Scurvy Research Articles

The influence of vitamin C deficiency on dermatosis in neonatal dairy calves

Vitamin C is an important water-soluble antioxidant, which plays necessary roles in an animal's body, especially in neonatal dairy calves. Neonatal dairy calves receive vitamin C from their dam, and in unique situations, it can cause problems within the calf, specifically skin lesions, or dermatosis. This study aims to determine the effects of vit. C deficiency on the skin and coat integrity of the neonate calves. In this study, 10 neonatal dairy calves were used. Five calves were served as the control group, and the other 5 calves were tested for clinically affected with ascorbic acid deficiency. The clinical findings showed that severe scaling, alopecia in different areas of the body, pinna erythematous, purpuric, and pruritus. Samples of plasma were collected to estimate the value of vitamin C and some blood film parameters. The findings also revealed that significant decreases in the level of vitamin C, counting of erythrocytes, concentration of haemoglobin, and packed cell volume. Furthermore, there were significant changes in the neutrophils. Histopathological results revealed hyperkeratosis and congestion in the skin layers. After affected calves were treated with vitamin C, there was improvement and gradual disappearing of the skin gross changes. This study found a close relationship between the vitamin C deficiency in dairy calves and dermatosis (skin integrity).

THE “OLD SAILORS “ ILLNESS MAKES A RETURN

Vitamin C, also known as ascorbic acid, is a co-factor in multiple enzymatic reactions including that of collagen synthesis. Due to the absence of the enzyme L-gulonolactone oxidase, humans are unable to synthesise ascorbic acid; hence it is recognised as an essential nutrient. Scurvy refers to the clinical presentation of a deficiency of ascorbic acid, which occurs as a result of inadequate dietary intake. It has long been considered an illness of historical rather than contemporary significance. However, a tendency towards Western diets rich in processed foods and lacking in fresh produce has given rise to the re-emergence of the condition in the developed world. Current evidence suggests that there is a resurgence of scurvy in Sydney. A case is highlighted of an otherwise healthy 35year old male who presented to a hospital emergency dental clinic with generalised red, boggy gingivae. Clinical examination revealed bilateral involvement of the buccal and lingual/palatal gingivae in both the mandibular and maxillary arches, predominantly affecting the interdental papillae. Radiographic examination confirmed there was no associated bone loss or bony pathology. The clinical differential diagnoses included leukaemia, Kaposi sarcoma or possible scurvy. A battery of serological investigations yielded the eventual diagnosis of severe ascorbic acid deficiency (vitamin C level

Behavioral and Neural Responses to Vitamin C Solution in Vitamin C-deficient Osteogenic Disorder Shionogi/Shi Jcl-od/od Rats.

To investigate the appetite for vitamin C (VC), we conducted behavioral and neural experiments using osteogenic disorder Shionogi/Shi Jcl-od/od (od/od) rats, which lack the ability to synthesize VC, and their wild-type controls osteogenic disorder Shionogi/Shi Jcl- +/+ (+/+) rats. In the behavioral study, rats were deprived of VC for 25 days and then received two-bottle preference tests with a choice between water and 10 mM VC. The preference for 10 mM VC solution of od/od rats was significantly greater than that of +/+ rats. In the neural study, the relative magnitudes of the whole chorda tympani nerve (CTN) responses to 100-1000 mM VC, 3-10 mM HCl, 100-1000 mM NaCl, and 20 mM quinine▪HCl in the VC-deficient rats were significantly smaller than those in the nondeficient ones. Further, we conducted additional behavioral experiments to investigate the appetite for sour and salty taste solutions of VC-deficient od/od rats. Preference scores for 3 mM citric acid increased in od/od rats after VC removal, compared with before, whereas preference scores for 100 and 150 mM NaCl were decreased in VC-deficient od/od rats. The preference for 300 mM NaCl was not changed. Hence, our results suggest that the reduction of the aversive taste of VC during VC deficiency may have involved the reduction of CTN responses to acids. Overall, our results indicate that VC-deficient rats ingest sufficient VC to relieve their deficiency and that VC deficiency causes changes in peripheral sensitivity to acids, but nongustatory factors may also affect VC intake and choice.

