Influence of dietary histidine on tissue histamine concentration, histidine decarboxylase and histamine methyltransferase activity in the rat

Lee, Nam Soo; Fitzpatrick, Dennis; Meier, Eileen; Fisher, Hans

doi:10.1007/bf01982463

Cited by 26 publications

(12 citation statements)

References 13 publications

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“…Supplemental histidine may have the potential to increase histamine production by gastric enterochromaffin cells and by mast cells. Indeed, one rat study has found that stomach levels of histamine are increased as histidine intake increases beyond normal dietary levels 49. Hence, in susceptible individuals, supplemental histidine could conceivably increase risk for peptic ulcers by boosting gastric acid secretion.…”

Section: Cautionsmentioning

confidence: 99%

Role of dietary histidine in the prevention of obesity and metabolic syndrome

2018

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Section: Cautionsmentioning

confidence: 99%

Role of dietary histidine in the prevention of obesity and metabolic syndrome

2018

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“…As was shown in a study with rats, the histamine content of many tissues was found to be in correlation with the histidine amount in the diet [17]. It is not impossible that this phenomenon plays also a role in man.…”

Section: Discussionmentioning

confidence: 88%

Urinary excretion of histamine and some of its metabolites in man: Influence of the diet

et al. 1984

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Urinary excretions of histamine, N tau-methylhistamine and N tau-methylimidazoleacetic acid have been determined in 10 normal subjects on 3 different diets, containing a very low protein, a low protein and a high protein amount. Foodstuffs which could contain histamine were excluded. The mean excretion of N tau-methylhistamine on the second day of each diet amounted to 0.861 mumol/24 h, 1.051 mumol/24 h and 1.378 mumol/24 h, respectively. The excretions of histamine and N tau-methylimidazoleacetic acid were not affected. In 6 normal persons on a protein low diet, the excretions of histamine, N tau-methylhistamine and N tau-methylimidazoleacetic acid have been determined for 10 days. On the fifth day, to 3 persons 200 mumol of histamine was given orally, the other 3 persons received a high protein diet. The persons receiving histamine showed a strongly enhanced excretion of N tau-methylimidazoleacetic acid, corresponding to 36.1% of the administered histamine, whereas the urinary excretions of histamine and N tau-methylhistamine were only slightly elevated. On the high protein diet, only the excretion of N tau-methylhistamine was slightly elevated. The urinary excretions of histamine in the female subjects sometimes showed unexpectedly high values. Most probably, this phenomenon is attributable to bacterial histamine production in the urogenital tract.

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“…Unexpectedly, the compensatory increase of Hdc expression was not observed in the LHD group. A previous study showed that an increase in dietary histidine enhanced Hdc enzymatic activity (41), suggesting that histidine itself might induce Hdc expression. The decreased histidine concentration in the cortex might reduce the expression of Hdc, although further studies are necessary to elucidate the mechanism of the mRNA expression.…”

Section: Downloaded Frommentioning

confidence: 99%

Insufficient Intake of L-Histidine Reduces Brain Histamine and Causes Anxiety-Like Behaviors in Male Mice

Yoshikawa

Nakamura

Shibakusa

et al. 2014

The Journal of Nutrition

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L-histidine is one of the essential amino acids for humans, and it plays a critical role as a component of proteins. L-histidine is also important as a precursor of histamine. Brain histamine is synthesized from L-histidine in the presence of histidine decarboxylase, which is expressed in histamine neurons. In the present study, we aimed to elucidate the importance of dietary L-histidine as a precursor of brain histamine and the histaminergic nervous system. C57BL/6J male mice at 8 wk of age were assigned to 2 different diets for at least 2 wk: the control (Con) diet (5.08 g L-histidine/kg diet) or the low L-histidine diet (LHD) (1.28 g L-histidine/kg diet). We measured the histamine concentration in the brain areas of Con diet-fed mice (Con group) and LHD-fed mice (LHD group). The histamine concentration was significantly lower in the LHD group [Con group vs. LHD group: histamine in cortex (means ± SEs): 13.9 ± 1.25 vs. 9.36 ± 0.549 ng/g tissue; P = 0.002]. Our in vivo microdialysis assays revealed that histamine release stimulated by high K(+) from the hypothalamus in the LHD group was 60% of that in the Con group (P = 0.012). However, the concentrations of other monoamines and their metabolites were not changed by the LHD. The open-field tests showed that the LHD group spent a shorter amount of time in the central zone (87.6 ± 14.1 vs. 50.0 ± 6.03 s/10 min; P = 0.019), and the light/dark box tests demonstrated that the LHD group spent a shorter amount of time in the light box (198 ± 8.19 vs. 162 ± 14.1 s/10 min; P = 0.048), suggesting that the LHD induced anxiety-like behaviors. However, locomotor activity, memory functions, and social interaction did not differ between the 2 groups. The results of the present study demonstrated that insufficient intake of histidine reduced the brain histamine content, leading to anxiety-like behaviors in the mice.

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Influence of dietary histidine on tissue histamine concentration, histidine decarboxylase and histamine methyltransferase activity in the rat

Cited by 26 publications

References 13 publications

Role of dietary histidine in the prevention of obesity and metabolic syndrome

Role of dietary histidine in the prevention of obesity and metabolic syndrome

Urinary excretion of histamine and some of its metabolites in man: Influence of the diet

Insufficient Intake of L-Histidine Reduces Brain Histamine and Causes Anxiety-Like Behaviors in Male Mice

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