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Effects of taurine treatment on body weight, visceral fat, food intake. Mice were treated with chow diet (C), Chow + Taurine (C + T), High-fat diet (HFD) or HFD + Taurine (HFD + T) for 10 weeks. (A) Body weight progression from the first day of taurine treatment until the 10 th week of treatment in mice fed with chow or HFD. (n = 8–10 mice per group). Differences between C vs HFD (*P < 0.05); HFD vs HFD+T ( # P < 0.05, ## P < 0.01). (B) Visceral fat weight after 10 weeks of taurine treatment in mice fed with chow or HFD. Differences between C vs HFD (*P < 0.05); HFD vs HFD+T ( # P < 0.05). (n = 8–10 mice per group). (C) Food intake progression from the first week until the 10th week of treatment. Differences between C vs HFD *P < 0.05. **P < 0.001, ***P < 0.0001. Differences between HFD vs HFD+ T ( # P < 0.05, ## P < 0.001). (D) Food intake at 10 th week of treatment during the light and dark cycle. Food was measured by weighing the food consumption separately during the day (from 8:00 to 20:00) and the food consumption during the night (from 20:00 to 8:00). Differences between C vs HFD (***P < 0.001); and HFD vs HFD+ T ( ## P < 0.01). (E) Water Intake at 10 th week of treatment. Data are expressed as mean ± SEM.
Source publication
Close ties have been made among certain nutrients, obesity, type 2 diabetes and circadian clocks. Among nutrients, taurine has been documented as being effective against obesity and type 2 diabetes. However, the impact of taurine on circadian clocks has not been elucidated. We investigated whether taurine can modulate or correct disturbances in dai...
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... groups until the 5 th week of treatment. In the HFD group, body weight increased from the 5 th week of treatment in both HFD and HFD+ T treated mice, as compared to controls. However, from the 8 th to the 10 th week of treatment, mice fed with HFD+ T prevented the increase in body weight, compared to mice fed with HFD until the end of treatment (Fig. 1A). After 10 weeks of treatment, visceral fat weight was comparable between the C and C+ T groups. As expected, mice treated with a HFD showed a significant increase in visceral fat, compared to the C group, whereas mice treated with HFD+ T had a decrease in visceral fat, compared to the HFD group (Fig. 1B). Interestingly, HFD-treated ...
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... fed with HFD until the end of treatment (Fig. 1A). After 10 weeks of treatment, visceral fat weight was comparable between the C and C+ T groups. As expected, mice treated with a HFD showed a significant increase in visceral fat, compared to the C group, whereas mice treated with HFD+ T had a decrease in visceral fat, compared to the HFD group (Fig. 1B). Interestingly, HFD-treated mice had increased food intake already at the first week of treatment with a peak of food con- sumption at the second week and a sustained elevation of food intake until the end of treatment. On the other hand, HFD+ T mice had decreased food intake already at the first week compared to the HFD group ...
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... HFD-treated mice had increased food intake already at the first week of treatment with a peak of food con- sumption at the second week and a sustained elevation of food intake until the end of treatment. On the other hand, HFD+ T mice had decreased food intake already at the first week compared to the HFD group (Fig.1C). Measurements of food intake at the end of treatment (10 th week) during the light cycle was similar between C and C+ T groups and increased during the dark cycle in both groups (P < 0.0001, respectively). ...
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... HFD group (Fig.1C). Measurements of food intake at the end of treatment (10 th week) during the light cycle was similar between C and C+ T groups and increased during the dark cycle in both groups (P < 0.0001, respectively). In contrast, mice fed a HFD exhibited an increase in food intake during both light and dark cycles, as compared to C group (Fig. 1D). Strikingly, taurine decreased food intake in both light and dark cycles. Water intake was similar in all experimen- tal groups at the 10 th week of treatment (Fig. 1E). The effects of the HFD and taurine treatment after 10 weeks on body weight gain, visceral fat and food intake and their interactions are also shown in Table 1. There ...
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... dark cycle in both groups (P < 0.0001, respectively). In contrast, mice fed a HFD exhibited an increase in food intake during both light and dark cycles, as compared to C group (Fig. 1D). Strikingly, taurine decreased food intake in both light and dark cycles. Water intake was similar in all experimen- tal groups at the 10 th week of treatment (Fig. 1E). The effects of the HFD and taurine treatment after 10 weeks on body weight gain, visceral fat and food intake and their interactions are also shown in Table 1. There was no effect of taurine treatment on body weight, visceral fat and food intake in the control group (Table 1). However, the effect of HFD alone when compared to the ...
