relative number of CD25 + FoxP3 + and CD25 - FoxP3 + cells in the spleen, blood, and the lesion. CD25 + FoxP3 + numbers decreased in response to anti-CD25 infusions in all the tissues examined. Dietary β-carotene favored an increase of 269% and 653% in CD25 - FoxP3 + Tregs in comparison to the Baseline of WD-Control groups, respectively. These effects occurred independently of changes in plasma lipids or changes in body weight. Our data show that β-carotene supplementation results in Treg expansion and acceleration of atherosclerosis resolution by increasing Treg number.

Composite dietary antioxidant intake and osteoporosis likelihood in premenopausal and postmenopausal women: a population-based study in the United States.

Osteoporosis is a skeletal disease characterized by low bone mass, reduced bone strength, and increased fracture risk. We aimed to investigate the association between combined dietary antioxidant intake and the likelihood of osteoporosis in premenopausal and postmenopausal women, based on data from the National Health and Nutrition Examination Survey. Nutrient intake data were obtained using two 24-hour recalls. Composite dietary antioxidant index (CDAI), which refers to the intake amounts of β-carotene, vitamin A, vitamin C, vitamin E, selenium, zinc, copper, and iron, was then constructed. Prevalent osteoporosis was defined according to bone mineral density T scores of ≤ -2.5 and self-reports. Multiple logistic and Poisson regression models were used for association analyses. A total of 3,418 participants (1,157 premenopausal and 2,261 postmenopausal women) 40 years or older were included, 776 (22.70%) of whom had prevalent osteoporosis. In terms of individual nutrients, postmenopausal women in the highest CDAI quartiles for dietary β-carotene, vitamin A, vitamin C, and iron intakes had a low likelihood of osteoporosis. Regarding the CDAI-osteoporosis association, postmenopausal women in the highest quartile were less likely to have osteoporosis (OR Q3 vs Q1 , 0.64; 95% CI, 0.43-0.96; OR Q4 vs Q1 , 0.56; 95% CI, 0.35-0.89; P for trend = 0.013), after controlling for covariates. CDAI was negatively associated with the likelihood of osteoporosis in postmenopausal women. Our findings suggest that the combined intake of antioxidant nutrients can help reduce the likelihood of osteoporosis in women.

Association of Dietary α-Carotene and β-Carotene Intake with Low Cognitive Performance in Older Adults: A Cross-Sectional Study from the National Health and Nutrition Examination Survey.

This study aims to examine the relationships of dietary α-carotene and β-carotene intake with cognitive function. The data were selected from the National Health and Nutrition Examination Survey (NHANES) 2011-2014. A total of 2009 participants were included in this analysis. Dietary α-carotene and β-carotene intake were averaged by two 24-h dietary recalls. The Consortium to Establish a Registry for Alzheimer's Disease Word Learning subset (CERAD W-L), Animal Fluency Test (AFT), and Digit Symbol Substitution Test (DSST) were used to evaluate cognitive function. Logistic regression and restricted cubic spline models were applied to explore the associations of dietary α-carotene and β-carotene intake with cognitive performance. After adjusting for all confounding factors, compared with individuals in the lowest quartile of β-carotene dietary intake, those in the highest quartile had lower risks of both CERAD W-L decline [odds ratio (OR) = 0.63, 95% confidence interval (CI): 0.44-0.90] and AFT decline (OR = 0.66, 95% CI: 0.47-0.94). In addition, the third quartile of β-carotene dietary intake had a significantly decreased risk of lower DSST (OR = 0.67, 95% CI: 0.48-0.83). Compared with the lowest quartile of α-carotene intake, the OR of AFT decline in the highest intake quartile was 0.66 (95% CI: 0.46, 0.94). For males, both dietary α-carotene and β-carotene intake were associated with a decreased risk of AFT decline (OR = 0.42, 95% CI: 0.25-0.71; OR = 0.51, 95% CI: 0.30-0.85, respectively). For females, dietary α-carotene intake was associated with a decreased risk of CERAD W-L decline (OR = 0.55, 95% CI: 0.33-0.91) and dietary β-carotene intake was associated with decreased risks of both CERAD W-L and AFT decline (OR = 0.37, 95% CI: 0.21-0.64; OR = 0.58, 95% CI: 0.37-0.91, respectively). Our results suggested that higher dietary α-carotene and β-carotene intake had inverse effects on cognitive function decline among older adults.

