Big little lizards: How hormones may affect species differently

When looking across many groups of organisms, we often see vast differences in body size when comparing males and females within a species. Sexual size dimorphism (SSD) describes this optimal difference in body size based on sex. Even closely related species may differ in whether they are considered female-larger or male-larger. Pituitary growth hormone (GH) is known to stimulate the production of hepatic insulin-like growth factor-1 (IGF-1). In vertebrates, this pathway is likely what causes tissues to grow. However, the mechanism of how hormones like testosterone regulate growth is not well known in all species. In male-larger species, it appears that testosterone stimulates growth. In female-larger species, testosterone may inhibit growth- but how?

Figure 1. Eastern fence lizard, S. undulatus, enjoying a little bask in the sunshine. Photo credit: Judy Gallagher.

Duncan et al. (2020) explores this mechanism in Eastern fence lizards (Sceloporus undulatus), a female-larger species. The authors offer two possible explanations for the mechanism in which testosterone affects growth:

 1.) the effects of testosterone are conserved in these lizards, and secondary mechanisms must be used to prevent growth stimulation.

2.) the effects of testosterone on IGF-1 are truly different in female-larger species, indicating an evolutionary reversal in the regulation of growth.

The authors compared the effects of hormone variation on growth and body sizes in adult and juvenile S. undulatus. They tested the effects of testosterone on body growth by studying several conditions, including placebo male and females, castrated males, castrated and hormone-implanted males, and hormone-implanted females. They also performed hormone assays to measure the amount of IGF-1 present in each group’s blood plasma after treatments.

Figure 2. (from Duncan et al. 2020). The snout-vent length (SVL) of juvenile S. undulatus lizards before and after the experimental treatments. Control females (JF-CON) exhibited the greatest SVL. Growth tapered in females treated with testosterone (JF-TEST), so that growth was similar to that of castrated males (JM-CAST). Males treated with testosterone (JM-TEST) had the lowest growth rate.  

Testosterone inhibited hepatic IGF-1 mRNA expression, which in turn reduced growth rate. This reduction in growth rate was seen comparatively in both sexes. The authors offered a proposed mechanism in which may simply explain these results: that testosterone interacts with androgen response elements to inhibit the expression of IGF-1 mRNA, rather than stimulate the expression.  

These results suggest that the mechanism in which testosterone affects growth in female-larger species may be caused from an evolutionary reversal in the role of testosterone. This would explain how the pathway is largely conserved, much like a reversal in the direction a light switch is wired. In the male-larger species, testosterone presence would turn the light switch “on” for growth. In the female-larger species, testosterone presence would turn the light switch “off” for growth. This and future studies will help us to better understand the regulation of hormones and the roles that hormones play across species. It is important to study the diversity in these mechanisms if we want to understand the endocrinology, physiology, and morphology of a wide range of vertebrate groups.

Amanda M. Palecek-McClung is a PhD student at Clemson University. She studies functional morphology, biomechanics, and adhesion mechanisms in fish and other vertebrates. You can find more about her at ampalecek.weebly.com or contact her at apalece@g.clemson.edu.

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