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... check the effect of taurine at the beginning of the treatment we next measured body weight, visceral fat, water and food intake at the first week of treatment. There was no difference in body weight, visceral fat and water intake in all experimental groups ( Supplementary Fig. 1A-C, respectively). Strikingly, mice fed a HFD had an increase in food intake during the light and dark cycles already at the first week of treatment whereas taurine was able to prevent the increase in food intake caused by HFD in both light and dark cycles ( Supplementary Fig. 1D). ...
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... was no difference in body weight, visceral fat and water intake in all experimental groups ( Supplementary Fig. 1A-C, respectively). Strikingly, mice fed a HFD had an increase in food intake during the light and dark cycles already at the first week of treatment whereas taurine was able to prevent the increase in food intake caused by HFD in both light and dark cycles ( Supplementary Fig. 1D). Moreover, one week of HFD treatment led to glucose intolerance (Supplementary Fig. 2A) and decreased insulin sensitivity ( Supplementary Fig. 2C) but taurine treatment in mice fed a HFD had a small effect on glucose tolerance and insulin sensitivity with no statistically significant results when calculating the area under the curve ( Supplementary Fig. 2B,D respectively). ...
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Objective
Circadian Clock gene mutant mice show dampened 24-h feeding rhythms and an increased sensitivity to high-fat diet (HFD) feeding. Restricting HFD access to the dark phase counteracts its obesogenic effect in wild-type mice. The extent to which altered feeding rhythms are causative for the obesogenic phenotype of Clock mutant mice, however,...
Aims: To investigate the central (hypothalamic) and peripheral effects of exercise without body weight change in diet-induced obesity. Methods: male 12-week old C57Bl/6 mice received a control (C) or a high-fat diet (H). Half of them had free access to running wheels 5days/week/10weeks (CE and HE, respectively). Hypothalamic expression of genes rel...
Citations
... Various animal models have shown the anti-obesity effects of taurine supplementation, tied to decreased body weight with inhibited expression of adipogenic genes but improved expression of hepatic genes involved in fatty acid metabolism [36,37]. The underlying pathways may include lower food/caloric intake via preserving hypothalamic leptin action and modulating circadian rhythms in high-fat diet-induced obese mice [38,39]. Moreover, taurine may also modulate energy metabolism to attenuate or prevent obesity [35]. ...
Red meat and animal-sourced protein are often disparaged as risk factors for developing metabolic syndrome, while emerging research has shown the beneficial effects of dietary taurine, creatine, carnosine, and anserine which are all exclusively abundant in red meat. Thus, it is imperative to highlight the available evidence to help promote red meat as part of a well-balanced diet to optimize human health. In this study, a bibliometric analysis was conducted to investigate the current research status of dietary taurine, creatine, carnosine, and anserine with metabolic syndrome, identify research hotspots, and delineate developmental trends by utilizing the visualization software CiteSpace. A total of 1094 publications were retrieved via the Web of Science Core Collection from 1992 to 2022. There exists a gradual increase in the number of publications on this topic, but there is still much room for research papers to rise. The United States has participated in the most studies, followed by China and Japan. The University of Sao Paulo was the research institute contributing the most; Kyung Ja Chang and Sanya Roysommuti have been identified as the most prolific authors. The analysis of keywords reveals that obesity, lipid profiles, blood pressure, and glucose metabolism, as well as ergogenic aid and growth promoter have been the research hotspots. Inflammation and diabetic nephropathy will likely be frontiers of future research related to dietary taurine, creatine, carnosine, and anserine. Overall, this paper may provide insights for researchers to further delve into this field and enlist the greater community to re-evaluate the health effects of red meat.
... NAC but not taurine prevented obesity development. As observed by others, HFD-induced glucose intolerance was prevented by treatment with taurine [45][46][47] and NAC [48]. Both treatments modulated circulating levels of adipokines, in line with possible effects of NAC [49] and taurine [50] on adipose tissue. ...