The conversion of β-carotene to vitamin A in adipocytes drives the anti-obesogenic effects of β-carotene in mice

ObjectiveThe β-carotene oxygenase 1 (BCO1) is the enzyme responsible for the cleavage of β-carotene to retinal, the first intermediate in vitamin A formation. Preclinical studies suggest that BCO1 expression is required for dietary β-carotene to affect lipid metabolism. The goal of this study was to generate a gene therapy strategy that over-expresses BCO1 in the adipose tissue and utilizes the β-carotene stored in adipocytes to produce vitamin A and reduce obesity. MethodsWe generated a novel adipose-tissue-specific, adeno-associated vector to over-express BCO1 (AT-AAV-BCO1) in murine adipocytes. We tested this vector using a unique model to achieve β-carotene accumulation in the adipose tissue, in which Bco1−/− mice were fed β-carotene. An AT-AAV over-expressing green fluorescent protein was utilized as control. We evaluated the adequate delivery route and optimized cellular and organ specificity, dosage, and exposure of our vectors. We also employed morphometric analyses to evaluate the effect of BCO1 expression in adiposity, as well as HPLC and mass spectrometry to quantify β-carotene and retinoids in tissues, including retinoic acid. ResultsAT-AAV-BCO1 infusions in the adipose tissue of the mice resulted in the production of retinoic acid, a vitamin A metabolite with strong effects on gene regulation. AT-AAV-BCO1 treatment also reduced adipose tissue size and adipocyte area by 35% and 30%, respectively. These effects were sex-specific, highlighting the complexity of vitamin A metabolism in mammals. ConclusionsThe over-expression of BCO1 through delivery of an AT-AAV-BCO1 leads to the conversion of β-carotene to vitamin A in adipocytes, which subsequently results in reduction of adiposity. These studies highlight for the first time the potential of adipose tissue β-carotene as a target for BCO1 over-expression in the reduction of obesity.

Effects of prepartum supplementation of β-carotene on colostrum and calves.

Little is known about transfer of dietary β-carotene into colostrum, its absorption by the calf, and its effects on retinol and α-tocopherol in the calf when the dam's dietary vitamin A is adequate. Our objective was to assess the effect of β-carotene supplementation during the close-up dry period on the colostrum and calf. The study was conducted on a large commercial dairy farm in Indiana during early summer of 2015. Ninety-four multiparous Holstein cows were blocked by calving data, parity, and previous production, and then randomly assigned to either control or β-carotene (BC) treatments. While locked in headgates each morning, each cow received a topdress of β-carotene (Rovimix, DSM Nutritional Products, 8 g/d; provided 800 mg β-carotene) or carrier from 21 d before expected calving until calving. Colostrum was collected within 2 h of parturition. Calf blood samples were obtained within 2 h of birth before receiving the dam's colostrum, at 24 h after birth, and at 7 d and 60 d of age. Blood serum was analyzed for β-carotene, retinol, α-tocopherol, and other metabolites and enzymes. Colostrum was analyzed for β-carotene, retinol, α-tocopherol, colorimetry profile, and milk components. Data were analyzed using mixed-effects models in SAS (SAS Institute Inc.). Calf serum β-carotene data were analyzed using the FREQ procedure. Colostrum β-carotene was higher for BC cows. Colostrum from BC cows had increased a* [measures red (positive) to green (negative)] and b* [measures yellow (positive) to blue (negative)] colorimeter values, indicating that β-carotene altered colostrum color toward red and yellow. Supplementation did not affect colostral or calf IgG concentrations. Colostrum color indices were correlated with IgG concentrations as well as concentrations of β-carotene, retinol, and α-tocopherol. Before receiving colostrum, the concentration of β-carotene in calf serum was below the detectable threshold of 0.05 μg/mL. At 24 h of age, the number of calves with detectable β-carotene concentrations increased, with more calves from BC cows (52.1%) having detectable concentrations than calves from cows in the control group (6.1%). No differences in concentrations of retinol or α-tocopherol were observed in calf serum. Supplementation of β-carotene to cows decreased activities of gamma-glutamyl transpeptidase and glutamate dehydrogenase in calf serum. In pregnant cows already receiving adequate vitamin A, supplementation of β-carotene increased concentration of β-carotene in colostrum, altered colostrum color, and increased serum β-carotene in calves at birth.

Dietary β-carotene and vitamin A and risk of Parkinson disease: A protocol for systematic review and meta-analysis.

Background:The beneficial effects of dietary β-carotene and vitamin A on Parkinson disease (PD) have been confirmed, but some studies have yielded questionable results. Therefore, this meta-analysis investigated the effect of dietary β-carotene and vitamin A on the risk of PD.Methods:The following databases were searched for relevant paper: PubMed, Embase, Medline, Scopus, Cochrane Library, CNKI, Wanfang Med online, and Weipu databases for the relevant paper from 1990 to March 28, 2022. The studies included were as follows: β-carotene and vitamin A intake was measured using scientifically recognized approaches, such as food frequency questionnaire (FFQ); evaluation of odds ratios using OR, RR, or HR; β-carotene and vitamin A intake for three or more quantitative categories; and PD diagnosed by a neurologist or hospital records.Results:This study included 11 studies (four cohort studies, six case–control studies, and one cross-sectional study). The high β-carotene intake was associated with a significantly lower chance of developing PD than low β-carotene intake (pooled OR = 0.83, 95%CI = 0.74‐0.94). Whereas the risk of advancement of PD was not significantly distinctive among the highest and lowest vitamin A intake (pooled OR = 1.08, 95%CI = 0.91‐1.29).Conclusions:Dietary β-carotene intake may have a protective effect against PD, whereas dietary vitamin A does not appear to have the same effect. More relevant studies are needed to include into meta-analysis in the further, as the recall bias and selection bias in retrospective and cross-sectional studies cause misclassifications in the assessment of nutrient intake.

Potential role of inflammation in relation to dietary sodium and β-carotene with non-alcoholic fatty liver disease: a mediation analysis

BackgroundHigh sodium intake has been linked to the prevalence of non-alcoholic fatty liver disease (NAFLD), but underlying mechanism remains unclear. This study aims to explore the role of chronic inflammation in the association between sodium and NAFLD. We also observed whether β-carotene, which had a strong anti-inflammatory effect, lowers the odds of NAFLD.MethodsWe performed mediation analyses to assess the mediating effects of C-reactive protein (CRP) and red cell distribution width (RDW) on the relationship between dietary sodium and NAFLD defined by the hepatic steatosis index (HSI) and the fatty liver index (FLI), respectively.ResultsA total of 6725 participants were included in this study. Compared with the high sodium-low carotene group, participants in the high sodium-high carotene group had 16% and 26% lower odds for HSI and FLI-defined NAFLD, respectively. There were positive indirect effects of dietary sodium intake on the HSI-defined NAFLD (indirect effect: 0.0057, 95% CI: 0.0021–0.0091, P < 0.0001), as well as the FLI defined NAFLD (indirect effect: 0.0081, 95% CI: 0.0024–0.0162, P < 0.0001) when C-reactive protein (CRP) was considered as a mediator. The mediating effects were somewhat attenuated after further adjusting for dietary β-carotene intake. Similar results were found when RDW was considered as a mediator in the HSI-defined NAFLD analysis.ConclusionsHigher sodium intake increases the odds of NAFLD by upregulating inflammation. Dietary β-carotene may attenuate this association by down regulating inflammation.

Captive diet does not influence exploration behavior upon reintroduction to the wild in a critically endangered amphibian

Exploration behavior can have profound effects on individual fitness. Consequently, knowledge of the proximate mechanisms underpinning exploration behavior may inform conservation breeding programs (CBPs) for threatened species. However, the environmental factors that influence exploration behavior in captivity and during the reintroduction process remain poorly understood. Dietary micronutrients, such as carotenoids, are known to affect the expression of energetically costly behavioral traits, and theoretically may also influence the degree of exploration behavior in various contexts. Here, we investigate whether dietary β-carotene supplementation in captivity influences exploration behavior upon reintroduction to the wild in the critically endangered southern corroboree frog,Pseudophryne corroboree.We conducted a manipulative dietary experiment where captive bredP. corroboreewere supplemented with different doses of β-carotene for 40 weeks prior to release. Frogs (n = 115) were reintroduced to the wild using a soft-release approach, where they were released into field enclosures specifically designed for this species. Upon reintroduction, the frogs’ initial exploration behavior was measured using a standardized behavioral assay. There was no effect of diet treatment on any measure of exploration behavior (mean latency to leave the initial refuge, time spent mobile within the release apparatus and latency to disperse into the field enclosure). However, there was a significant relationship between individual body size and latency to leave the refuge, whereby smaller individuals left the refuge more rapidly. While these findings provide no evidence that β-carotene at the dosages tested influencesP. corroboreeexploration behavior in a reintroduction context, the effect of body size draws attention to the potential for bodily state to influence exploration behavior. We discuss the need for ongoing research investigating the influence of captive diet on post release behavior, and highlight how knowledge concerning state-dependent behavior might help to inform and direct reintroduction programs.

