Evidence map›Paper›PMID 25926796›Full record

ArticleFrontiers in pharmacology2015

Early pharmacological inhibition of angiotensin-I converting enzyme activity induces obesity in adulthood.

Kely de Picoli Souza, Elton D da Silva, Elice C Batista, Felipe C G Reis, Sylvia M A Silva, Charlles H M Castro, Jaqueline Luz, Jorge L Pesquero, Edson L Dos Santos, João B Pesquero

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

10 authors at 3 institutions in 1 country.

Kely de Picoli SouzaSchool of Environmental and Biological Science, Universidade Federal da Grande Dourados Dourados, Brazil.
Elton D da SilvaDepartment of Biophysics, Escola Paulista de Medicina, Universidade Federal de São Paulo São Paulo, Brazil.
Elice C BatistaDepartment of Biophysics, Escola Paulista de Medicina, Universidade Federal de São Paulo São Paulo, Brazil.
Felipe C G ReisDepartment of Biophysics, Escola Paulista de Medicina, Universidade Federal de São Paulo São Paulo, Brazil.
Sylvia M A SilvaDepartment of Physiology, Escola Paulista de Medicina, Universidade Federal de São Paulo São Paulo, Brazil.
Charlles H M CastroDepartment of Rheumatology, Escola Paulista de Medicina, Universidade Federal de São Paulo São Paulo, Brazil.
Jaqueline LuzDepartment of Physiology, Escola Paulista de Medicina, Universidade Federal de São Paulo São Paulo, Brazil.
Jorge L PesqueroDepartment of Physiology and Biophysics, Universidade Federal de Minas Gerais Belo Horizonte, Brazil.
Edson L Dos SantosSchool of Environmental and Biological Science, Universidade Federal da Grande Dourados Dourados, Brazil.
João B PesqueroDepartment of Biophysics, Escola Paulista de Medicina, Universidade Federal de São Paulo São Paulo, Brazil.
Universidade Federal de São Paulo · BRUniversidade Federal de Minas Gerais · BRUniversidade Federal da Grande Dourados · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have investigated early programming of body mass in order to understand the multifactorial etiology of obesity. Considering that the renin-angiotensin system (RAS) is expressed and functional in the white adipose tissue (WAT) and modulates its development, we reasoned whether early transitory inhibition of angiotensin-I converting enzyme activity after birth could modify late body mass development. