An interesting paper has appeared that shows that a gene present in most vertebrates is absent in snakes. The gene is responsible for the production of the unpronounceable peptide ghrelin. Discovered in 1999, ghrelin is produced by a number of organs in the body and has a multitude of actions, sometimes acting as a true hormone via circulation in the blood and sometimes, it would seem, locally on cells in close proximity. The main source of ghrelin is the lining of the stomach and a major target for its action is the brain.
There are a lots of hormones acting within the body that have an effect on such physiological processes as appetite, satiety, metabolism and gut motility. There is what is perhaps best described as a control network rather than simple cause and effect pathways. There is clearly a great deal of redundancy in the sense of safety-net measures, parallel signalling, cross-talk and feedback that ensure a chemical signal gets through to its intended target, enable effects to come into play in response to changes in food intake, reproductive state etc, and for key variables, like blood glucose concentration to be regulated. One agent of this control network is Glucagon-like Peptide 1 (GLP-1), with which the obese and those who think they are obese are stuffing themselves, is one of those agents. Ghrelin is another. Ghrelin has been called the ‘hunger hormone’ because it promotes the desire to eat when injected. It also seems to have effects on the gut associated with food intake, on glucose metabolism as well as other functions in the brain like learning and memory. It also stimulates the storage of fat.
The authors of the paper pin the reason for the absence of ghrelin in snakes to their ability to go for very long periods without food. Although some snakes may lack that ability, the argument is still valid since the ancestors of snakes may have found selective advantage—or at least found no disadvantage from—a mutation that obliterated the ability to produce ghrelin. Thus it can be argued that all snakes, even those that can, do, or must, eat regularly inherited the condition from a common ancestor.
However, interpretation along those lines gets more complicated because the authors found the gene for ghrelin to be absent in the four species of chameleon examined and in two species of agama. In other words, the loss of ghrelin has happened independently at least three times in the snake-lizard lineage. The authors suggest that chameleons and the particular agamas (two species of Phrynocephalus) have similar lifestyles to the snakes as ‘sit-and-wait’ predators. That may be so but the chameleons do not sit and wait for that long, as anybody who has kept, bred and reared chameleons knows. Therefore, I am not convinced that the loss of ghrelin in particular lizards is necessarily connected with the ability to go without food for long periods.
In a similar vein, members of other groups that go without food for long periods do not lack ghrelin, the crocodilians coming immediately to mind.
A reminder that if you are reading this article other than on ‘Zoology Jottings’ it has been stolen.
Defining with any degree of certainty what ghrelin does in mammals also seems problematic. Mice in which the gene for ghrelin has been knocked out seem to get along fine with only seemingly minor physiological changes, sometimes in unexpected ways. The general view seems to be that in terms of appetite control, for example, it is part of a signalling pathway with a great deal of redundancy.
Ascribing presumed function to biologically active substances found in extant animals to what may have happened in evolutionary history falls into the category of a ‘just-so story’ after Rudyard Kipling’s book of children’s stories including such gems as ‘How the leopard got its spots’. In living animals I have long railed against assumptions that biologically active substances found in milk have a particular or, indeed, any function in the infant, and have suggested the evidence that must be obtained to test each hypothetical function. When applied to evolutionary matters the task is even more difficult or impossible. Fossils, infuriatingly, are not amenable to experiment.
I would argue that it is a pity the authors of the paper on the absence of ghrelin in snakes have written their account almost as a test of the hypothesis that the phenomenon can be explained by the ability to go without food for long periods. Other just-so stories could be plausible: the short alimentary canal with long transit times for digesta, with all that implies for digestion, absorption of nutrients, and gut motility, could be another. Or was loss of ghrelin in their early evolution of no selective consequence to snakes and chameleons; in other words just neutral?
Studies in comparative molecular endocrinology are extremely valuable in stimulating the sort of questions that need to be answered in extant snakes. In short, is the rest of the control network similar to that of other vertebrates, minus grhelin,
‘My conclusion on the story at present: ‘Just so’ but not ‘quite so’.
Pinto RR, Ruivo R, Stiller J, Oliveira D, Castro LFC, da Fonseca RR. 2026. Ghrelin and MBOAT4 are lost in Serpentes. Open Biology. 16: 250162.
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| ‘Sit-and-wait’ is the name of the game for these Common Boas (Boa constrictor) on Cayos Grande, one of the islets of the Cayos Cochinos archipelago off the Caribbean coast of Honduras. They lie on the branches waiting for a bird to land within striking distance since there are no mammals on the island. Our guess was that they were most likely to get the chance of a feed during the migration of large numbers of birds from and to North America. In the shade the boas are difficult for the untrained eye to spot. Once you eye is ‘in’ they are easy to spot in the undergrowth behind the beach. Their coloration is distinctive compared to those on the mainland and the pinkish hue gives rise to their local name of ‘pink’ boa. And if you are staying for lunch the fish and chips are excellent. |
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