Evidence map›Paper›PMID 30236792›Full record

ArticleClinical therapeutics2018

Maternal Lipids and Fetal Overgrowth: Making Fat from Fat.

Linda A Barbour, Teri L Hernandez

Open access · greenAbstract read
In one paragraph

Article in Clinical therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Linda A BarbourDepartment of Medicine, Division of Endocrinology, Metabolism, and Diabetes. University of Colorado, Anschutz Medical Campus, Aurora, Colorado; Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado. Electronic address: lynn.barbour@ucdenver.edu.
Teri L HernandezDepartment of Medicine, Division of Endocrinology, Metabolism, and Diabetes. University of Colorado, Anschutz Medical Campus, Aurora, Colorado; College of Nursing, University of Colorado, Anschutz Medical Campus, Aurora, Colorado.
University of Colorado Anschutz Medical Campus · US

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Wendy M Kohrt · 1995 to 2026
$32.6M
Randomized Trial of Diet in GDM: Metabolic Consequences to Mother and OffspringR01DK101659 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI HERNANDEZ, TERI L · 2014 to 2018
$3.1M
Regulation of Maternal Fuel Supply and Neonatal AdiposityR01DK078645 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BARBOUR, LINDA ANNE · 2010 to 2014
$2.6M
NIDDK NIH HHS R01 DK078645NIDDK NIH HHS R01 DK101659
6 · The paper itself

Abstract

There is increasing recognition that maternal glucose concentrations lower than those previously used for diagnosis of gestational diabetes mellitus (GDM) and targeted for treatment can result in excess fetal growth. Yet, mothers with GDM who appear to have optimal glycemic control and mothers with obesity and normal glucose tolerance still have a significantly increased risk for delivering infants who are large for gestational age, or even more importantly, who have increased adiposity at birth. What is less appreciated is that in addition to glucose, maternal lipids are also substrates for fetal fat accretion and that placental lipases can hydrolyze maternal triglycerides (TGs) to free fatty acids for fetal-placental availability. Maternal TG levels are 40% to 50% higher on average in mothers with obesity and GDM compared to those in normal-weight mothers early in pregnancy and are sustained at higher levels throughout gestation. Increasing evidence supports that maternal TG, both fasting and postprandial, are also predictors of newborn adiposity (newborn %fat), a risk factor for childhood obesity, and that early exposure is at least as strong of a risk factor as later exposure in mothers with obesity. In the setting of maternal nutrient excess and maternal insulin resistance, which lead to fetal hyperinsulinemia, excess free fatty acid exposure in the fetus may result in lipid storage and fetal fat development in subcutaneous and possibly other depots. In this commentary, we provide further evidence to make a case for targeting maternal fasting and postprandial TG in mothers with obesity who have elevated TG in early pregnancy to determine whether a TG-lowering interventional approach might limit fetal overgrowth and potentially mitigate the intrauterine contribution to childhood obesity and metabolic disease.

Indexed as

Birth WeightBlood GlucoseChildDiabetes, GestationalFatty Acids, NonesterifiedFemaleFetal DevelopmentFetusGestational AgeHumansInfant, NewbornInsulin ResistanceLipid MetabolismObesityPlacentaPregnancyBlood GlucoseFatty Acids, NonesterifiedTriglyceridesfetal growthgestational diabetesinsulin resistancelipidsmaternal obesitynewborn fattriglycerides

Identifiers

PMID30236792
PMCPMC6195465
OpenAlexW2892316717

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.