Hypothalamic and Brain Thyrotropin-Releasing Hormone Content and Pituitary-Thyroid Function in Histidine-Deficient Rats

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Abstract
Because starvation is known to depress pituitary-thyroid function, and the essential amino acid histidine is a precursor of thyrotropin releasing hormone (TRH, pyroglutamyl-histidyl-prolinamide) the hypothesis was tested that histidine deficiency would decrease the secretion of TRH, and influence its concentration in extrahypothalamic brain. Rats given an histidine-deficient diet ad lib for 4 days lost weight compared with controls (-25 .+-. 3 vs. +15 .+-. 4 g; P < 0.001), showed a reduction in serum histidine (4.8 .+-. 0.9 vs. 11.6 .+-. 0.6 .mu.g/ml; P < 0.01) and brain histidine (2.4 .+-. 0.6 vs. 4.7 .+-. 0.7 .mu.g/g; P < 0.05), and a lowered serum thyroxine (T4) level (4.5 .+-. 0.4 vs. 5.7 .+-. 0.4 .mu.g/dl; P < 0.05), with non-significant reductions in serum thyroid stimulating hormone (TSH) and triiodothyronine (T3). There were no significant changes in the immunoreactive TRH levels in brain, hypothalamus and stalk median eminence (SME). In a 2nd experiment lasting 9 days, the controls were pair-fed, with both groups losing weight equally, serum and brain histidine levels were again markedly reduced in the rats receiving the histidine-deficient diet, but thyroid function (serum TSH, T4 and T3), a reflection of TRH secretion, was unaltered and the TSH levels in brain, hypothalamus, SME, anterior and posterior pituitary were similar in both groups. Histidine deficiency is not the cause of depressed thyroid function in starvation. In the rat dietary availability of histidine is not rate-limiting for TRH synthesis and secretion over a period of 9 days, although it is important for normal body growth.