First, 4 glycine supplementation studies since I last scanned in August-to-November 2016:
Vargas et al, 2017. Effect of oral glycine on the clinical, spirometric and inflammatory status in subjects with cystic fibrosis: a pilot randomized trial. BMC pulm med, 17(1), p.206.
Subjects with CF received, in random order, oral glycine (0.5 g/kg/day, dissolved in any liquid) and placebo...pulse oximetry improved after glycine intake (p = 0.04 vs. placebo). TNF-α in serum and IL-6 and G-CSF in sputum tended to decline at the end of the glycine period (p = 0.061, p = 0.068 and p = 0.04, respectively, vs placebo)...The clinical, spirometric and inflammatory status of subjects with CF improved after just 8 weeks of glycine intake, suggesting that this amino acid might constitute a novel therapeutic tool for these patients.
Heidari et al., 2018. Mitochondria protection as a mechanism underlying the hepatoprotective effects of glycine in cholestatic mice. Biomedi Pharmacother, 97, pp.1086-1095.
Mice underwent BDL operation and received glycine (0.25% and 1% w:v in drinking water) ... Glycine supplementation (0.25% and 1%) decreased mitochondrial swelling, reactive oxygen species, and lipid peroxidation. Moreover, glycine treatment improved mitochondrial membrane potential and restored liver mitochondrial ATP. On the other hand, it was found that glycine supplementation attenuated oxidative stress markers in the liver of BDL animals. Moreover, liver histopathological changes and collagen deposition were markedly mitigated by glycine treatment.
Venkatesh et al, 2017. Effect of arginine: lysine and glycine: methionine intake ratios on dyslipidemia and selected biomarkers implicated in cardiovascular disease: A study with hypercholesterolemic rats. Biomedi Pharmacother, 91, pp.408-414.
The effect of intake ratios of arginine (Arg): lysine (Lys) and glycine (Gly): methionine (Met) on lipid profile and selected cardiovascular disease markers, was studied, in rats maintained on a hypercholesterolemic diet. The rise in blood cholesterol was countered by 32%, 24%, and 49%, respectively, through increased oral supplementation of Arg, Gly, and Arg + Gly; a corresponding increase in plasma phospholipids at the end of the 8-week study was observed. The elevated plasma cholesterol to phospholipids ratio was countered by 27, 40, and 57%, respectively, through oral supplementation of Arg, Gly, and Arg + Gly. The elevation in hepatic cholesterol was lowered by 18, 29, and 51%, respectively, while phospholipids concentration was concomitantly increased by these amino acids. The elevated cholesterol to phospholipids ratio was, thus, significantly countered in the hypercholesterolemic situation by orally supplemented Arg, Gly, and Arg + Gly. Increased plasma asymmetric dimethylarginine (ADMA) levels, under hypercholesterolemic conditions, were lowered by 12, 15 and 34%, respectively, while plasma symmetric dimethylarginine (SDMA) levels were lowered by 14, 10 and 17%, respectively, with orally supplemented Arg, Gly and Arg + Gly. Only Gly and Arg + Gly decreased plasma homocysteine levels. Total nitric oxide (NO) concentration was considerably increased by Gly supplementation in hypercholesterolemic rats. Thus, altered ratios of Arg:Lys or Gly:Met offered beneficial influence on the lipid profile and plasma levels of ADMA, SDMA and homocysteine in hypercholesterolemic rats. Optimal beneficial effects, among ratios tested, was observed when Arg:Lys and Gly:Met ratios were maintained in ratios of 1:1 and 2:1, respectively.
Zeb and Rahman, 2017. Protective effects of dietary glycine and glutamic acid toward the toxic effects of oxidized mustard oil in rabbits. Food & function, 8(1), pp.429-436.
Oxidized, un-oxidized mustard oils, glycine and glutamic acid were given to rabbits alone or in combination. The biochemical responses were studied in terms of haematological and biochemical parameters and histopathology. It has been observed that biochemical and haematological parameters were adversely affected by the oxidized oil, while supplementation of both amino acids was beneficial in normalizing these parameters. Both amino acids alone have no significant effects, however, oxidized oil affected the liver by enhancing fat accumulation, causing hepatitis, reactive Kupffer cells and necrosis. The co-administration of oxidized oils with glycine or glutamic acid revealed significant recovery of the liver structure and function.
Not supplementation studies, but noteworthy:
José Alburquerque-Béjar et al, 2017. Remote ischemic conditioning provides humoural cross-species cardioprotection through glycine receptor activation. Cardiovasc res, 113(1), pp.52-60.
Remote ischaemic conditioning (RIC) (4 × 5min femoral occlusion/5min reperfusion) was applied to 10 male pigs, and blood was taken before and after the manoeuvre. Discriminant analysis of 1H-NMR spectra obtained from plasma dialysates allowed to demonstrate a different metabolic profile between control and postRIC samples, with lactate (2.671 vs. 3.666 μmol/mL), succinate (0.062 vs. 0.082 μmol/mL) and glycine (0.055 vs. 0.471 ± μmol/mL) being the main responsible for such differences. Plasma dialysates were then given to isolated mice hearts submitted to global ischaemia (35 min) and reperfusion (60 min), for 30 min before ischaemia or during the first 15 min of reflow. Infarct size was significantly reduced when postRIC dialysate was applied before ischaemia as compared with hearts pretreated with control dialysate (44.81 vs. 55.55%). Blockade of glycine receptors with strychnine 10 μM inhibited the protective effect caused by pretreatment with postRIC dialysate (52.76 vs. 51.92%), whereas pretreatment with glycine 3 mmol/L, but not succinate 100 μmol/L, mimicked RIC protection (41.90 in glycine-treated vs. 61.51 and 64.73% in succinate-treated and control hearts, respectively).
Lu et al, 2017. Glycine prevents pressure overload induced cardiac hypertrophy mediated by glycine receptor. Biochem pharmaco, 123, pp.40-51.
pre-treatment with glycine significantly attenuated murine cardiac hypertrophy induced by transverse aortic constriction or by administration of angiotensin II (Ang II). This action was associated with a suppressive extracellular signal-regulated kinase 1/2 phosphorylation in myocardium. The cardioprotective effect of glycine disappeared when endogenous glycine receptor α2 was knocked down by mRNA interference in rats. Co-culture experiments revealed that glycine could also antagonize Ang II stimulated release of transforming growth factor β and endothelin-1 by cardiomyocytes, which prevented an over-production of collagens in rat fibroblasts.
This one concurs with past studies finding mTORC1 activation, good for muscle hypertrophy or preventing sarcopenia, not so good in other studies for longevity:
Sun et al, 2016. Glycine regulates protein turnover by activating protein kinase B/mammalian target of rapamycin and by inhibiting MuRF1 and atrogin-1 gene expression in C2C12 myoblasts. J Nut, 146(12), pp.2461-2467.
Compared with control cells, 0.25-1.0 mmol glycine/L enhanced cell growth (by 12-15%) after 24 h (P < 0.05). Glycine treatment led to increased DNA replication (by 70-80%) while enhancing mTORC1 activation by upregulating Akt and inhibiting AMPK signaling (P < 0.05). Accordingly, glycine exposure increased (P < 0.05) the rate of protein synthesis (by 20-80%) and inhibited (P < 0.05) the rate of protein degradation (by 15-30%) in a concentration-dependent manner in C2C12 cells. These observations were validated by the use of an Akt inhibitor, LY294002, or an AMPK activator, AICAR.
There's also a new open access review:
Razak, et al, 2017. Multifarious beneficial effect of non-essential amino acid, glycine: a review. Oxid Med Cell Longevity, 2017.