Ascorbic acid deficiency increases hepatic expression of acute phase proteins through the intestine-derived IL-6 and hepatic STAT3 pathway in ODS rats

We have previously shown that ascorbic acid (AsA) deficiency elevates hepatic expression of acute phase proteins (APPs), inflammatory markers, in Osteogenic Disorder Shionogi (ODS) rats, which are unable to synthesize AsA. However, the precise mechanisms of this elevation are unknown. Signal transducer and activator of transcription 3 (STAT3) is one of the transcription factors inducing the expression of APPs and is activated by several cytokines including interleukin-6 (IL-6). The aim of this study was to determine whether AsA deficiency stimulates hepatic STAT3 activation and increases intestinal production of proinflammatory cytokines such as IL-6. Male ODS rats (6 weeks old) were fed either a basal diet containing 300 mg AsA/kg (control group) or an AsA-free diet (AsA-deficient group) for 18 days. AsA deficiency gradually and simultaneously elevated both mRNA levels of APPs (haptoglobin, α1-acid glycoprotein, C-reactive protein and α2-macroglobulin) and nuclear level of phosphorylated STAT3 (activated STAT3) in the liver. These results showed that the AsA-deficiency-induced expression of hepatic APPs is stimulated by proinflammatory cytokines activating STAT3. On day 14, AsA deficiency significantly elevated IL-6 mRNA level in the ileum and the concentration of IL-6 in portal blood. Furthermore, the portal concentration of IL-6 positively correlated with hepatic mRNA levels of STAT3-regulated genes. These findings suggest that IL-6, produced in the intestine as a result of AsA deficiency, is recruited to the liver via the portal vein and contributes to hepatic STAT3 activation and the elevated expression of APPs.

Sperm agglutination: Prevalence and contributory factors

Agglutination is a finding noted in semen analyses (SAs) that often causes confusion as to its significance. While some have attributed agglutination to antisperm antibodies (ASAs), there are other causes as well, such as genital tract infection and ascorbic acid deficiency. Additionally, it is known that patients with ASAs often have risk factors such as a history of scrotal trauma or surgery. Therefore, we sought to determine the prevalence of agglutination in our patient population and correlate it with these risk factors, regardless of the presence/absence of ASAs. A retrospective study was conducted on the SAs of men seen at a single academic Reproductive Center. Of the 1,095 SAs identified, 133 (12.1%) patients experienced agglutination (61.7% scant, 21.8% moderate and 16.5% excessive). Of patients who underwent multiple SAs, 24 (12.2%) showed variability. Furthermore, patients who underwent scrotal surgery carried 3.4 times the risk of agglutination (X2 p<0.01) and 5.5 times the risk of variability (X2 p<0.01) as compared to those patients without a history significant for scrotal surgery. Agglutination is a relatively common finding in men presenting to a reproductive clinic with little intrapatient variability. Scrotal surgery confers a higher risk of agglutination and variability.

Ascorbic acid insufficiency impairs spatial memory formation in juvenile AKR1A-knockout mice.

AKR1A, an aldo-keto reductase, is involved in the synthesis of ascorbic acid as well as the reduction of a variety of aldehyde compounds. AKR1A−/− mice produce considerably less ascorbic acid (about 10%) compared to AKR1A+/+ mice and require ascorbic acid supplementation in order to breed. To elucidate the roles played by AKR1A in spatial memory, AKR1A−/− male mice were weaned at 4 weeks of age and groups that received ascorbic acid supplementation and no supplementation were subjected to a Morris water maze test. Juvenile AKR1A−/− mice that received no supplementation showed impaired spatial memory formation, even though about 70% of the ascorbic acid remained in the brains of the AKR1A−/− mice at day 7 after weaning. To the contrary, the young adult AKR1A−/− mice at 13–15 weeks of age maintained only 15% of ascorbic acid but showed no significant difference in the spatial memory compared with the AKR1A+/+ mice or ascorbic acid-supplemented AKR1A−/− mice. It is conceivable that juvenile mice require more ascorbic acid for the appropriate level of formation of spatial memory and that maturation of the neural system renders the memory forming process less sensitive to an ascorbic acid insufficiency.

