Hi /r/diabetes. I don’t have diabetes. I’m an MDMA (ecstasy) user who has been looking into the possibility that taurine supplementation may help prevent some of the neurotoxic effects of MDMA. Here’s my big post about that if you wanna read it.
While I was doing that research, I also kept coming across papers mentioning that taurine may help prevent some of the complications caused by diabetes. To quote one of the papers below research:
There is overwhelming evidence that taurine treatment diminishes the severity of complications among the major targets of diabetes, namely, the retina, the neuron, and the kidney.
I was surprised to see there hasn’t been much discussion of this on reddit, so I’m posting this here to bring it to your attention. If you want to see more of what Google Scholar has to offer, I recommend starting with a search for “taurine diabetes” and sorting by:
Below are the papers, I’ve singled out as giving the best overview of the evidence and proposed mechanisms of action. They are sorted from most recent to oldest. If the sci-hub links are blocked in your country, you can try the mirrors by changing the .tw in the URL to:
- .se
- .ltd
- .ren
- .zone
Effects and Mechanisms of Taurine as a Therapeutic Agent (2018)
There is overwhelming evidence that taurine therapy reduces pathology associated with diabetes, obesity and the metabolic syndrome (Schaffer et al., 2009; Ito et al., 2012; Imai et al., 2014; Murakami, 2015; Chen et al., 2016). In many animal studies, particularly of type II diabetes, taurine treatment diminishes the degree of hypoglycemia, an effect that in turn attenuates diabetic complications (Nakaya et al., 2000; Winiarska et al., 2009; Das and Sil, 2012; Kim et al., 2012; Chiang et al., 2014; Koh et al., 2014). Several mechanisms may contribute to the regulation of hyperglycemia in diabetic animals treated with taurine. First, taurine improves respiratory function and increases ATP production, effects that should improve pancreatic β-cell function and insulin secretion (Sivitz and Yorek, 2010; Schaffer et al., 2016). Second, hyperglycemia and lipidemia are associated with elevations in mitochondrial ROS generation. In pancreatic β-cells, fatty acid-mediated ROS generation appears to decrease insulin secretion, an effect attenuated by taurine treatment (Oprescu et al., 2007). Third, mitochondrial dysfunction can provoke insulin resistance (Sivitz and Yorek, 2010). Haber et al. (2003) found that taurine treatment prevents hyperglycemia-induced insulin resistance and oxidative stress. Together, these findings indicate that taurine protects against type 2 diabetes-mediated complications, but the mechanism by which taurine diminishes the development of the complications of type 2 diabetes remain unclear, largely because it is virtually impossible to separate the mitochondrial actions of taurine from its effects on insulin secretion and action.
On the other hand, in the streptozotocin-induced model of type 1 diabetes, plasma glucose levels remain unaltered by taurine treatment while the severity of the diabetic complications are diminished. Because diabetic status in the streptozotocin model of type 1 diabetes is unaffected by taurine, one can readily establish the mechanism underlying taurine’s effectiveness against the development of diabetic complications. According to several investigators, taurine-mediated reductions in the severity of type 2 diabetic complications are more closely linked to improvements in cellular stresses (ER, oxidative and inflammatory) and mitochondrial dysfunction (Schaffer et al., 2009; Ito et al., 2012; Imai et al., 2014). Trachtman et al. (1995) were the first group to recognize the benefit of taurine treatment against the development of diabetic complications. They reported that male rats administered streptozotocin developed a diabetic nephropathy characterized by elevated glomerular filtration rate, glomerular hypertrophy and proteinuria and albuminuria. Administration of taurine (1% in the drinking water) reduced proteinuria by 50% and dramatically suppress glomerular hypertrophy and tubointerstitial fibrosis without affecting blood glucose. Because the amino acid also abolished the elevation in renal cortical malondialdehyde, a marker of oxidative stress, and of advanced glycoloxidation products, a marker of advanced glycosylation end products, the protective effects of taurine were attributed to suppression of oxidative stress and advanced glycosylation. Recently, the effectiveness of taurine therapy against the development of diabetic nephropathy has been confirmed (Pandya et al., 2013; Koh et al., 2014). In a related study, Ikubo et al. (2011) found that streptozotocin-treated diabetic rats developed vascular defects that were associated with oxidative stress without a change in blood glucose. Interestingly, taurine also protects against apoptosis in cellular models of glucose toxicity (Ulrich-Merzenich et al., 2007).