Can dietary β-carotene supplementation provide an alternative to astaxanthin on the performance of growth, pigmentation, biochemical, and immuno-physiological parameters of Litopenaeus vannamei ?

The present study aimed to investigate the effect of dietary β-carotene (β-car) compared with astaxanthin (Ax) and their combination on the performances of white shrimp (Litopenaeus vannamei). Eight experimental diets containing 0, 100, 200, 300, 400, 500 mg/kg β-car, 200 mg/kg Ax, and the combination of 100 mg/kg Ax with 200 mg/kg β-car were provided for 56-days. The results indicated that shrimp fed β-car at 300–400 mg/kg had significantly higher growth performance and survival than the other β-car supplemented treatments without significant differences from shrimp fed Ax200 and the combination. The redness (a*) of shrimp increased as the β-car level increased up to 300 mg/kg diet. Furthermore, shrimp fed carotenoid combinational diet developed the deepest red color, consistent with the highest shell Ax contents. Hepatopancreatic total antioxidant capacity (T-AOC) and malondialdehyde (MDA) content showed significantly better performance in shrimp fed carotenoids including diets than the control. Significantly positive relationships were detected on alkaline phosphatase (AKP) activities and dietary β-car levels. The combination treatment recorded the significantly highest lysozyme activity. Broken-line analysis indicated that the optimal dietary β-car levels ranged from 265.2 to 341.28 mg/kg diet. In conclusion, data suggested that dietary β-car could provide an alternative to Ax referring to its efficiency in improving the overall performance of L. vannamei.

Effects of prepartum supplementation of β-carotene in Holstein cows

Whether supplemental dietary β-carotene affects periparturient cows and vitamins A and E in cows when dietary vitamin A is adequate remains uncertain. Our objective was to assess the effect of β-carotene supplementation during the close-up dry period in a herd with adequate status of vitamins A and E but low in β-carotene. The study was conducted on a large commercial dairy farm in Indiana during early summer of 2015. Ninety-four multiparous Holstein cows were assigned to either control (CON; n = 47) or β-carotene (BC; n = 47) treatments. When locked in headgates each morning, each cow received a topdress of β-carotene (Rovimix, 8 g/d; provided 800 mg of β-carotene) or carrier from 21 d before expected calving until calving. Blood samples were collected at 21 ± 1 d (mean ± standard deviation) before expected calving (before treatments began), 7 ± 1 d before calving, immediately following parturition, and 7 ± 1 d postpartum. Blood serum was analyzed for vitamins A and E, β-carotene, cholesterol, and other metabolites and enzymes. Data were analyzed using the MIXED procedure in SAS (SAS Institute Inc.). Cows had low β-carotene concentrations (0.85 μg/mL) in blood serum before treatments began. Compared with CON cows, BC cows had higher overall mean concentrations of β-carotene (2.87 μg/mL vs. 0.73 μg/mL) and retinol (165 vs. 143 ng/mL). Cows fed BC had lower α-tocopherol in serum than cows fed CON (2.26 vs. 2.46 µg/mL). Cows fed BC had lower peak milk than cows fed CON (50.9 vs. 55.3), but total lactation milk yield did not differ significantly. No effects of BC were observed on days to conception (100 d) or times bred (2.4). Treatments did not affect incidences of ketosis, retained placenta, displaced abomasum, off feed, lameness, footrot, mastitis, or metritis. In conclusion, in pregnant cows already receiving adequate vitamin A but with low serum β-carotene concentration, supplementation of β-carotene increased concentrations of β-carotene and vitamin A in blood serum, but did not affect production, reproduction, or health.

