Table 2.
Effect of L-arginine in the treatment of lipid metabolism disorders.
| Cell Testing | ||||||
| Study (Year) | Cell Line |
Dose(s) of
L-Arginine Tested |
Control Culture | Outcome | ||
| Tsao et al. (1994a) [79] | mononuclear cells of New Zealand White rabbits + WEHI 78/24 | 2.25% L-arginine HCl in water (animals) |
+ | Endothelial adhesiveness is attenuated by L-arginine; NO acts as an endogenous antiatherogenic agent; L-arginine normalizes NO-dependent vasodilation and inhibits atherogenesis in a hypercholesterolaemic rabbits | ||
| Zhang et al. (2020) [80] | aortic endothelial cells of Sprague-Dawley rats | 1 g/kg bw/day (injection to animals) + 5, 25, 50 mM (isolated cells) | + | L-arginine inhibits the expression of miR-221 and increases the expression of eNOS in cells; L-arginine exerts milder effects than simvastatin, but presumably has fewer side effects | ||
| Animal Testing | ||||||
| Study, Year |
Duration
of Experiment |
Dose(s) of
L-Arginine Tested |
Control
Group |
Number
of Animals per Group |
Animal
Model |
Outcome |
| Cooke et al. (1992) [81] | 10 weeks | 2.25% L-arginine HCI in water |
+ | 16–20 | New Zealand White rabbits | L-arginine, as a endothelium-derived relaxing factor precursor, improves endothelium-dependent vasorelaxation |
| Tsao et al. (1994b) [82] | 10 weeks | 2.25% L-arginine HCI in water |
+ | 3 | New Zealand White rabbits | L-arginine has antiatherogenic properties and inhibits platelet aggregation in hypercholesterolaemic rabbits; the effect is presumably due to the increase in NO production |
| Nematbakhsh et al. (2008) [83] | 4 weeks | 3% L-arginine in water |
+ | 14–16 | white rabbits | L-arginine exerts no effect on T-C level, but increases nitrite concentration; L-arginine restores endothelial function in hypercholesterolaemic rabbits by the inhibition of apoptosis in endothelial cells |
| Méndez and Balderas (2001) [84] | 12 days | 10 mM/day (intraperitoneal injection) | + | 5–48 | Sprague-Dawley rats | L-arginine normalizes glycaemia and alleviate hyperlipidaemia by reducing TG, T-C and LDL-C levels in diabetic rats |
| El-Kirsh et al. (2011) [85] | 8 weeks | 100 mg/kg bw/day orally | + | 8 | albino rats | L-arginine has hypocholesterolaemic and hypolipidaemic effects; it regulates AST and ALT activities, urea level and lipid profile biomarkers; L-arginine, by promoting NO production, regulates biochemical disturbances and progression of aortic diseases; in high-fat and high-cholesterol diet fed rats. |
| Aly et al. (2014) [86] | 8 weeks | 10 mM/kg bw/day orally | + | 15 | Sprague-Dawley rats | L-arginine increases insulin and HDL-C levels, and decreases glucose, LDL-C, T-C and TG levels; L-arginine attenuates insulin resistance in diabetic rats |
| Human Research | ||||||
| Study, Year |
Duration
of Experiment |
Dose(s) of
L-Arginine Tested |
Control
Group |
Number
of Subjects per Group |
Outcome | |
| Hurson et al. (1995) [87] | 2 weeks | 17 g/day orally | + | 15–30 | L-arginine improves nitrogen balance, elevates serum IGF-1 concentrations, and reduces T-C and LDL-C levels in elderly humans; no adverse effects were observed | |
| Clarkson et al. (1996) [88] | 12 weeks (4 weeks of intervention) |
3 × 7 g/day orally | cross-over study | 27 | L-arginine has no effect on lipid profile (TG, T-C, HDL-C, LDL-C levels); L-arginine improves endothelium-dependent dilation in hypercholesterolaemic young adults, which might attenuate atherogenic processes | |
| Blum et al. (2000) [89] | 3 months (1 month of intervention) |
3 × 3 g/day orally | cross-over study | 10 | L-arginine increases growth hormone level, but does not affect insulin, catecholamines and lipid profile (TG, T-C, HDL-C, LDL-C, VLDL-C levels) in postmenopausal women | |
| Schulze et al. (2009) [90] | 18 weeks (6 weeks of intervention) |
2 × 1.5 g/day orally | + | 11–22 | L-arginine + simvastatin reduces TG level compared to placebo + simvastatin; L-arginine attenuates increases in AST and fibrinogen induced by simvastatin; L-arginine intensifies effects of simvastatin on lipid metabolism markers, but it has no effects when given alone in patients with hypertriglyceridaemia | |
| Nascimento et al. (2014) [91] | 3 weeks (1 week of intervention) |
3 × 2 g/day orally | cross-over study | 7 | No effects on TG, T-C and adiponectin levels were observed; L-arginine decreases LDL-C and non-esterified fatty acids levels; L-arginine can enhance effects of exercise inducing changes in lipid profile in overweight men | |
| Tripathi et al. (2012) [92] | 15 days | 3 g/day orally | + | 60–70 | L-arginine administration was found to improve the lipid profile in patients with acute myocardial infarction; L-arginine regulates modified cholesterol levels and increases HDL-C; L-arginine might be useful against precipitation of myocardial ischemia in elderly population | |
| Pahlavani et al. (2017) [93] | 45 days | 2 g/day orally | + | 28 | L-arginine improves glycaemia and lipid profile (TG, T-C, LDL-C, HDL-C), but has no effect on blood pressure in male athletes | |
| Dashtabi et al. (2016) [94] | 8 week | 3 × 3 or 6 g/day orally | + | 27–28 | L-arginine decreases, blood pressure, glycaemia, MDA, TG, T-C, LDL-C and levels and increases HDL-C level; L-arginine improves anthropometric parameters, blood pressure and blood biochemical indices in patients with obesity | |
| Schulman et al. (2006) [35] | 6 months | 3 × 3 g/day orally | + | 28–30 | L-arginine does not improve measurements related to vascular stiffness or ejection fraction; supplementary L-arginine might be associated with higher postinfarction mortality and should not be recommended for elderly patients after acute myocardial infarction | |