Ameliorative effects of taurine against diabetes: a review (2017)
Sci-hub link to full text: https://sci-hub.tw/10.1007/s00726-018-2544-4
Abstract:
Diets in rats and humans have shown promising results. Taurine improved glucagon activity, promoted glycemic stability, modified glucose levels, successfully addressed hyperglycemia via advanced glycation end-product control, improved insulin secretion and had a beneficial effect on insulin resistance. Taurine treatment performed well against oxidative stress in brain, increased the secretion of required hormones and protected against neuropathy, retinopathy and nephropathy in diabetes compared with the control. Taurine has been observed to be effective in treatments against diabetic hepatotoxicity, vascular problems and heart injury in diabetes. Taurine was shown to be effective against oxidative stress. The mechanism of action of taurine cannot be explained by one pathway, as it has many effects. Several of the pathways are the advanced glycation end-product pathway, PI3-kinase/AKT pathway and mitochondrial apoptosis pathway. The worldwide threat of diabetes underscores the urgent need for novel therapeutic measures against this disorder. Taurine (2-aminoethane sulfonic acid) is a natural compound that has been studied in diabetes and diabetes-induced complications.
Conclusion:
Diabetes is gaining the status of a global epidemic, and interest in therapeutic research on diabetes is prevalent. Taurine is a non-proteinaceous amino acid, and its role in diabetes has been well studied, showing it is a promising therapeutic agent. Various studies have found that Taurine modifes glucose in diabetes, addresses hyperglycemia and modifies diabetes mellitus as well as secretion. It has a protective effect in diabetic neuropathy, brain damage, retinopathy, liver injury caused by diabetes and cardiovascular problems. The protective effect of taurine has been observed in the advanced glycation end-product pathway and the PI3-kinase/AKT and mitochondrial apoptosis pathways. Overall, taurine could be a good therapeutic strategy for diabetes.
The potential usefulness of taurine on diabetes mellitus and its complications (2012)
Abstract:
Taurine (2-aminoethanesulfonic acid) is a free amino acid found ubiquitously in millimolar concentrations in all mammalian tissues. Taurine exerts a variety of biological actions, including antioxidation, modulation of ion movement, osmoregulation, modulation of neurotransmitters, and conjugation of bile acids, which may maintain physiological homeostasis. Recently, data is accumulating that show the effectiveness of taurine against diabetes mellitus, insulin resistance and its complications, including retinopathy, nephropathy, neuropathy, atherosclerosis and cardiomyopathy, independent of hypoglycemic effect in several animal models. The useful effects appear due to the multiple actions of taurine on cellular functions. This review summarizes the beneficial effects of taurine supplementation on diabetes mellitus and the molecular mechanisms underlying its effectiveness.
Discussion:
As described in this article, numerous studies revealed that taurine supplementation is beneficial to diabetes and its complications in several animal models. Moreover, multiple actions of taurine coordinate to protect from diabetes and complications. Especially, suppressive effect of taurine against oxidative stress is associated with various pathways in diabetic condition. First, reactivity of taurine against aldehyde can contribute to the reduction of AGE and modified LDL. Second, scavenging action against HClO can reduce the LDL modification and increase in bioavailability of the NO. Finally, taurine is likely to inhibit the ROS production via regulation of mitochondria (reviewed in Schaffer et al. 2009). While very high taurine concentration is found in mitochondria, several roles of taurine in mitochondria have been proposed. Taurine-containing modified uridine has recently been discovered at wobble position in mitochondrial transfer RNA (tRNA) (Suzuki et al. 2002). Taurine-modified tRNA may play a crucial role in the translation of proteins responsible for electron transport (Kirino et al. 2004), suggesting that taurine depletion might cause a decrease in taurine-modified tRNA and impairs electron transport capacity. Moreover, buffering property of taurine in mitochondrial matrix has been reported (Hansen et al. 2010). Therefore, taurine depletion in diabetes may contribute to mitochondrial dysfunction and it is possible that restoration of taurine contributes to normalize mitochondrial function, which may associate with inhibition of the ROS production from mitochondria. To elucidate the role of taurine depletion in mitochondrial function and in the development of diabetic complications, further studies, such as investigations using taurine transporter knock-out animals (Ito et al. 2008), will be required.
Nevertheless, most of clinical studies failed to prove the beneficial role of taurine on insulin resistance and diabetic complications, whereas the others revealed the effectiveness. The discrepancies between animal experiments and clinical trials might be due to some limitations of clinical studies, such as a severity of the disease, other medications, given dose, duration of trial etc. Especially, the given dose of taurine per body weight is more than 10 times higher in animal experiments (e.g. diet containing 5% taurine) than in clinical trials (1.5–3 g taurine per day). Intake of taurine is thought to be quite safe as well as the amino acids found in food. While several reports strongly support that taurine is safe at levels up to 3 g/day, several clinical trials tested higher taurine dosages without adverse effects (Azuma et al. 1983, 1985; Shao and Hathcock 2008). Furthermore, since the pharmacological effect of taurine seems mild but not powerful, simultaneous therapy by using some medicines is also a problem. At present none of clinical studies have a sufficient numbers of patients. Therefore, long-term surveillance with large numbers of patients may be necessary to elucidate the effectiveness of taurine against diabetes or its complications in clinical study. Moreover, life style, such as diet, and genetic factors, such as genomic polymorphisms which relate to individual differences, can affect to the result of trials. It is known that urinary taurine concentration in human varies widely among individuals (Yamori et al. 2001). Brons et al. (2004) reported a wide variation in the increasing rate of plasma taurine concentration after taurine administration among individuals. These variations of taurine movement among individuals must differ dependent not only on life style but also genomic polymorphisms in taurine-related genes associated with the kinetics of taurine, such as taurine transporter. Therefore, we believe that the discovery of the genetic factors which determine the variation of taurine movement will help to elucidate the effectiveness of taurine against diabetes and its complications in humans.
