ArdisLabs Taurine (90 Count)

Taurine supplementation has anti-atherogenic and anti-inflammatory effects before and after incremental exercise in heart failure

• https://journals.sagepub.com/doi/10.1177/1753944717711138
• Patients with HF and left ventricle ejection fraction less than 50%, and placed in functional class II or III, were randomly assigned to two groups: (1) taurine supplementation; or (2) placebo.
• The taurine group received oral taurine (500 mg) 3 times a day for 2 weeks, and performed exercise before and after the supplementation period. The placebo group followed the same protocol, but with a starch supplement (500 mg) rather than taurine
• Our results indicate that inflammatory indices [C-reactive protein (CRP), platelets] decreased in the taurine group in pre-exercise, post-supplementation and post-exercise, post-supplementation as compared with pre-exercise, pre-supplementation ( p < 0.05) whereas these indices increased in pre-exercise, post-supplementation and post-exercise, post-supplementation as compared with pre-exercise, pre-supplementation in the placebo group ( p < 0.05).
• Our results also show that atherogenic indices [Castelli's Risk Index-I (CRI-I), Castelli's Risk Index-II (CRI-II) and Atherogenic Coefficient (AC)] decreased in the taurine group in pre-exercise, post-supplementation and post-exercise, post-supplementation as compared with pre-exercise, pre-supplementation ( p < 0.05). No such changes were noted in the placebo group ( p > 0.05).
• our results suggest that 2 weeks of oral taurine supplementation increases the taurine levels and has anti-atherogenic and anti-inflammatory effects

Ameliorative effects of taurine against diabetes

• https://link.springer.com/article/10.1007/s00726-018-2544-4
• Taurine modifies the glucose level in diabetes
• Tau alone lowered fructosamine and serum glucose levels, improved β-cell performance and decreased MDA and TAOC contents
• Tau improved blood glucose in a time-dependent manner (Rashid et al. 2013). In addition, 0.5 g Tau consumption twice per day in patients with type 1 diabetes who had already received insulin (n = 10) decreased triglycerides and improved carbohydrate metabolism (Elizarova and Nedosugova 1996), but 1.5 g/day (n = 30) for 90 days had no effect on glucose metabolism in patients with T2DM
• administration of 3 g/day Tau to patients with type 2 diabetes showed that (n = 32) administration for 4 months elevated Tau levels in plasma
• Among six men who were overweight or obese, intravenous lipid infusion for 48 h caused insulin resistance (IR), but a 2-week pretreatment with Tau 3 g/day improved insulin sensitivity and prevented the elevation of lipid peroxidation products (plasma). This result suggested that oral consumption of Tau administration ameliorated fatty acid-induced DM in humans.
• Taurine improves hyperglycemia
• Hyperglycemia leads to the accumulation of advanced glycation end products (AGEs) that have important functions in diabetic complications. As Tau is highly reactive with aldehydes, it has been thought to have a protective effect.
• In fact, Tau reduced the synthesis of glycated proteins, i.e., glycated hemoglobin, in rats fed fructose (Nandhini et al. 2004). Tau repressed hyperglycemia, lowered glycated hemoglobin in plasma, triglycerides and cholesterol in type I diabetic rats induced by STZ
• Taurine improves insulin resistance and secretion
• Tau supplementation restored insulin sensitivity in 11-week-old female progeny of low protein-fed dams,
• Tau strongly repressed glucose-stimulated insulin secretion in isolated mouse islets (Tokunaga et al. 1983), and intra-peritoneal injection of Tau inhibited the rise in serum insulin stimulated by glucose
• In contrast, Tau enhanced insulin secretion (induced by glucose) from cultured rat fetal islets (Cherif et al. 1996). Tau repressed hyperglycemia and improved IR (insulin resistance) in a rat model reared on a high fat diet (El Mesallamy et al. 2010) and enhanced insulin sensitivity and secretion following a large lipid infusion or in glucose models (Haber et al. 2003).
• The effect of Tau was observed to be similar to the maternal model of protein restriction, in which insulin secretion in response to the glucose load was reduced, and the decrease in pancreatic islet mass was prevented, perhaps due to a preventive effect on mitochondrial dysfunction in β-cells (Sturman 1993).
• Tau use hindered the start of diabetes in non-obese mice (Sturman, 1993). Tau increased Ca⁺² influx in mitochondria through the Ca⁺² uniporter, leading to increased mitochondrial metabolic activity and the ATP:ADP ratio and restored glucose-stimulated insulin secretion.
• Tau led to improvements in insulin sensitivity in diabetic rats (Haber et al. 2003). Tau intravenous injection protected GSIS (glucose-stimulated insulin secretion) impairment by lipids, as expected based on their ability to ameliorate the lipid-induced rise in islet ROS (Oprescu et al. 2007).

