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Evidence that Human Growth Hormone Is a Potent Lactogen in Primates^*

Department of Medicine, New York University School of Medicine New York, New York 10016 Medical Service, Veterans Administration Medical Center New York, New York 10010

Address requests for reprints to: Dr. David L. Kleinberg, Veterans Administration Medical Center, 408 First Avenue, New York, New York 10010.

To help determine if human GH (hGH) plays a physiological role in normal mammary function or diseases of the human breast, a study was undertaken to examine the lactogenic potency of hGH in a subhuman primate system. hGH was previously considered a relatively weak lactogen when tested in avian crop sac and rodent mammary assays. The effect of hGH on the production of -lactalbumin in organ cultures of primate mammary tissue was compared with the effect of equal concentrations of ovine PRL (oPRL).

Mammary tissues from seven adult rhesus monkeys were maintained in culture for 9 days (medium changed every 3 days) without and with oPRL or hGH in doses ranging from 30–1000 ng/ml. hGH was consistently more effective than oPRL in the stimulation of -lactalbumin production in over 90% of the cases. For example, mean (±SEM) -lactalbumin production at the 6-day time period in response to 1000 ng/ml hormone was 12.9 ± 3.3 ng/ml for oPRL and 61.9 ± 18 ng/ml for hGH. Overall, it was calculated that hGH had 328% the potency of oPRL in adult rhesus monkey mammary tissue.

In pigtail macaques, hGH was also a more potent stimulant of -lactalbumin production than oPRL, but the differences were not as great as in rhesus monkeys. -Lactalbumin in medium was higher in hGH-containing dishes than in those containing oPRL in over 85% of the cases. It was calculated that the lactogenic potency of hGH in macaque tissue was 160.5% that of oPRL. The differences between species were significant.

These results indicate that hGH is a more effective lactogen in subhuman primates than oPRL and suggest the possibility that GH may be a lactogen which has physiological importance.

^* This work was supported by the National Cancer Institute (Grant CA-16149), the Medical Research Service of the V.A., and NIH Grant RR-00166.

Received December 6, 1979.

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