Tryptophan Prevents the Development of Non-Alcoholic Fatty Liver Disease

Figures & data

Figure 1 The addition of L-tryptophan (80 mg/kg) to a high-calorie diet (HCD) reduced lipid metabolism disorders in the liver. L-tryptophan reduced visceral fat accumulation (A), decreased total liver lipids (B) and triglycerides (C) compared to HCD rats but had no effect on hepatic total cholesterol (D). *Different from group I at p<0.05, ^#Different from group II at p<0.05 (One way ANOVA followed by Bonferroni post hoc test, N=10 rats/group).

Abbreviations: I, control rats; II, rats on HCD for 12 weeks; III, rats treated with L-tryptophan in addition to HCD.

Table 1 Histomorphometric Parameters of the Liver

Indicators	Control	High-Calorie Diet	High-Calorie Diet + L-Tryptophan (80 mg/kg)
Area, μm^2:
Hepatocyte	255.2±9.6	352.3±9.3*	293.9±13.0^#
Nucleus	34.8±1.8	38.7±1.6	37.9±1.4
Cytoplasm	220.4±8.1	313.6±8.5*	256.0±11.8^#
Nuclear-cytoplasmic ratio	0.158±0.005	0.123±0.007*	0.148±0.008^#
Number of hepatocytes, pcs (on an area of 23.000 μm^2)
Total	67.6±1.9	50.5±1.6*	58.9±1.8*^#
Mononuclear	65.4±2.0	48.7±1.5*	56.8±1.6*^#
Binuclear	2.2±0.2	1.8±0.2	2.1±0.3
Number of nucleolus in the hepatocyte nucleus	2.41±0.09	1.43±0.05*	1.77±0.05*^#
Number of lipid droplets (S >100 μm^2 on an area of 93.000 μm^2)	–	10.8±0.9	8.1±0.5^#
Relative area of sinusoids, %	12.3±0.6	4.9±0.3*	10.4±0.6^#
Vizotto coefficient	0.14±0.01	0.06±0.003*	0.13±0.01^#

Notes: Data are presented as mean ± sd. *Different from control group at p<0.05, ^#Different from rats, which exposure to high-calorie diet at p<0.05 (One way ANOVA followed by Bonferroni post hoc test, N=10 rats/group).

Figure 2 Representative images of histological slides of liver tissue ((A) Control rats, (B) Rats on high-calorie diet for 12 weeks and (C) Rats treated with L-tryptophan (80 mg/kg) in addition to high-calorie diet, Van Gieson stain, x800). 1 – mononuclear hepatocyte; 2 – binuclear hepatocyte; 3 – connective tissue cell; 4 – sinusoids; 5 – hepatocyte with numerous intracellular lipid drops; 6 – lipid drop S > 100 μm².

Table 2 Parameters of Respiration and Oxidative Phosphorylation of Hepatocyte Mitochondria

Parameters (nmol O2/min^−1/mg^−1)	Control	High-Calorie Diet	High-Calorie Diet + L-Tryptophan (80 mg/kg)
Oxidation substrate 5mM sodium succinate
V^S4	11.9±1.0	7.1±1.0*	9.4±1.2
V3	45.8±2.7	31.6±1.6*	36.8±1.6*
V4^ATP	12.6±1.3	11.7±0.9	12.3±1.3
V3 / V4^ATP	3.63±0.09	2.70±0.02*	2.99±0.09*^#
Oxidation substrate 5mM sodium glutamate + 2.5 mM malate
V^S4	8.3±1.0	9.2±1.2	8.8±1.7
V3	39.0±1.9	25.6±1.2*	32.5±1.8*^#
V4^ATP	9.8±0.7	10.4±1.0	10.5±1.2
V3 / V4^ATP	3.97±0.01	2.46±0.06*	3.09±0.05*^#

Notes: Data are presented as mean ± sd. *Different from control group at p<0.05, ^#Different from rats, which exposure to high-calorie diet at p<0.05 (One way ANOVA followed by Bonferroni post hoc test, N=10 rats/group).

Abbreviations: V^S₄, resting mitochondrial respiration; V₃, active respiration with ADP addition; V₄^ATP, controlled respiration; V₃ / V₄^ATP, respiratory control.

Figure 3 L-tryptophan (80 mg/kg) prevented disturbances in the impedance and reactivity of the liver tissue. L-tryptophan reduced the high-calorie diet (HCD) induced increase in impedance on 10⁴ Hz (A) and 10⁶ Hz (B), and also reduced the HCD-induced increase in reactance on 10⁴ Hz (C) and 10⁶ Hz (D) in liver. L-tryptophan neutralized the effect of HCD on the reactivity dispersion coefficient (E) in the liver tissue (E). *Different from group I at p<0.05, ^#Different from group II at p<0.05 (One way ANOVA followed by Bonferroni post hoc test, N=10 rats/group).

Abbreviations: I, control rats; II, rats on HCD for 12 weeks; III, rats treated with L-tryptophan in addition to HCD.

Data Sharing Statement

The datasets used and analyzed during the current study are included in this published article.