Dual-Emitting Eu(III)–Cu(II) Heterometallic–Organic Framework: Simultaneous, Selective, and Sensitive Detection of Hydrogen Sulfide and Ascorbic Acid in a Wide Range

As important biomolecules, the deficiency or maladjustment of hydrogen sulfide (H2S) or ascorbic acid (AA) is associated with the symptoms of the same disease (e.g., cardiovascular disease or cancer). There is an urgent need to develop a fluorescent probe capable of distinguishing between H2S and AA simultaneously. Here, we report the syntheses, structure, and property of the first dual-detection fluorescent probe which can differentiate H2S or/and AA in aqueous media. Accordingly, a novel [EuCu(pydc)2(ox)0.5(H2O)3·1.5H2O]2 n (1, H2pydc = 2,3-pyridinedicarboxylic acid and ox = oxalic acid) for selective and sensitive detection of H2S and AA in a wide range has been constructed (H2S: [130 nM, +∞); AA: [55 nM, +∞)), exhibiting excellent catalytic activity comparable to horseradish peroxidase. In addition, the highly efficient detection in human serum sample also proves the potential application in medical diagnosis. Meanwhile, a combinatorial logic gate (AND(INH)-OR) based on activated 1 has also been constructed. Furthermore, this approach for simultaneous H2S and AA detection suggests that the current work will expand the potential application of metal-organic frameworks for dual or multiple detections in biomedical fields.

Vitamin C and Helicobacter pylori Infection: Current Knowledge and Future Prospects.

The gram-negative bacterium, Helicobacter pylori (H. pylori), infection is predominantly known for its strong association with development of gastric diseases, including gastritis, peptic ulcers, and stomach cancer. Numerous clinical reports show that ascorbic acid deficiency has been connect with gastritis. Vitamin C levels both in gastric acid and serum have constantly been affirmed to be low in subjects with H. pylori infected gastritis and peptic ulcers. Ascorbic acid supplementation likely relates to reduced incidences of bleeding from peptic ulcers and gastric cancer. H. pylori eradication is shown to increase vitamin C levels, while the benefits of ascorbic acid oral intake to increase the effectiveness of H. pylori-eradication therapy are controversial. Recent studies suggest that ascorbate intake intravenously, but not orally; pharmacologic ascorbate concentrations up to 30 mmol/L in blood, several millimolar in tissues as well as in interstitial fluid, are easily and safely achieved. Pharmacologic ascorbate can exert pro-oxidant effects locally as a drug by mediating hydrogen peroxide (H2O2) formation, which was applied to animal and clinical trials of cancer, sepsis, and severe burns etc. In this review, we summarize current understanding of the associations of vitamin C and H. pylori infection, and outline some potential strategies for H. pylori intervention from emerging advances on ascorbic acid physiology and pharmacology.

Ethylene signaling triggered by low concentrations of ascorbic acid regulates biomass accumulation in Arabidopsis thaliana

Ascorbic acid (AA) is a major redox buffer in plant cells. The role of ethylene in the redox signaling pathways that influence photosynthesis and growth was explored in two independent AA deficient Arabidopsis thaliana mutants (vtc2-1 and vtc2-4). Both mutants, which are defective in the AA biosynthesis gene GDP-L-galactose phosphorylase, produce higher amounts of ethylene than wt plants. In contrast to the wt, the inhibition of ethylene signaling increased leaf conductance, photosynthesis and dry weight in both vtc2 mutant lines. The AA-deficient mutants showed altered expression of genes encoding proteins involved in the synthesis/responses to phytohormones that control growth, particularly auxin, cytokinins, abscisic acid, brassinosterioids, ethylene and salicylic acid. These results demonstrate that AA deficiency modifies hormone signaling in plants, redox-ethylene interactions providing a regulatory node controlling shoot biomass accumulation.

Vitamin C and Skin

Vitamin C (VC) is one of nine water-soluble vitamins. VC is known as ascorbic acid (AA), which is a reduced form of VC. AA plays some essential roles in the human body: (1) protecting skin against UV damage; (2) preventing hyperpigmentation of the skin; (3) improving skin inflammation and reducing photocarcinogenesis; (4) increasing collagen fiber; (5) reducing oxidative stress; and (6) immuno-modulating effects. AA deficiency affects collagen and vessels structure, wound healing and hemostasis, and scurvy. VC and AA are essential for life. We hope development of new medicines using VC or AA because of few adverse side effects of VC and AA.

Micronutrient Alterations During Continuous Renal Replacement Therapy in Critically Ill Adults: A Retrospective Study.

