l-Tryptophan alleviates fatty liver and modifies hepatic microsomal mixed function oxidase in laying hens

Akiba, Yukio; Takahashi, Kyoko; Horiguchi, Michiko; Ohtani, Hiromi; Saitoh, S.; Ohkawara, Hiroshi

doi:10.1016/0300-9629(92)90738-c

Cited by 16 publications

(15 citation statements)

References 36 publications

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“…In close relation to our findings, a recent study has indicated positive effects of indoleamine 2,3-dioxygenase, an enzyme that mediates the catabolism of L-TRP to L-kynurenine, on liver inflammation and fibrosis (32) . In earlier studies, TRP supplementation has been found to attenuate the development of NAFLD in laying hens (23,24) .…”

Section: Discussionmentioning

confidence: 91%

Effect of tryptophan supplementation on diet-induced non-alcoholic fatty liver disease in mice

et al. 2014

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Intestinal serotonin (5-hydroxytrypamine, 5-HT) metabolism is thought to play a role in gut functions by regulating motility, permeability and other functions of the intestine. In the present study, we investigated the effect of tryptophan (TRP), the precursor of 5-HT, supplementation on intestinal barrier functions and non-alcoholic fatty liver disease (NAFLD). An established mouse model of NAFLD induced by feeding a fructose-rich diet (N group) was used in the present study. TRP was administered orally for 8 weeks to C57BL/6J control or NAFLD mice. NAFLD-related liver parameters (hepatic TAG and Oil Red O staining), intestinal barrier parameters (tight-junction protein occludin and portal plasma lipopolysaccharides (LPS)) and 5-HT-related parameters (5-HT, 5-HT transporter (SERT) and motility) were measured. We observed reduced duodenal occludin protein concentrations (P¼0·0007), high portal plasma LPS concentrations (P¼0·005) and an elevated liver weight:body weight ratio (P¼ 0·01) in the N group compared with the parameters in the control group. TRP supplementation led to an increase in occludin concentrations (P¼ 0·0009) and consecutively reduced liver weight:body weight ratio (P¼ 0·009) as well as overall hepatic fat accumulation in the N group (P¼ 0·05). In addition, the N group exhibited reduced SERT protein expression (P¼ 0·002), which was normalised by TRP supplementation (P¼0·02). For the first time, our data indicate that oral TRP supplementation attenuates experimental NAFLD in mice. The underlying mechanisms are not clear, but probably involve stabilisation of the intestinal barrier in the upper small intestine and amelioration of the dysregulated intestinal serotonergic system.

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Section: Discussionmentioning

confidence: 91%

Effect of tryptophan supplementation on diet-induced non-alcoholic fatty liver disease in mice

et al. 2014

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“…Earlier studies conducted in hens have suggested that supplementation with the amino acid tryptophan (Trp) reduces hepatic lipid accumulation [ 56 ]. Recently, the influence of Trp supplementation on NAFLD induced by a fructose-rich diet was studied in C57BL/6J mice, as precursor of serotonin, a regulator of the intestinal motility and permeability [ 51 ].…”

Section: Therapeutic Agentsmentioning

confidence: 99%

Relevant Aspects of Nutritional and Dietary Interventions in Non-Alcoholic Fatty Liver Disease

Hernández-Rodas

Valenzuela

Videla

2015

IJMS

114

101

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Non-alcoholic fatty liver disease (NAFLD) is the main cause of liver disease worldwide. NAFLD is linked to circumstances such as type 2 diabetes, insulin resistance, obesity, hyperlipidemia, and hypertension. Since the obesity figures and related comorbidities are increasing, NAFLD has turned into a liver problem that has become progressively more common. Currently, there is no effective drug therapy for NAFLD; therefore, interventions in lifestyles remain the first line of treatment. Bearing in mind that adherence rates to this type of treatment are poor, great efforts are currently focused on finding novel therapeutic agents for the prevention in the development of hepatic steatosis and its progression to nonalcoholic steatohepatitis and cirrhosis. This review presents a compilation of the scientific evidence found in the last years showing the results of interventions in lifestyle, diet, and behavioral therapies and research results in human, animal and cell models. Possible therapeutic agents ranging from supplementation with vitamins, amino acids, prebiotics, probiotics, symbiotics, polyunsaturated fatty acids and polyphenols to interventions with medicinal plants are analyzed.

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“…TRP has been used to alter the intestinal serotonin homeostasis, since intra peritoneal treatment with TRP enhances 5-HT levels [20,21]. Surprisingly, it also has been reported that TRP is capable of reducing hepatic lipid accumulation in particular animal models [22,23] and plasma triglycerides in humans [24]. In addition, TRP is able to exert anti-inflammatory effects in the liver [25].…”

Section: Introductionmentioning

confidence: 99%

Role of serotonin in fatty acid-induced non-alcoholic fatty liver disease in mice

et al. 2013

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BackgroundSaturated fatty acids are thought to be of relevance for the development of non-alcoholic fatty liver disease and obesity. However, the underlying mechanisms are poorly understood. In previous studies we found that food-derived carbohydrates such as fructose alter the intestinal serotonergic system while inducing fatty liver disease in mice. Here, we examined the effect of fatty acid quantity (11% versus 15%) and quality (saturated, monounsaturated, or polyunsaturated fatty acids) on hepatic fat accumulation, intestinal barrier and the intestinal serotonergic system.MethodsC57BL/6 mice had free access to diets enriched with one of the three fatty acids or standard diet, for 8 weeks. In an additional experiment mice were fed diets enriched with saturated, monounsaturated fatty acids or standard diet supplemented with tryptophan (0.4 g/(kg.d), 8 weeks) or not. Hepatic fat accumulation, small intestinal barrier impairment and components of the serotonergic system were measured with RT-PCR, western blot or immunoassays. For statistical analysis t-test and one-way ANOVA with Tukey’s post hoc test and Bartlett’s test for equal variances was used.ResultsHepatic triglycerides, liver weight and liver to body weight ratio were significantly changed depending on the fat quality but not fat quantity. In contrast, fat quantity but not quality decreased the expression of the tight junction proteins occludin and claudin-1 in the small intestine. These changes seemed to result in enhanced portal vein endotoxin concentrations and fatty liver disease after feeding diet enriched with saturated and monounsaturated fatty acids but not polyunsaturated fatty acids. Neither fatty acid quantity nor quality significantly influenced the intestinal serotonergic system. Similarly, tryptophan supplementation had no impact on small intestinal barrier or fatty liver disease.ConclusionIn conclusion, diets rich in saturated or monounsaturated fatty acids promote the development of fatty liver disease in mice, likely by a dysfunction of the small intestinal mucosal barrier.

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l-Tryptophan alleviates fatty liver and modifies hepatic microsomal mixed function oxidase in laying hens

Cited by 16 publications

References 36 publications

Effect of tryptophan supplementation on diet-induced non-alcoholic fatty liver disease in mice

Effect of tryptophan supplementation on diet-induced non-alcoholic fatty liver disease in mice

Relevant Aspects of Nutritional and Dietary Interventions in Non-Alcoholic Fatty Liver Disease

Role of serotonin in fatty acid-induced non-alcoholic fatty liver disease in mice

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