β-carotene improves fecal dysbiosis and intestinal dysfunctions in a mouse model of vitamin A deficiency

Vitamin A deficiency (VAD) results in intestinal inflammation, increased redox stress and reactive oxygen species (ROS) levels, imbalanced inflammatory and immunomodulatory cytokines, compromised barrier function, and perturbations of the gut microbiome. To combat VAD dietary interventions with β-carotene, the most abundant precursor of vitamin A, are recommended. However, the impact of β-carotene on intestinal health during VAD has not been fully clarified, especially regarding the VAD-associated intestinal dysbiosis. Here we addressed this question by using Lrat−/-Rbp−/− (vitamin A deficient) mice deprived of dietary preformed vitamin A and supplemented with β-carotene as the sole source of the vitamin, alongside with WT (vitamin A sufficient) mice. We found that dietary β-carotene impacted intestinal vitamin A status, barrier integrity and inflammation in both WT and Lrat−/-Rbp−/− (vitamin A deficient) mice on the vitamin A-free diet. However, it did so to a greater extent under overt VAD. Dietary β-carotene also modified the taxonomic profile of the fecal microbiome, but only under VAD. Given the similarity of the VAD-associated intestinal phenotypes with those of several other disorders of the gut, collectively known as Inflammatory Bowel Disease (IBD) Syndrome, these findings are broadly relevant to the effort of developing diet-based intervention strategies to ameliorate intestinal pathological conditions.

Microsomal triglyceride transfer protein-mediated transfer of β-carotene from donor to acceptor vesicles in vitro.

Dietary β-carotene is the most abundant vitamin A precursor. Once absorbed by the enterocytes, the provitamin A carotenoid can either be cleaved into retinoids (vitamin A and its derivatives) or incorporated in its intact form within chylomicrons to be distributed throughout the body for utilization and/or storage by other tissues. From the liver, together with endogenous lipids, intact β-carotene can also be incorporated within very low-density lipoprotein/low-density lipoprotein (VLDL/LDL) for transport to other tissues and organs. Microsomal triglyceride transfer protein (MTP) is a key regulator of lipoprotein biosynthesis in intestine and liver as it facilitates the incorporation of dietary and endogenous lipids into nascent lipoproteins. MTP is also critical for transferring β-carotene into lipoprotein particles for secretion. Here, we present an in vitro method to assess the transfer of β-carotene by MTP from donor to acceptor vesicles. This transfer can be assessed by precipitating donor vesicles and measuring amounts of β-carotene transferred to acceptor vesicles. The levels of transferred β-carotene are quantified by HPLC analysis and intrinsic fluorescence of β-carotene. This chapter demonstrates the feasibility of this method which is also useful to study the role of MTP for incorporation of other carotenoids that are known to be carried within VLDL/LDL and chylomicrons for organ distribution.

Carotenoid transporter CD36 expression depends on hypoxia-inducible factor-1α in mouse soleus muscles.

Dietary β-carotene induces muscle hypertrophy and prevents muscle atrophy in red slow-twitch soleus muscles, but not in white fast-twitch extensor digitorum longus (EDL) muscles and gastrocnemius muscles. However, it remains unclear why these beneficial effects of β-carotene are elicited in soleus muscles. To address this issue, we focused on carotenoid transporters in skeletal muscles. In mice, Cd36 mRNA levels were higher in red muscle than in white muscle. The siRNA-mediated knockdown of CD36 decreased β-carotene uptake in C2C12 myotubes. In soleus muscles, CD36 knockdown inhibited β-carotene-induced increase in muscle mass. Intravenous injection of the hypoxia marker pimonidazole produced more pimonidazole-bound proteins in soleus muscles than in EDL muscles, and the hypoxia-inducible factor-1 (HIF-1) α protein level was higher in soleus muscles than in EDL muscles. In C2C12 myotubes, hypoxia increased the expression of CD36 and HIF-1α at the protein and mRNA levels, and HIF-1α knockdown reduced hypoxia-induced increase in Cd36 mRNA level. In soleus muscles, HIF-1α knockdown reduced Cd36 mRNA level. These results indicate that CD36 is predominantly involved in β-carotene-induced increase in soleus muscle mass of mice. Furthermore, we demonstrate that CD36 expression depends on HIF-1α in the soleus muscles of mice, even under normal physiological conditions.