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Histidine supplementation ameliorates metabolic syndrome
A recent Chinese supplementation study, in which obese middle-aged women diagnosed with metabolic syndrome received 12 weeks of supplemental histidine (2 g, twice daily) or matching placebo, achieved remarkable findings.1 Insulin sensitivity improved significantly in the histidine-supplemented subjects, and this may have been partially attributable to loss of body fat. Body mass index (BMI), waist circumference and body fat declined in the histidine-supplemented group relative to the placebo group; the average fat loss in the histidine group was a robust 2.71 kg. Markers of systemic inflammation such as serum tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-6, non-esterified fatty acids and oxidative stress also decreased in the histidine group. Subsequently, precisely parallel findings were reported in female rats rendered obese with a high-fat diet.2
Brain histamine influences appetite and metabolic rate
These intriguing findings were not altogether unexpected, as earlier rodent studies had shown that supplemental histidine tends to inhibit food intake, via an impact on the hypothalamus that is mediated by the neurotransmitter histamine.3–6 Acting via H1 receptors in the ventromedial and paraventricular hypothalamic nuclei, histamine suppresses feeding behaviour, promotes adipocyte lipolysis via sympathetic activation and raises metabolic rate.3 7 8 These effects are analogous to those of leptin on the brain, and indeed histamine has been shown to be a key mediator of leptin signalling in the hypothalamus.4 9 Leptin triggers histamine release in the hypothalamus, and histamine in turn prevents the downregulation of leptin receptors which mediates leptin resistance. Crucially, whether administered intraperitoneally or intraventricularly, histidine dose dependently increases hypothalamic levels of histamine as well as hypothalamic activity of histidine decarboxylase, the enzyme which converts histidine to histamine.10 Such administration also inhibits food consumption—an effect that is blocked in animals pretreated with an irreversible inhibitor of histidine decarboxylase.
Neuronal histamine release in the hypothalamus is subject …
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