Background: Obesity constitutes a risk factor for cognitive impairment. In rodent models, long-term exposure to obesogenic diets leads to hippocampal taurine accumulation. Since taurine has putative cyto-protective effects, hippocampal taurine accumulation in obese and diabetic models might constitute a counteracting response to metabolic stress. Objective: We tested the hypothesis that treatment with taurine or with N-acetylcysteine (NAC), which provides cysteine for the synthesis of taurine and glutathione, prevent high-fat diet (HFD)-associated hippocampal alterations and memory impairment. Methods: Female mice were fed either a regular diet or HFD. Some mice had access to 3%(w/v) taurine or 3%(w/v) NAC in the drinking water. After 2 months, magnetic resonance spectroscopy (MRS) was used to measure metabolite profiles. Memory was assessed in novel object and novel location recognition tests. Results: HFD feeding caused memory impairment in both tests, and reduced concentration of lactate, phosphocreatine-to-creatine ratio, and the neuronal marker N-acetylaspartate in the hippocampus. Taurine and NAC prevented HFD-induced memory impairment and N-acetylaspartate reduction. NAC, but not taurine, prevented the reduction of lactate and phosphocreatine-to-creatine ratio. MRS revealed NAC/taurine-induced increase of hippocampal glutamate and GABA levels. Conclusion: NAC and taurine can prevent memory impairment, while only NAC prevents alterations of metabolite concentrations in HFD-exposed female mice.
... The peripheral clock receives signals from the central clock through hormones and synaptic projections and is affected by the autonomic nervous system as well as by external factors (such as light, sleep, physical activity, feeding, etc.) (2). The circadian rhythm system is closely integrated with energy metabolism through both central and peripheral clocks (3,4). The master regulators of the circadian clock, Brain and Muscle Aryl Hydrocarbon Receptor Nuclear Translocation 1 (BMAL1 (Arntl)) and CLOCK (Clock), form heterodimers and combine with E-box elements to regulate the expression of target genes, such as Per1/Per2 and cryptochrome 1/cryptochrome 2 (Cry1/Cry2). ...
... LC-MS analysis and chromatographic separation conditions were as follows: analysis platform: ACQUITYTM UPLC QTOF; column: XBridge TM C18 2.5 μm, 2.1 mm × 50 mm Column, Waters, USA; column temperature: 30°C; mobile phase A: 0.05% HCOOH-Water; mobile phase B: 0.05% HCOOH-CH 3 ...
Background: Disturbance of circadian rhythm leads to abnormalities in bile acid (BA) and lipid metabolism, and it is of great significance to explore the relationship between them. This study explored the effects of circadian dysregulation on the rhythms of intestinal BA metabolism. Method: Period circadian clock 1/period circadian clock 2 (Per1/Per2) double gene knockout (DKO) and wild-type (WT) male C57BL/6 mice were fed with a control or high-fat diet for 16 weeks. We measure plasma parameters of mice. Pathological changes including those in liver and intestine were detected by hematoxylin and eosin (H&E) and oil O staining. Western blot was used to detect the intestinal core rhythm protein clock circadian regulator (CLOCK), nuclear receptor subfamily 1, group D, member 1 (REV-ERBα), Farnesoid X receptor (FXR), Small heterodimer partner (SHP), and Fibroblast growth factor 15 (FGF15) expressions. We analyzed the bile acid and intestinal flora profile in the mice intestine tissues by BA-targeted metabolomics detection and high-throughput sequencing. Results: Rhythmic chaos affected lipid metabolism and lipid accumulation in mice liver and intestine, and diurnal fluctuations of plasma triglycerides (TGs) were absent in normal-feeding DKO mice. The normal circadian fluctuations of the CLOCK and REV-ERBα observed in wild mice disappeared (normal diet) or were reversed (high-fat diet) in DKO mice. In WT mice intestine, total BA and conjugated BA were affected by circadian rhythm under both normal and high-fat diets, while these circadian fluctuations disappeared in DKO mice. Unconjugated BA seemed to be affected exclusively by diet (significantly increased in the high-fat group) without obvious fluctuations associated with circadian rhythm. Correlation analysis showed that the ratio of conjugated/unconjugated BA was positively correlated with the presence of Bacteroidetes and displayed a circadian rhythm. The expression levels of BA receptor pathway protein FXR, SHP, and FGF15 were affected by the ratio of conjugated/unconjugated BA. Conclusion: Bacteroidetes-related diurnal changes to intestinal ratios of conjugated/unconjugated BA have the potential to regulate diurnal fluctuations in liver BA synthesis via FXR-FGF15. The inverted intestinal circadian rhythm observed in DKO mice fed with a high-fat diet may be an important reason for their abnormal circadian plasma TG rhythms and their susceptibility to lipid metabolism disorders.
