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Relationships of maternal and paternal birthweights to features of the metabolic syndrome in adult offspring: an inter-generational study in South India

Relationships of maternal and paternal birthweights to features of the metabolic syndrome in adult offspring: an inter-generational study in South India
Relationships of maternal and paternal birthweights to features of the metabolic syndrome in adult offspring: an inter-generational study in South India
AIMS/HYPOTHESIS: The association between lower birthweight and metabolic syndrome may result from fetal undernutrition (fetal programming hypothesis) and/or genes causing both low birthweight and insulin resistance (fetal insulin hypothesis). We studied associations between the birthweight of parents and metabolic syndrome in the offspring.
METHODS: We identified men and women (aged 35-68 years), who had been born in Holdsworth Memorial Hospital, Mysore, India. We also identified the offspring (20-46 years) of these men and women. In total, 283 offspring of 193 mothers and 223 offspring of 144 fathers were studied. Investigations included anthropometry, oral glucose tolerance, plasma insulin and lipid concentrations and blood pressure. The metabolic syndrome was defined using WHO criteria.
RESULTS: Among the offspring, lower birthweight was associated with an increased risk of glucose intolerance (impaired glucose tolerance, impaired fasting glucose or type 2 diabetes) and higher cholesterol and triacylglycerol concentrations (p < 0.05 for all adjusted for sex and age). Most outcomes in the offspring, including most individual components of the metabolic syndrome, were unrelated to parental birthweight. However, both maternal and paternal birthweight were inversely related to offspring metabolic syndrome (odds ratio [OR] 0.36 [95% CI: 0.13-1.01] per kg, p = 0.053 for mother-offspring pairs; OR 0.26 [0.07-0.93], p = 0.04 for father-offspring pairs, adjusted for offspring age, sex, BMI and socioeconomic status). Maternal birthweight was inversely related to offspring systolic blood pressure (beta = -2.5 mmHg [-5.00 to 0.03] per kg maternal birthweight; p = 0.052).
CONCLUSIONS/INTERPRETATION: Factors in both parents may influence the risk of metabolic syndrome in their offspring. There are several possible explanations, but the findings are consistent with the fetal insulin (genetic) hypothesis.
cholesterol, plasma, metabolic syndrome, fasting, mothers, undernutrition, women, syndrome, blood, risk, fathers, anthropometry, hypothesis, india, glucose, glucose tolerance, diabetes, fetal, adult, aged, gene, insulin resistance, parents, methods, blood pressure, maternal, glucose intolerance, cardiovascular disease, insulin, odds ratio
0012-186X
43-54
Veena, S.R.
2acd1a9f-ce06-4cd2-bbdb-8f0057308e0e
Geetha, S.
c21d5a91-5301-4e42-a4df-38badd76ee96
Leary, S.D.
7d73ca65-d303-40d4-964b-ff0fb6635a70
Saperia, J.
f2156914-ce9d-4861-97f2-23901f89e0d1
Fisher, D.J.
a22f14ff-7cc9-4e74-ae56-85b0f8b648cc
Kumaran, K.
ea8fa175-5f63-4c5b-a9b2-e6861a59d89e
Coakley, P.
6d68ba63-ddf6-499c-9507-9106618f0a47
Stein, C.E.
e0a5e068-9730-401a-aed7-8ae32973fb2d
Fall, C.H.
7171a105-34f5-4131-89d7-1aa639893b18
Veena, S.R.
2acd1a9f-ce06-4cd2-bbdb-8f0057308e0e
Geetha, S.
c21d5a91-5301-4e42-a4df-38badd76ee96
Leary, S.D.
7d73ca65-d303-40d4-964b-ff0fb6635a70
Saperia, J.
f2156914-ce9d-4861-97f2-23901f89e0d1
Fisher, D.J.
a22f14ff-7cc9-4e74-ae56-85b0f8b648cc
Kumaran, K.
ea8fa175-5f63-4c5b-a9b2-e6861a59d89e
Coakley, P.
6d68ba63-ddf6-499c-9507-9106618f0a47
Stein, C.E.
e0a5e068-9730-401a-aed7-8ae32973fb2d
Fall, C.H.
7171a105-34f5-4131-89d7-1aa639893b18

Veena, S.R., Geetha, S., Leary, S.D., Saperia, J., Fisher, D.J., Kumaran, K., Coakley, P., Stein, C.E. and Fall, C.H. (2007) Relationships of maternal and paternal birthweights to features of the metabolic syndrome in adult offspring: an inter-generational study in South India. Diabetologia, 50 (1), 43-54. (doi:10.1007/s00125-006-0516-9).

Record type: Article

Abstract

AIMS/HYPOTHESIS: The association between lower birthweight and metabolic syndrome may result from fetal undernutrition (fetal programming hypothesis) and/or genes causing both low birthweight and insulin resistance (fetal insulin hypothesis). We studied associations between the birthweight of parents and metabolic syndrome in the offspring.
METHODS: We identified men and women (aged 35-68 years), who had been born in Holdsworth Memorial Hospital, Mysore, India. We also identified the offspring (20-46 years) of these men and women. In total, 283 offspring of 193 mothers and 223 offspring of 144 fathers were studied. Investigations included anthropometry, oral glucose tolerance, plasma insulin and lipid concentrations and blood pressure. The metabolic syndrome was defined using WHO criteria.
RESULTS: Among the offspring, lower birthweight was associated with an increased risk of glucose intolerance (impaired glucose tolerance, impaired fasting glucose or type 2 diabetes) and higher cholesterol and triacylglycerol concentrations (p < 0.05 for all adjusted for sex and age). Most outcomes in the offspring, including most individual components of the metabolic syndrome, were unrelated to parental birthweight. However, both maternal and paternal birthweight were inversely related to offspring metabolic syndrome (odds ratio [OR] 0.36 [95% CI: 0.13-1.01] per kg, p = 0.053 for mother-offspring pairs; OR 0.26 [0.07-0.93], p = 0.04 for father-offspring pairs, adjusted for offspring age, sex, BMI and socioeconomic status). Maternal birthweight was inversely related to offspring systolic blood pressure (beta = -2.5 mmHg [-5.00 to 0.03] per kg maternal birthweight; p = 0.052).
CONCLUSIONS/INTERPRETATION: Factors in both parents may influence the risk of metabolic syndrome in their offspring. There are several possible explanations, but the findings are consistent with the fetal insulin (genetic) hypothesis.

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More information

Published date: 2007
Keywords: cholesterol, plasma, metabolic syndrome, fasting, mothers, undernutrition, women, syndrome, blood, risk, fathers, anthropometry, hypothesis, india, glucose, glucose tolerance, diabetes, fetal, adult, aged, gene, insulin resistance, parents, methods, blood pressure, maternal, glucose intolerance, cardiovascular disease, insulin, odds ratio

Identifiers

Local EPrints ID: 61582
URI: http://eprints.soton.ac.uk/id/eprint/61582
ISSN: 0012-186X
PURE UUID: f5538a25-ab05-458d-b10c-7ae8a706b08a
ORCID for C.H. Fall: ORCID iD orcid.org/0000-0003-4402-5552

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Date deposited: 11 Sep 2008
Last modified: 16 Mar 2024 02:38

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Contributors

Author: S.R. Veena
Author: S. Geetha
Author: S.D. Leary
Author: J. Saperia
Author: D.J. Fisher
Author: K. Kumaran
Author: P. Coakley
Author: C.E. Stein
Author: C.H. Fall ORCID iD

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