Role of antioxidant activity of taurine in diabetes (2009)
Sci-hub link to full text: https://sci-hub.tw/10.1139/Y08-110
Abstract:
The unifying hypothesis of diabetes maintains that reactive oxygen species (ROS) generated in the mitochondria of glucose-treated cells promote reactions leading to the development of diabetic complications. Although the unifying hypothesis attributes the generation of oxidants solely to impaired glucose and fatty acid metabolism, diabetes is also associated with a decline in the levels of the endogenous antioxidant taurine in a number of tissues, raising the possibility that changes in taurine status might also contribute to the severity of oxidant-mediated damage. There is overwhelming evidence that taurine blocks toxicity caused by oxidative stress, but the mechanism underlying the antioxidant activity remains unclear. One established antioxidant action of taurine is the detoxification of hypochlorous acid. However, not all of the antioxidant actions of taurine are related to hypochlorous acid because they are detected in isolated cell systems lacking neutrophils. There are a few studies showing that taurine either modulates the antioxidant defenses or blocks the actions of the oxidants, but other studies oppose this interpretation. Although taurine is incapable of directly scavenging the classic ROS, such as superoxide anion, hydroxyl radical, and hydrogen peroxide, there are numerous studies suggesting that it is an effective inhibitor of ROS generation. The present review introduces a novel antioxidant hypothesis, which takes into consideration the presence of taurine-conjugated tRNAs in the mitochondria. Because tRNA conjugation is required for normal translation of mitochondrial-encoded proteins, taurine deficiency reduces the expression of these respiratory chain components. As a result, flux through the electron transport chain decreases. The dysfunctional respiratory chain accumulates electron donors, which divert electrons from the respiratory chain to oxygen, forming superoxide anion in the process. Restoration of taurine levels increases the levels of conjugated tRNA, restores respiratory chain activity, and increases the synthesis of ATP at the expense of superoxide anion production. The importance of this and other actions of taurine in diabetes is discussed. Key words: taurine, oxidative stress, taurine chloramines, antiinflammatory activity, mitochondria, tRNA conjugation, diabetes.
(This paper concludes with some words of caution that I wanted to highlight)
There is also reason to further evaluate the utility of taurine as a therapeutic agent. Animal studies showing that taurine supplementation increase insulin secretion and action have prompted the use of taurine as a potential therapeutic modality in the treatment of diabetes mellitus (Lampson et al. 1983; Mozaffari and Schaffer 2002, 2003; Tenner et al. 2003; Patriarca et al. 2005). These clinical trials have met with mixed results. Franconi et al. (1995) reported that plasma taurine levels, which are reduced in the untreated type 1 diabetic patient, are restored upon taurine supplementation. This restoration of taurine levels was associated with reduced platelet aggregation. However, in a similar study of type 2 diabetic patients, Spohr et al. (2005) failed to detect a beneficial effect of taurine supplementation on platelet aggregation. The same group also observed no difference in insulin-mediated glucose disposal in type 2 diabetic patients treated with taurine, suggesting to them that taurine supplementation does not prevent the development of type 2 diabetes (Brøns et al. 2004). Chauncey et al. (2003) also failed to find an improvement in glucose, lipid and insulin serum levels in the type 2 diabetic patient treated with taurine.
Because of the paucity of clinical studies, it is unclear whether the differences in response to taurine in the 4 studies relate to the unique properties of type 1 and type 2 diabetes, the period of intervention, the doses of taurine used in the antidiabetic supplement, the use of other agents to prevent diabetic complications, or the severity of the diabetic condition. Clinical trials using various antioxidants to treat cardiovascular disease have often proven disappointing. Therefore, it is unclear whether taurine will prevent diabetic complications ascribed to oxidative stress. Because the antioxidant actions of taurine are indirect, taurine therapy may represent a novel approach toward the treatment of oxidative injury. Therefore, clinical use of taurine must await the outcome of large-scale double-blind clinical trials to establish its efficacy and safety.
Social Plugin