Evidence map›Paper›PMID 39823439›Full record

ArticleEndocrinology2025

Hepatic and Pancreatic Cellular Response to Early Life Nutritional Mismatch.

Shubhamoy Ghosh, Amit Ganguly, Manal Habib, Bo-Chul Shin, Shanthie Thamotharan, Sture Andersson, Sherin U Devaskar

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

7 authors.

Shubhamoy GhoshDivision of Neonatology & Developmental Biology, Department of Pediatrics, UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, USA.
Amit GangulyDivision of Neonatology & Developmental Biology, Department of Pediatrics, UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, USA.
Manal HabibDivision of Endocrinology, Department of Pediatrics, UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, USA.
Bo-Chul ShinDivision of Neonatology & Developmental Biology, Department of Pediatrics, UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, USA.
Shanthie ThamotharanDivision of Neonatology & Developmental Biology, Department of Pediatrics, UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, USA.
Sture AnderssonDepartment of Pediatrics, Helsinki University Central Hospital, 00290 Helsinki, Finland.
Sherin U DevaskarDivision of Neonatology & Developmental Biology, Department of Pediatrics, UCLA Children's Discovery & Innovation Institute at the David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1752, USA.ORCID 0000-0002-7313-1189

Funding

In utero metabolic programming of the offspringR01HD041230 · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2001 to 2005
$1.9M
NICHD NIH HHS R01 HD041230NICHD NIH HHS R01 HD081206NIH HHS HD41230
6 · The paper itself

Abstract

To determine the basis for perinatal nutritional mismatch causing metabolic dysfunction-associated steatotic liver disease and diabetes mellitus, we examined adult phenotype, hepatic transcriptome, and pancreatic β-islet function. In prenatal caloric-restricted rats with intrauterine growth restriction (IUGR) and postnatal exposure to high fat with fructose (HFhf) or high carbohydrate, we investigated male and female IUGR-HFhf and IUGR-high carbohydrate, vs HFhf and control offspring. Males more than females displayed adiposity, glucose intolerance, insulin resistance, hyperlipidemia, and hepatomegaly with hepatic steatosis. Male hepatic triglyceride synthesis, de novo lipogenesis genes increased, while female lipolysis, β-oxidation, fatty acid efflux, and FGF21 genes increased. IUGR-HFhf males demonstrated reduced β-islet insulin and humanin, and type 1 diabetes mellitus human amniotic fluid increased humanin. Humanin suppression disabled glucose stimulated insulin, ATP production, with apoptotic diminished β-islet viability. Humanin and FGF21 may reverse perinatal nutritional mismatched phenotype by restoring functional β islets and preventing metabolic dysfunction-associated steatotic liver disease and diabetes mellitus.

Indexed as

Fetal Growth RetardationLiverPancreasPrenatal Exposure Delayed EffectsAnimalsDiet, High-FatFatty LiverFemaleFibroblast Growth FactorsHumansInsulin ResistanceInsulin-Secreting CellsMalePregnancyRatsRats, Sprague-Dawleyfibroblast growth factor 21Fibroblast Growth Factorsdiabetes mellitusFGF21glucose metabolismhumaninlipid metabolismmetabolic dysfunction associated steatotic liver disease

Identifiers

PMID39823439
PMCPMC11815087

What Socratic holds

Textmetadata
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 Socratic graph.