Evidence map›Paper›PMID 37876538›Full record

ArticleFrontiers in endocrinology2023

High-fat diet impairs glucose homeostasis by increased p16 beta-cell expression and alters glucose homeostasis of the progeny in a parental-sex dependent manner.

Rene Escalona, Carlos Larqué, Daniela Cortes, Ricardo Vilchis, Emiliano Granados-Delgado, Abigail Sánchez, Guadalupe Sánchez-Bringas, Haydée Lugo-Martínez

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Rene EscalonaLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Carlos LarquéLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Daniela CortesLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Ricardo VilchisLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Emiliano Granados-DelgadoLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Abigail SánchezLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Guadalupe Sánchez-BringasLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Haydée Lugo-MartínezLaboratory of Embryology and Genetics, Departamento de Embriología y Genética, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Obesity consists in the accumulation of adipose tissue accompanied by low grade chronic inflammation and is considered a pandemic disease. Recent studies have observed that obesity affects females and males in a sex-dependent manner. In addition, several works have demonstrated that parental obesity increases the risk to develop obesity, insulin resistance, diabetes, and reproductive disorders. Considering that intergenerational effects of obesity may occur in a sex-dependent manner, we studied male Methods: Five-week-old female and male Results and conclusions: HFD altered plasma fasting glucose, insulin and leptin levels, glucose tolerance, adiposity, and beta-cell expression of p16 in F0 rats. Particularly, HFD showed sexual dimorphic effects on body weight gain and insulin sensitivity. Moreover, we observed that parental HFD feeding exerts parental-sex-specific metabolic impairment in the male progeny. Finally, parental metabolic dysfunction could be in part attributed to the increased beta-cell expression of p16; other mechanisms could be involved in the offspring glucose homeostasis.

Indexed as

Insulin ResistanceLeptinAnimalsDiet, High-FatFemaleGlucoseHomeostasisInsulinMaleObesityRatsRats, WistarWeight GainGlucoseInsulinLeptinadiposityhyperinsulinemiaimpaired-glucose toleranceintergenerationalobesityparental-obesitysexual dimorphism

Identifiers

PMID37876538
PMCPMC10591070
OpenAlexW4387454212

What Socratic holds

Textmetadata
LicenceCC BY
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.