... 28 The anti-obesity effects of taurine might result from lower food/caloric intake. 29,30 Mice administered 2% taurine in their drinking water for 10 weeks gained less weight on a high-fat diet and showed significantly lower visceral fat weight than control mice. 30 In that study, mice administered taurine showed decreased food intake. ...
... 29,30 Mice administered 2% taurine in their drinking water for 10 weeks gained less weight on a high-fat diet and showed significantly lower visceral fat weight than control mice. 30 In that study, mice administered taurine showed decreased food intake. ...
Taurine (2-aminoethane sulfonic acid) is a non-essential amino acid mainly obtained through diet in humans. Despite the lack of research on the health effects of taurine in animals and humans, it is widely used as a dietary supplement. Evidence from human and animal studies indicates that taurine is involved in conjugation of bile acids and regulation of blood pressure and has anti-oxidative, anti-inflammatory, and anti-obesogenic properties. Taurine can benefit both human and non-human animal health in multiple ways. However, few interventional and epidemiological studies regarding the beneficial impacts of taurine in humans and other animals have been conducted. Here, we review the evidence from animal and human studies showing that taurine protects against dyslipidemia, obesity, hypertension, and diabetes mellitus.
... NAC but not taurine prevented obesity development. As observed by others, HFD-induced glucose intolerance was prevented by treatment with taurine [45][46][47] and NAC [48]. Both treatments modulated circulating levels of adipokines, in line with possible effects of NAC [49] and taurine [50] on adipose tissue. ...
Obesity impacts brain metabolism and function, and constitutes a risk factor for dementia development. Long-term exposure to obesogenic diets leads to taurine accumulation in the hippocampus of rodents. Taurine has putative beneficial effects on cell homeostasis, and is reported to improve cognition. Therefore, hippocampal taurine accumulation in obese and diabetic models might constitute a counteracting response to metabolic stress. This study tested the hypothesis that treatment with taurine or with N-acetylcysteine (NAC), which provides cysteine for the synthesis of taurine and the antioxidant glutathione, prevent obesity-associated hippocampal alterations and memory impairment. Female mice were fed either a regular diet or a high-fat diet (HFD). For the same period, some mice had access to 3%(w/v) taurine or 3%(w/v) NAC in the drinking water. After 2 months, magnetic resonance spectroscopy was used to measure metabolite profiles. Then, memory was assessed in novel object and novel location recognition tests. HFD feeding caused memory impairment in both tests, and reduced concentration of lactate, phosphocreatine-to-creatine ratio, and the neuronal marker N-acetylaspartate in the hippocampus. Both taurine and NAC prevented HFD-induced memory impairment and N-acetylaspartate reduction. NAC, but not taurine, prevented the HFD-induced reduction of lactate and phosphocreatine-to-creatine ratio. Analysis of the metabolite profile further revealed prominent NAC/taurine-induced increase of glutamate and GABA levels in the hippocampus. We conclude that NAC and taurine prevent of neuronal dysfunction, while only NAC prevents energy metabolism dysregulation in HFD-induced obesity in female mice.
... Under our conditions, we found no significant differences in relation to the amount of food consumed in 9-month-old sham-castrated mice. Similarly, other studies observed that taurine (2%) treatment for 10 weeks reduces food intake and body weight in obese mice with no effect in control mice [21]; other study reported that 5% taurine in drinking water reduces food intake and body weight in 30-days-old mice treated for 6 weeks [22]; also, taurine administered via Ip (100 mg/kg) for 30 days, reduced food intake in rats [23]. Additionally, taurine applied directly in brain (Icv cannulated) for 8 weeks in food deprived old rats showed a spontaneous reduction of food intake [24]. ...
Taurine is an abundant metabolite associated with regulation of cell volume. Several signaling pathways are stimulated at a micromolar concentrations of taurine. However, most of the experimental studies employ this compound at a very high concentration (tens of millimolar). In this study, the role of a chronic treatment with a micromolar dosage of taurine in the physical performance of skeletal muscle of castrated-aged mice was characterized.
