Evidence map›Paper›PMID 20062558›Full record

ArticleInternational journal of diabetes in developing countries2009

An investigation into genetic contribution to the relationship between insulin resistance and birth weight.

Samsad Jahan, Rahelee Zinnat, Zahid Hasan, Chowdhury Meshkat Ahmed, Samira Humaria Habib, Soma Saha, Liaquat Ali

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Article in International journal of diabetes in developing countries, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 82% of its field
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 4 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Samsad JahanDepartment of Gynecology and Obstetrics, BIRDEM, Dhaka, Bangladesh.
Rahelee Zinnat
Zahid Hasan
Chowdhury Meshkat Ahmed
Samira Humaria Habib
Soma Saha
Liaquat Ali
Bangladesh Institute of Research and Rehabilitation for Diabetes Endocrine and Metabolic Disorders · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin resistance has been proposed to be the most likely phenotypic trait that could represent a genetic link between low birth weight and type 2 diabetes, especially in Southeast Asia. Insulin resistance can persist for many years, even decades, before the manifestation of overt diabetes. There have been many studies suggesting a strong genetic basis in the etiology of type 2 diabetes mellitus. There is also ample evidence providing a link with low birth weight and type 2 diabetes in later life. Hence, parental insulin sensitivity could well serve as a representation of the offspring's future insulin resistance state. Association between maternal insulin sensitivity and the incidence of type 2 diabetes mellitus in low birth weight babies is confounded by many factors and hence, has limited value in the determination of any genetic origin of the disease. Therefore, the present study was done to investigate the relationship between paternal insulin sensitivity and the growth parameters of the foetus to determine a genetic link between poor early growth and the increased risk of type 2 diabetes mellitus in later life. MATERIALS AND

methodsThe study was performed on 30 healthy fathers and their babies born from nondiabetic mothers. Each father underwent a low-dose short insulin tolerance test (ITT) as a measure of insulin sensitivity. Placental weight was recorded and a blood sample was collected from the placental side of the umbilical cord at birth for measurement of insulin. Measurement of birth weight, length, and head circumference were recorded and ponderal index was calculated from the formula: weight (kg)/ length (cm)(3). Individual parameters of insulin resistance syndrome were measured in the fathers.

resultsThe degree of insulin sensitivity, K(m) (constant for insulin tolerance test) did not correlate with the fetal growth parameters (Ponderal Index r = 0.031, P = 0.870; weight of baby r = 0.010, P = 0.959; length of baby r = 0.087, P = 0.464; head circumference r = 0.280, P = 0.142) or with the fathers' anthropometric measures: body mass index (BMI), blood pressure, fasting glucose, insulin, and lipid profiles.

conclusionThe data suggest that the mechanism linking insulin resistance with low birth weight is not a genetically determined defect.

Indexed as

Birth weightgenetic contributioninsulin resistancetype 2 diabetes mellitus

Identifiers

PMID20062558
PMCPMC2802359
OpenAlexW2170676272

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.