The Relationship between Plasma Taurine Levels and Diabetic Complications in Patients with Type 2 Diabetes Mellitus

• https://www.mdpi.com/2218-273X/9/3/96
• Fifty-nine patients with type 2 diabetes mellitus (T2DM), and 28 healthy control subjects between the ages of 32 and 82 were included in the study.
• The mean age of subjects was 55.6 ± 10.3 and mean diabetes duration was 10.2 ± 6.0 years.
• Plasma taurine concentrations were significantly lower in diabetic patients (0.6 ± 0.1 mmol/L) than controls (0.8 ± 0.2 mmol/L) and in hypertensive (0. 6 ± 0.1 mmol/L) patients (p = 0.000, p = 0.027 respectively)
• Plasma taurine levels were decreased in patients with T2DM, taurine levels may be more important in the development of diabetes

Tauroursodeoxycholic acid prevents hearing loss and hair cell death in Cdh23(erl/erl) mice

• https://linkinghub.elsevier.com/retrieve/pii/S0306452215011434
• Tauroursodeoxycholic acid (TUDCA), a taurine-conjugated bile acid, has been used in experimental research and clinical applications related to liver disease, diabetes, neurodegenerative diseases, and other diseases associated with apoptosis.
• Because hair cell apoptosis was implied to be the cellular mechanism leading to hearing loss in Cdh23(erl/erl) mice (erl mice), this study investigated TUDCA's otoprotective effects in erl mice: preventing hearing impairment and protecting against hair cell death.
• Our results showed that systemic treatment with TUDCA significantly alleviated hearing loss and suppressed hair cell death in erl mice. Additionally, TUDCA inhibited apoptotic genes and caspase-3 activation in erl mouse cochleae. The data suggest that TUDCA could be a potential therapeutic agent for human DFNB12.
• Article is purchasable

Taurine in sports and exercise

• https://www.tandfonline.com/doi/full/10.1186/s12970-021-00438-0 
• Peer-reviewed studies that investigated taurine as a single ingredient at dosages of < 1 g - 6 g, ranging from 10 to 15 min-to-2 h prior to exercise bout or chronic dose (7 days- 8 weeks)
• Key results include improvements in the following: VO2max, time to exhaustion (TTE; n = 5 articles), 3 or 4 km time-trial (n = 2 articles), anaerobic performance (n = 7 articles), muscle damage (n = 3 articles), peak power (n = 2 articles), recovery (n = 1 article). Taurine also caused a change in metabolites: decrease in lactate, creatine kinase, phosphorus, inflammatory markers, and improved glycolytic/fat oxidation markers (n = 5 articles). Taurine dosing appears to be effective at ~ 1–3 g/day acutely across a span of 6–15 days (1–3 h before an activity) which may improve aerobic performance (TTE), anaerobic performance (strength, power), recovery (DOMS), and a decrease in metabolic markers (creatine kinase, lactate, inorganic phosphate).

Taurine and atherosclerosis

• https://link.springer.com/article/10.1007/s00726-012-1432-6 
• Epidemiological studies have suggested that a high regular intake of taurine is associated with a reduced risk of developing cardiovascular disease (Yamori et al. 2001, 2009). It has also been reported that taurine is the second most abundant amino acid in the aorta (Kempf et al. 1970).
• Taurine has been shown to prevent the development of atherosclerosis in various kinds of animal models, including mice, rabbits, and quails.
• In one study, taurine supplementation prevented arterial lipid accumulation and decreased plasma levels of low density lipoprotein (LDL) and very low density lipoprotein (VLDL) cholesterol in mice fed with a high-fat/high-cholesterol diet (Murakami et al. 1999). In hyperlipidemia- and atherosclerosis-prone Japanese (LAP) quails, which develop severe atherosclerotic lesions in response to high-cholesterol diet, taurine supplementation markedly prevented the elevation of serum LDL and VLDL cholesterol levels and suppressed lesion formation (Murakami et al. 2010a).
• The data obtained from these diet-induced models of hyperlipidemia suggest that taurine prevents the elevation of non-high density lipoprotein (HDL) cholesterol and thereby retards the development of atherosclerosis.
• Taurine supplementation has been shown to reduce aortic lipid accumulation in apolipoprotein E (apoE)-deficient mice, a well-established animal model used for studying atherosclerosis (Kondo et al. 2001). taurine has been shown to suppress the progression of atherosclerosis in spontaneously hyperlipidemic (SHL) mice, Japanese wild mice with apoE gene disruption (Matsushima et al. 2003)
• taurine suppresses the development of atherosclerotic lesion formation without reducing serum cholesterol levels, suggesting the involvement of mechanisms other than cholesterol-lowering actions.
• Taurine supplementation has been shown to decrease serum and aorta levels of lipid peroxide in these animals. Similar anti-oxidative effects of taurine have also been observed in rabbits fed with a high-cholesterol diet (Balkan et al. 2002).
• Therefore, anti-oxidative effect exerted by taurine, in addition to cholesterol-lowering effects, may be associated with the prevention of atherosclerosis.