Taurine was administered in drinking water (800 μM) to 9-months-old castrated (or sham) mice at approximately 20 mg/kg per day for 12 weeks. The weight of the mice, grip strength, food and water intake were monitored. Soleus or EDL muscles were dissected for determinations of force and fatigue.
Castrated mice show a slow increase in body mass and a sustained reduction of grip strength. The taurine treatment delays the weigh recovery and generates a decrease in force of castrated and sham mice. No effect of taurine was observed in young mice. The food intake was significantly reduced in castrated mice treated with taurine (with no effect in water intake). The raw force generation or muscle mass in EDL and soleus muscle were similar in treated mice in comparison with control groups. Interestingly, the taurine treatment generated an increased fatigability in both EDL and soleus muscle.
We suggest that a submillimolar concentration of taurine chronically administered during aging produce negative effect in physical performance. Caution should be taken when this compound is routinely consumed by old adults.
... Our findings revealed that TAU supplementation enhance effectively the concentration Camargo et al. (2015) demonstrated that TAU could modulate gene expression of leptin for suppressing neuropeptides in hypothalamus, that decrease food intakes through reduction hypothalamic resistance to leptin. Prevention of daily plasma leptin disruption caused by the high fat diet was confirmed (Figueroa et al., 2016). Regarding adiponectin, Chen et al. (2009) found that TAU supplementation could improve expression the circulating adiponectin through prevention ethanol-induced oxidative stress and attenuated tumor necrosis factor expression and steatosis, in part, by increasing expression of genes involved in fatty acid oxidation. ...
This study was aimed to investigate the effect of Taurine on albino rats with different MDs (obesity, diabetes and hypoprotein). A total of, 30 male albino rats subjected to preparatory period, and then, divided into five groups; control (C), TAU-supplementation (TS), cholesterol (Ch), diabetes (D) and hypoprotein (Hp) groups. Post-experimental period, direct blood sampling was performed to detect the levels of TAU, leptin, adiponectin and the blood biomarkers. The findings TS showed a significant elevation in levels of leptin, adiponectine and HDL, whereas, there was significant reduction in values of cholesterol, triglyceride, LDL and VLDL. For Ch group, significant increases were detected in levels of insulin, cholesterol, LDL and VLDL. The values of glucose were increased significantly among D and Ch groups. The levels of GSH and SOD increased significantly in TS group, and reduced in D and Ch groups. Correlation between TAU and liver enzymes revealed a significant decrease in ALT and AST among TS rats, and increased among the Ch and D groups. Although, the findings of total protein differed insignificantly among all study groups. Levels of creatinine and urea reduced in TS group, increased in Ch, D and Hp. The findings concluded that TAU has many advantages and can be used to improvement of body health in both diseased (obese and diabetic) and healthy individuals.
... Improves plasma glucose levels (around −20 mg/dL in all timepoint compared to control) disturbance plasma insulin (between −4 and −10 ng/ml in different timepoint compared to control) and leptin (between −5 and −50 ng/ml in different timepoint compared to control) and Per1 expression in pancreatic islets. [102] (Continued) 10 in taurine-supplemented group ...
... Moreover, nutrients reset peripheral circadian clocks and the local clock genes control downstream metabolic processes [107] and, specially, the circadian system which has been shown to regulate glucose metabolism . [108] Concretely, taurine supplementation in mice model demonstrated the modulation of clock genes expression in β cells in those consuming a diet rich in high fat diet [102] which is linked to an improvement with sleep quality [109] and negatively associated with obesity and T2D development . [110] Furthermore, the supplementation through the combination between omega-3 + taurine in humans has shown a cardioprotective and anti-inflammatory effect greater than both elements separately . ...
There are many studies regarding stop the progression to type 2 diabetes (T2D) through dietary control but there is no global recommendation for a specific diet. The strongest evidence is weight control through nutritional education but it does not include elderly people because of the risk of malnutrition that would entail. Therefore, the search for specific foods that can help slow down the progress towards T2D are of great interest. Although the controversy between fish consumption and the risk of developing T2D, it has been observed that oily fish could play a protective role. This type of fish may contain large amounts of persistent organic pollutants (POPs) but, on the contrary, contain omega-3 with effects on the cardiovascular system. In addition, the presence of taurine, a semi-essential amino acid very present in oily fish and which has been studied its antidiabetogenic effect, could play an essential role in the protective effect of this type of fish against T2D. Among them, the one with the highest concentrations of omega-3 and taurine as well as low concentration of POPs is sardine. An integrative review of observational studies and clinical trials was performed to investigate the association between sardine consumption and T2D prevention.
