The University of Southampton
University of Southampton Institutional Repository

Programming of hormonal axes contributing to the link between fetal growth, diabetes and cardiovascular disease

Programming of hormonal axes contributing to the link between fetal growth, diabetes and cardiovascular disease
Programming of hormonal axes contributing to the link between fetal growth, diabetes and cardiovascular disease

Type 2 diabetes is though to be the result of a combined defect in the ability of the body to respond to insulin (insulin resistance) and an inability to compensate for this by increasing insulin secretion.

Previous work has suggested that babies that are born small are more insulin resistant as adults in middle age and later life. Previous studies have also indicated that alterations in other hormonal axes may be contributing to the insulin resistant state. Possible mechanisms include increased sympatho-adrenal activity or alterations in the hypothalamic pituitary adrenal axis leading to insulin resistance.

I have studied a cohort of 20 year old men and women in whom detailed information on birthsize was available. Using an established measure of insulin sensitivity, the intravenous glucose tolerance test, I have examined the relationship between size at birth, insulin sensitivity and insulin secretion in young adults where the confounding influences of obesity and physical inactivity are minimised. Male babies born small were less insulin sensitive but showed no defect in insulin secretion. The same trends were not seen in women.

Using spectral analysis of heart rate variability I have shown a relationship between the autonomic control of heart rate and insulin sensitivity. Men with increased cardiac sympathetic activity were more insulin resistant but this did not show relationships with birthsize. Again these trends were not seen in women. I have also studied the relationship between size at birth and plasma cortisol levels. Again men who were small at birth show higher 9.00 cortisol levels but there was no relationship with features of the insulin resistance syndrome. Subjects were small at birth show lower levels of overnight growth hormone hormone and melatonin production suggesting that fetal programming is occurring at the hypothalamic/pituitary level.

In conclusion size at birth predicts insulin resistance, an established cardiovascular risk, in young adult life. A number of other hormonal axes may be contributing to this risk.

University of Southampton
Flanagan, Daniel Edward Henry
03babc39-d808-4732-8688-b62f4a055caa
Flanagan, Daniel Edward Henry
03babc39-d808-4732-8688-b62f4a055caa

Flanagan, Daniel Edward Henry (1999) Programming of hormonal axes contributing to the link between fetal growth, diabetes and cardiovascular disease. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

Type 2 diabetes is though to be the result of a combined defect in the ability of the body to respond to insulin (insulin resistance) and an inability to compensate for this by increasing insulin secretion.

Previous work has suggested that babies that are born small are more insulin resistant as adults in middle age and later life. Previous studies have also indicated that alterations in other hormonal axes may be contributing to the insulin resistant state. Possible mechanisms include increased sympatho-adrenal activity or alterations in the hypothalamic pituitary adrenal axis leading to insulin resistance.

I have studied a cohort of 20 year old men and women in whom detailed information on birthsize was available. Using an established measure of insulin sensitivity, the intravenous glucose tolerance test, I have examined the relationship between size at birth, insulin sensitivity and insulin secretion in young adults where the confounding influences of obesity and physical inactivity are minimised. Male babies born small were less insulin sensitive but showed no defect in insulin secretion. The same trends were not seen in women.

Using spectral analysis of heart rate variability I have shown a relationship between the autonomic control of heart rate and insulin sensitivity. Men with increased cardiac sympathetic activity were more insulin resistant but this did not show relationships with birthsize. Again these trends were not seen in women. I have also studied the relationship between size at birth and plasma cortisol levels. Again men who were small at birth show higher 9.00 cortisol levels but there was no relationship with features of the insulin resistance syndrome. Subjects were small at birth show lower levels of overnight growth hormone hormone and melatonin production suggesting that fetal programming is occurring at the hypothalamic/pituitary level.

In conclusion size at birth predicts insulin resistance, an established cardiovascular risk, in young adult life. A number of other hormonal axes may be contributing to this risk.

This record has no associated files available for download.

More information

Published date: 1999

Identifiers

Local EPrints ID: 463828
URI: http://eprints.soton.ac.uk/id/eprint/463828
PURE UUID: c447d282-21af-427d-b9c2-02d200fe855e

Catalogue record

Date deposited: 04 Jul 2022 20:57
Last modified: 23 Jul 2022 02:15

Export record

Contributors

Author: Daniel Edward Henry Flanagan

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×