Effect of taurine on chronic and acute liver injury: Focus on blood and brain ammonia

• https://www.sciencedirect.com/science/article/pii/S2214750016300336?via%3Dihub
• The present study was conducted to evaluate the role of taurine (TA) administration on plasma and brain ammonia and its consequent events in different models of chronic and acute liver injury and hyperammonemia.
• Bile duct ligated (BDL) rats were used as a model of chronic liver injury
• Thioacetamide and acetaminophen-induced acute liver failure were used as acute liver injury models. A high level of ammonia was detected in blood and brain of experimental groups. An increase in brain ammonia level coincided with a decreased total locomotor activity of animals and significant changes in the biochemistry of blood and also liver tissue.
• TA administration (500 and 1000 mg/kg, i.p), effectively alleviated liver injury and its consequent events including rise in plasma and brain ammonia and brain edema.
• The data suggested that TA is not only a useful and safe agent to preserve liver function, but also prevented hyperammonemia as a deleterious consequence of acute and chronic liver injury.

Taurine and its analogs in neurological disorders: Focus on therapeutic potential and molecular mechanisms

• https://www.sciencedirect.com/science/article/pii/S2213231719301971?via%3Dihub
• Taurine significantly increased functional recovery and decreased glial fibrillary acidic protein accumulation and water content in the penumbral region after induced traumatic brain injury (TBI). It significantly prevented growth-related oncogene and interleukin (IL)-1β levels whereas elevating the levels of regulated on activation, normal T cell-expressed and -secreted (RANTES) in comparison with the TBI group.
• a one week treatment with taurine noticeably reduced levels of 17 cytokines, IL-1α, IL-1β, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-13, IL-17, tumor necrosis factor (TNF)-α, interferon-gamma, eotaxin, granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, leptin, monocyte chemotactic protein-1, and vascular endothelial growth factor (VEGF), while elevating the level of macrophage inflammatory protein 1 alpha only.
• The treatment with taurine effectually reversed brain injury severity in TBI by ameliorating brain edema, elevated activity of astrocytes and proinflammatory cytokines.
• Taurine (50 mg/kg) efficiently ameliorated pathological inflammation and injury in white matter after intracerebral hemorrhage, and upregulation of H2S content and reduction of P2X purinoceptor 7 expression may be connected to those effects
• Afterward, taurine prevented paraquat- and maneb-induced microglial M1 polarization and proinflammatory mediator expression. To initiate and maintain the M1 microglial inflammatory response, the p47phox and nuclear factor-κB (NF-κB) pathways are crucial. Taurine treatment inhibited the activation of NADPH oxidase by affecting both factors
• Taurine treatment (20–160 mM) shows a significant preventive action on cell proliferation while promoting the induction of hepatocellular carcinoma HepG2 cell apoptosis [44]. It can inhibit the proliferation of human lung cancer cell line A549 and the growth of transplanted tumors in nude mice
• Taurine also promotes the apoptosis in A549 cells by increasing the protein level of p53 upregulated modulator of apoptosis (PUMA) and bcl-2-like protein 4 (Bax) and decreasing the protein level of B-cell lymphoma 2 (Bcl-2)
• Taurine prevented nitric oxide-induced apoptotic cell death in murine RAW264.7 macrophages [46] and myocardial ischemia-induced apoptosis by preventing the assembly of the Apaf-1/caspase-9 apoptosome [47].
• Taurine displays neuroprotective activity against hypoxia-induced injury in rats by modulating apoptotic damage. Treatment with taurine (30 mg/kg, i.p., 18 days) increased Bcl-2 expression but reduced Bax and caspase-3 expression.