... As l-arginine modulates leptin function [76], it was possible that HMDP and HMPH improved leptin resistance at least in part via the action of l-arginine and thereby enhanced glucose utilization, stimulated energy expenditure and subsequently decreased body weight. Taurine, another important amino acid in HMPH or HMDP, is reported to restore leptin signaling in neurons and improve leptin resistance [77,78]. The reduction in serum leptin levels by HMDP and HMPH might be a consequence of improved leptin resistance or a confounded effect of improving both leptin and insulin resistances. ...
Although genetic predisposition influences the onset and progression of insulin resistance and diabetes, dietary nutrients are critical. In general, protein is beneficial relative to carbohydrate and fat but dependent on protein source. Our recent study demonstrated that 70% replacement of dietary casein protein with the equivalent quantity of protein derived from herring milt protein hydrolysate (HMPH; herring milt with proteins being enzymatically hydrolyzed) significantly improved insulin resistance and glucose homeostasis in high-fat diet-induced obese mice. As production of protein hydrolysate increases the cost of the product, it is important to determine whether a simply dried and ground herring milt product possesses similar benefits. Therefore, the current study was conducted to investigate the effect of herring milt dry powder (HMDP) on glucose control and the associated metabolic phenotypes and further to compare its efficacy with HMPH. Male C57BL/6J mice on a high-fat diet for 7 weeks were randomized based on body weight and blood glucose into three groups. One group continued on the high-fat diet and was used as the insulin-resistant/diabetic control and the other two groups were given the high-fat diet modified to have 70% of casein protein being replaced with the same amount of protein from HMDP or HMPH. A group of mice on a low-fat diet all the time was used as the normal control. The results demonstrated that mice on the high-fat diet increased weight gain and showed higher blood concentrations of glucose, insulin, and leptin, as well as impaired glucose tolerance and pancreatic β-cell function relative to those on the normal control diet. In comparison with the high-fat diet, the replacement of 70% dietary casein protein with the same amount of HMDP or HMPH protein decreased weight gain and significantly improved the aforementioned biomarkers, insulin sensitivity or resistance, and β-cell function. The HMDP and HMPH showed similar effects on every parameter except blood lipids where HMDP decreased total cholesterol and non-HDL-cholesterol levels while the effect of HMPH was not significant. The results demonstrate that substituting 70% of dietary casein protein with the equivalent amount of HMDP or HMPH protein protects against obesity and diabetes, and HMDP is also beneficial to cholesterol homeostasis.
... Traditionally, taurine is administered as a dietary supplement in therapeutic trials. [23][24][25] Dietary taurine could be absorbed into the circulation system, whereas this process is highly dependent on the taurine transporters in intestinal epithelium. Herein, we show that the directly intravenous delivery can act as an efficient approach to enhance the retinal taurine level. ...
Objective
Retinitis pigmentosa causes progressive photoreceptor degeneration in the subjects while no clinical therapy exists. The present study sought to evaluate the potential protective effects of taurine on a pharmacologically induced RP animal model.
Methods
Photoreceptor degeneration in mice was induced by an intraperitoneal injection of N-methyl-N-nitrosourea (MNU). The MNU-administrated mouse received taurine treatment and then they were examined by electroretinography, spectral-domain optical coherence tomography, optokinetic test, and histological and immunohistochemistry assay.
Results
Prominent taurine deficiency was found in the retinas of MNU-administered mice. Intravenous taurine treatment increased significantly the retinal taurine level. Morphological studies showed that taurine could alleviate the retinal disorganizations in the MNU-induced mice. Taurine also ameliorated the visual impairments in the MNU-induced mice as evidenced by functional examinations. Immunostaining experiments demonstrated that both the M-cone and S-cone populations in the degenerative retinas are rescued by taurine. In particular, the M-cone photoreceptors in superior-temporal quadrant and the S-cone photoreceptors in inferior-nasal quadrant were preferentially rescued. Mechanism study showed that the photoreceptor apoptosis and oxidative stress in the degenerative retina were effectively alleviated by taurine treatment.
Conclusion
Taurine is protective against the MNU-induced photoreceptor degeneration. Systemic taurine administration may act as a promising therapeutic potion for retinopathies with chronic cycle.
