How does hyperthyroidism cause diarrhea?

[Polycherry]

According to Robbin's Pathology, hyperthyroidism leads to an overactivity of the sympathetic system.

It also goes on to mention that this sympathetic hyperstimulation in the gut leads to increased motility leading to diarrhea and malabsorption.

How would sympathetic stimulation cause hypermotility? Isn't the parasympathetic system responsible for it?

Also, how does hyperthyroidism increase the sympathetic tone?

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[gettheleadout]

The mechanism seems to be incompletely understood, but the interplay between thyroid hormone actions and responses to catecholamines throughout the body are quite complex. The distilled version for why thyrotoxicosis results in hypersympathetic manifestations like tachycardia is that the genes for β1-adrenergic receptors are under transcriptional control of a TRE, and so are upregulated by increased TR-signaling. If we conceptualize "sympathetic tone" to be central sympathoadrenal outflow, it's actually reduced in thyrotoxicosis / hyperthyroidism (the mechanism essentially being increased feedback inhibition by the thyroid hormones), but the increased peripheral sensitivity (via, among others, the mechanism above) overcomes this and results in the clinical picture of hypersympathetic symptoms.

Oh, and it's actually hyperdefecation [edit:typo corrected] ("pseudodiarrhea") that is seen, not frank diarrhea with watery stool and such. Frequency of defecation is increased, but stool is normally-formed.

For further reading, see: J. Enrique Silva and Suzy D.C. Bianco. Thyroid. February 2008, 18(2): 157-165. doi:10.1089/thy.2007.0252.

 

[Polycherry]

Thanks a lot!!
A couple of questions persist.

1. How is the sympathetic tone feedback inhibited? Is it due to the increased expression of adrenergic receptors on the presynaptic or something else?
2. Hyperdefecation is due to hyperstimulation of the gut peristalsis, right? So, how does thyroxine increase gut motility? Wouldn't upregulation of adrenergic receptors slow down the gut?

 

[gettheleadout]

Thanks a lot!!
A couple of questions persist.

1. How is the sympathetic tone feedback inhibited? Is it due to the increased expression of adrenergic receptors on the presynaptic or something else?
2. Hyperdefecation is due to hyperstimulation of the gut peristalsis, right? So, how does thyroxine increase gut motility? Wouldn't upregulation of adrenergic receptors slow down the gut?

Unfortunately I don't know the answers to those!

 

[liujw124]

ASAP, thyroid hormone increases the expression of β1-adrenergic receptor but this receptor is not expressed in GI tract. But meanwhile, TH also stimulates, in GI tract, α2 receptors the function of which is to contract sphincters of GI tract. That's why GI mobility is increased in hyperthyroidism.