Continuous renal replacement therapy (CRRT) is commonly used to provide renal replacement therapy in the intensive care unit. Limited published data suggest that CRRT may lead to depletion of water-soluble vitamins and trace elements. The goal of this study was to identify the incidence of trace element and vitamin deficiencies in critically ill patients during CRRT. This study is based on a retrospective chart review of patients who were referred to Emory University Hospital's nutrition support services and had at least 1 serum micronutrient level measured during CRRT (thiamin, pyridoxine, ascorbic acid, folate, zinc, and copper) between April 1, 2009, and June 1, 2012. Seventy-five patients were included in the study. Nine of 56 patients (16%) had below-normal whole blood thiamin concentrations, and 38 of 57 patients (67%) had below-normal serum pyridoxine levels. Serum ascorbic acid and folate deficiencies were identified among 87% (13 of 15) and 33% (3 of 9) of the study patients, respectively. Nine of 24 patients had zinc deficiency (38%), and 41 of 68 patients had copper deficiency (60%). Of the 75 total subjects, 60 patients (80%) had below-normal levels of at least 1 of the micronutrients measured. The incidence of various micronutrient deficiencies in critically ill patients who required CRRT was higher than previously reported. Prospective studies are needed to determine the impact of CRRT on micronutrient status and the potential clinical and metabolic efficacy of supplementation in the intensive care unit setting.

ビタミンC欠乏は表皮萎縮およびUVB照射による色素沈着を増加する : SMP30/GNL-ノックアウトヘアレスマウスでの解析

ビタミンC欠乏は表皮萎縮およびUVB照射による色素沈着を増加する : SMP30/GNL-ノックアウトヘアレスマウスでの解析

Upregulation of TET activity with ascorbic acid induces epigenetic modulation of lymphoma cells

The Ten Eleven Translocation (TET) enzymes have been found to be mutated in both diffuse large B-cell (DLBCL) and peripheral T-cell (PTCL) lymphomas resulting in DNA hypermethylation. Recent studies in embryonal stem cells showed that ascorbic acid (AA) is a cofactor for TET with a binding site at the catalytic domain, and enhances TET activity. We hypothesized that AA could potentially enhance TET activity in lymphoma cells to cause DNA demethylation, reactivate expression of tumor suppressor genes and enhance chemosensitivity. We demonstrate in vitro that AA treatment of DLBCL and PTCL cells using AA concentrations achievable intravenously increased TET activity leading to DNA demethylation. This epigenetic effect is independent of hydrogen peroxide. AA treatment increased the expression of SMAD1, a tumor suppressor gene known to be suppressed by methylation, and increased chemosensitivity of lymphoma cells. Twenty-nine percent (10/34) of unselected lymphoma patients had plasma AA levels that were deficient suggesting an additional clinical mechanism of TET hypofunction. These data indicate that AA has the potential to modify TET function in lymphoma and enhance chemosensitivity. In addition, the AA deficiency seen in some patients may further impair TET function and contribute to resistance. Clinical trials testing intravenous AA with chemotherapy are warranted.

Transcriptome Analysis of Skin from SMP30/GNL Knockout Mice Reveals the Effect of Ascorbic Acid Deficiency on Skin and Hair.

Senescence marker protein-30/gluconolactonase knockout mice (SMP-30/GNL-KO) are a very useful model for clarifying the involvement of vitamin C (VC) in aging-related diseases. In this study, the effects of VC deficiency on skin and hair growth were investigated using SMP-30/GNL-KO mice by RNA sequencing. SMP-30/GNL-KO mice were given water containing 1.5 g/l VC until up to 8 weeks after birth to maintain a VC concentration in their organs and plasma equivalent to that in wild-type mice. The mice were then divided into two groups: a VC(+) group, where VC was administered, and a VC(-) group, where VC was not administered. Skin samples were collected at 4 and 8 weeks after the treatment. RNA was extracted from each skin sample, followed by cDNA synthesis and RNA-seq. In addition, hair growth was compared between the VC(-) and VC(+) groups after shaving. Skin samples were collected from the shaved area for histological examination by hematoxylin & eosin (HE) staining. RNA-seq revealed that there were 1,736 (FDR<0.001) differentially expressed genes in the VC(-) and VC(+) groups. From the functional analysis of the differentially expressed genes in the VC(-) and VC(+) groups, predicted functionalities including cell death and cytotoxicity increased in the VC(+) group. Furthermore, it was predicted that the difference in hair growth between the VC(-) and VC(+) groups was caused by the expression of genes including keratin-related genes and the Sonic hedgehog gene. It was confirmed that hair growth was significantly promoted; hair growth from hair papilla cells was also confirmed by HE staining of the shaved backs of SMP-30/GNL-KO mice in the VC(+) group. RNA-seq of the skin from VC-deficient mice showed the effects of VC deficiency on the expression of genes involved in cell growth and the hair cycle. Visual inspection suggested that changes in the expression of the genes are involved in delaying hair growth in the VC(-) group. Further research on the relationship among VC deficiency, the hair cycle, and skin cell growth may contribute to research on hair restoration and skin aging.

