From a flounder pituitary cDNA library, cDNA clones encoding a 28-kDa glycoprotein produced by the pars intermedia of the pituitary were isolated and characterized. Nucleotide sequencing demonstrated a precursor of the 28-kDa protein, which consisted of 231 amino acid residues, to be cleaved into a signal peptide (24 amino acids) and a mature protein (207 amino acids) containing one N-glycosylation site. By comparison of amino acid sequences, the 28-kDa protein was found to be distantly and similarly related to growth hormone and prolactin. Consequently, it was named somatolactin. Somatolactin mRNAs were specifically expressed as 1.2 and 1.8 kb poly(A)+ RNAs in flounder pituitary.

Abstract. Children with simple obesity (SO) show increased linear growth with normal or high serum insulin-like growth factor-I (IGF-I) levels during prepubertal period, despite low GH secretion. We measured IGF-I, IGFBP-1, GHBP and other factors to clarify the hormonal relation between the nutrition and the linear growth in SO and compared these factors with children with normal short stature (NS). Subjects were 23 SO and 19 NS children, and their height standard deviation (SD) scores were 0.7 ± 0.2 SD and -3.4 ± 0.3 SD (mean ± SEM) (P<0.01), respectively. Oral glucose tolerance test (OGTT) was performed in all the subjects and GH-releasing factor (GRF) test was also performed in 13 of SO and 17 of NS. The peak levels of GH in the GRF test were significantly lower in SO than in NS (12.8 ± 1.7 vs. 39.8 ± 6.9 ng/ml) and showed a significantly positive correlation with IGFBP-1 (r= 0.63, P<0.01). Serum GHBP level and IGF-I level were significantly higher in SO than in NS on pubertal stage matching. There was a positive correlation between GHBP and insulin during OGTT (r=0.75, P<0.01). When the sum of the values during OGTT was expressed as L insulin, ~C-peptide and glucose were significantly higher in SO than in NS on pubertal stage matching. Basal and IGFBP-1 were significantly lower in SO than in NS, but IGFBP-3 levels showed no significant difference between the two groups either in prepuberty or midpuberty.In conclusion, it can be hypothesized that the overnutrition causes hyperinsulinemia which increases GH receptor and IGF-I secretion despite low GH secretion. Hyperinsulinemia also may increase free IGF-I by lowering IGFBP-1. These two mechanism are supposed to be the nutrition related hormonal changes in SO and can explain the growth of SO. In addition, the increased free IGF-I may contribute the decreased GH secretion due to negative feedback in SO.

Tanaka T, Satoh M, Yasunaga T, Horikawa R, Tanae A, Katsumata N, Tachibana K, Nose O, Hibi I. When and how to combine growth hormone with a luteinizing hormone‐releasing hormone analogue. Acta Pædiatr 1999; Suppl 428: 85–8. Stockholm. ISSN 0803–5326 The effect of combined treatment with growth hormone (GH) and a luteinizing hormone‐releasing hormone (LHRH) analogue, or GH alone, on pubertal height gain was assessed in an uncontrolled study in 15 boys and 10 girls with GH deficiency (GHD). Seven boys and six girls were treated with GH alone (group 1), and eight boys and four girls were treated with a combination of GH and an LHRH analogue during puberty (group 2). Mean ages (□ SD) at the start of GH treatment and at the onset of puberty were significantly lower in group 2 (8.0 □ 3.3 years and 11.2 □ 0.8 years, respectively, in boys, and 6.3 □ 1.6 years and 10.8 □ 0.7 years in girls) than in group 1 (12.8 □ 1.9 years and 13.7 □ 1.4 years in boys, and 11.2 □ 1.0 years and 12.5 □ 1.2 years in girls). Height at the onset of puberty was less in group 2 than in group 1, but the difference was significant only for the boys. Combination treatment was started at a mean age of 11.7 □ 1.2 years in boys and 11.5 □ 1.0 years in girls. The duration of the combination treatment was 5.1 □ 1.5 years in boys and 2.3 □ 0.7 years in girls. The duration of the period between the onset of puberty and the end of GH treatment was significantly longer in group 2 (6.8 □1.2 years in boys and 5.5 □ 1.0 years in girls) than in group 1 (4.3 □ 1.6 years in boys and 3.6 □1.4 years in girls). The pubertal height gain was also significantly greater in group 2 (36.7 □ 6.5 cm in boys and 29.0 □ 8.3 cm in girls) than in group 1 (21.9 □ 4.1 cm in boys and 18.6 □ 4.1 cm in girls). Final height was significantly greater in group 2 than in group 1 in boys. Although there was no significant difference in final height between groups in the girls, the change in height SDS from the start of GH treatment until final height was significantly greater in group 2 (2.7 □ 1.6 in boys and 4.5 □ 0.5 SD in girls) than in group 1 (1.0 □ 0.8 in boys and 1.8 □ 0.9 SD in girls), in both boys and girls. In conclusion, it appears that combination of an LHRH analogue and GH may increase the pubertal height gain and the final height of children with GHD. The improvement is attributed to the prolongation of the treatment period, permitting slow bone maturation, and to the maintenance of height velocity. This combination treatment appears to be more effective in boys than girls. To fully assess this therapeutic approach, prospective controlled studies are needed. □Growth hormone deficiency, growth hormone treatment, luteinizing hormone‐releasing hormone analogue, pubertal height gain

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