Vitamin C deficiency exacerbates diabetic glomerular injury through activation of transforming growth factor-β signaling

BackgroundThe hyperglycemia and hyperoxidation that characterize diabetes lead to reduced vitamin C (VC) in diabetic humans and experimentally diabetic animals. Herein, we access the effects of VC deficiency on the diabetic kidney injury and explore the underlying mechanism. Methodsl-gulonolactone oxidase conventional knockout (Gulo−/−) mice genetically unable to synthesize VC were subjected to streptozotocin-induced diabetic kidney injury and the role of VC deficiency was evaluated by biochemical and histological approaches. Rat mesangial cells were cultured to investigate the underlying mechanism. ResultsFunctionally, VC deficiency aggravates the streptozotocin-induced renal insufficiency, exhibiting the increased urine albumin, water intake, and urine volume in Gulo−/− mice. Morphologically, VC deficiency exacerbates the streptozotocin-induced kidney injury, exhibiting the increased glomerular expansion, deposition of Periodic Acid-Schiff- and Masson-positive materials, and expression of α-smooth muscle actin, fibronectin and type 4 collagen in glomeruli of Gulo−/− mice. Mechanistically, VC activates protein kinase B (Akt) to destabilize Ski and thereby induce the expression of Smad7, resulting in suppression of TGF-β/Smad signaling and extracellular matrix deposition in mesangial cells. ConclusionsVC is essential for the renal function maintenance in diabetes. General significanceCompensation for the loss of VC could be an effective remedy for diabetic kidney injury.

Ascorbic acid deficiency in patients with lichen planus

ABSTRACTObjectives. Recent studies have highlighted the role of oxidative stress in the pathogenesis of lichen planus (LP). In the present study, the interest of the authors is focused on the investigation of ascorbic acid status in patients with LP and identification of parameters that might influence the level of this vitamin.Material and method. We analyzed the level of urinary ascorbic acid (reflectometric method) in 77 patients with LP (cutaneous LP (CLP)—49 cases; oral LP (OLP)—28 cases) and 50 control subjects. The evaluation of all participants included clinical examination and laboratory and imaging tests.Results. Compared to the control group (19.82 mg/dl) the level of ascorbic acid was significantly lower both in patients with CLP (8.47 mg/dl, p = 0.001) and in those with OLP (8.04 mg/dl, p = 0.001). In patients with LP it was found that the deficiency of ascorbic acid increases with age (r = -0.318, p = 0.032). The urinary concentrations of ascorbic acid were significantly lower in patients with LP associated with infections compared to patients with LP without infections.Conclusions. The urinary ascorbic acid level may be a useful parameter in identifying patients with LP who are at risk of developing viral or bacterial infections.

Acerola (Malpighia emarginata DC.) Juice Intake Suppresses UVB-Induced Skin Pigmentation in SMP30/GNL Knockout Hairless Mice.

Background/AimsAcerola (Malpighia emarginata DC.) is a fruit that is known to contain high amounts of ascorbic acid (AA) and various phytochemicals. We have previously reported that AA deficiency leads to ultraviolet B (UVB)-induced skin pigmentation in senescence marker protein 30 (SMP30)/gluconolactonase (GNL) knockout (KO) hairless mice. The present study was undertaken to investigate the effects of acerola juice (AJ) intake on the skin of UVB-irradiated SMP30/GNL KO mice.Research design/Principal findingsFive-week old hairless mice were given drinking water containing physiologically sufficient AA (1.5 g/L) [AA (+)], no AA [AA (-)] or 1.67% acerola juice [AJ]. All mice were exposed to UVB irradiation for 6 weeks. UVB irradiation was performed three times per week. The dorsal skin color and stratum corneum water content were measured every weekly, and finally, the AA contents of the skin was determined. The skin AA and stratum corneum water content was similar between the AA (+) and AJ groups. The L* value of the AA (+) group was significantly decreased by UVB irradiation, whereas AJ intake suppressed the decrease in the L* value throughout the experiment. Moreover, in the AJ group, there was a significant decrease in the expression level of dopachrome tautomerase, an enzyme that is involved in melanin biosynthesis.ConclusionThese results indicate that AJ intake is effective in suppressing UVB-induced skin pigmentation by inhibiting melanogenesis-related genes.

Ascorbic acid deficiency leads to increased grain chalkiness in transgenic rice for suppressed of L-GalLDH

The grain chalkiness of rice (Oryza sativa L.), which determines the rice quality and price, is a major concern in rice breeding. Reactive oxygen species (ROS) plays a critical role in regulating rice endosperm chalkiness. Ascorbic acid (Asc) is a major plant antioxidant, which strictly regulates the levels of ROS. l-galactono-1, 4-lactone dehydrogenase (L-GalLDH, EC 1.3.2.3) is an enzyme that catalyzes the last step of Asc biosynthesis in higher plants. Here we show that the L-GalLDH-suppressed transgenic rice, GI-1 and GI-2, which have constitutively low (between 30% and 50%) leaf and grain Asc content compared with the wild-type (WT), exhibit significantly increased grain chalkiness. Further examination showed that the deficiency of Asc resulted in a higher lipid peroxidation and H2O2 content, accompanied by a lower hydroxyl radical scavenging rate, total antioxidant capacity and photosynthetic ability. In addition, changes of the enzyme activities and gene transcript abundances related to starch synthesis were also observed in GI-1 and GI-2 grains. The results we presented here suggest a close correlation between Asc deficiency and grain chalkiness in the L-GalLDH-suppressed transgenics. Asc deficiency leads to the accumulation of H2O2, affecting antioxidant capacity and photosynthetic function, changing enzyme activities and gene transcript abundances related to starch synthesis, finally leading to the increased grain chalkiness.

Evidence for chronic omega-3 fatty acids and ascorbic acid deficiency in Palaeolithic hominins in Europe at the emergence of cannibalism

At the Middle-Upper Palaeolithic (M/UP) transition in Western Europe, hominins depended mostly on terrestrial mammals for subsistence, being pointed out that reliance on reindeer (Rangifer tarandus) would have promoted declines in human population densities during that period. Food-composition tables have been compiled for hominins at the M/UP transition, listing protein, fat, energy, different omega-3 fatty acids and ascorbic acid concentrations. These data were used to compute the regular relations between fatty and lean tissues of the main hunted food-animals to meet hominin energy needs. Then, with daily protein intake considered critical, the optimal contribution of the different omega-3 fatty acids from different hunted species to hominin diets were computed. Several faunal assemblages from different human sites at different M/UP periods were used to assess the overall daily intake of the various omega-3 fatty acid classes. The results of the calculations made in this work are quite clear; hominins at the M/UP transition had a deficit of both omega-3 fatty acids and ascorbic acid. Data on human organs summarized here are also conclusive: these contain such nutrients in amounts much higher than reached in the corresponding mammal organs consumed, and thus could have been alternative sources of those nutrients for Palaeolithic hominins. Therefore, nutritional cannibalism detected at such times could have had the function of alleviating these deficits. The evolutionary advantages gained by the consumption of the various omega-3 fatty acids of human origin are also discussed.

A novel osteoporosis model with ascorbic acid deficiency in Akr1A1 gene knockout mice.

The AKR1A1 protein is a member of the aldo-keto reductase superfamily that is responsible for the conversion of D-glucuronate to L-gulonate in the ascorbic acid (vitamin C) synthesis pathway. In a pCAG-eGFP transgenic mouse line that was produced by pronuclear microinjection, the integration of the transgene resulted in a 30-kb genomic DNA deletion, including the Akr1A1 gene, and thus caused the knockout (KO) of the Akr1A1 gene and targeting of the eGFP gene. The Akr1A1 KO mice (Akr1A1eGFP/eGFP) exhibited insufficient serum ascorbic acid levels, abnormal bone development and osteoporosis. Using micro-CT analysis, the results showed that the microarchitecture of the 12-week-old Akr1A1eGFP/eGFP mouse femur was shorter in length and exhibited less cortical bone thickness, enlargement of the bone marrow cavity and a complete loss of the trabecular bone in the distal femur. The femoral head and neck of the proximal femur also showed a severe loss of bone mass. Based on the decreased levels of serum osteocalcin and osteoblast activity in the Akr1A1eGFP/eGFP mice, the osteoporosis might be caused by impaired bone formation. In addition, administration of ascorbic acid to the Akr1A1eGFP/eGFP mice significantly prevented the condition of osteoporotic femurs and increased bone formation. Therefore, through ascorbic acid administration, the Akr1A1 KO mice exhibited controllable osteoporosis and may serve as a novel model for osteoporotic research.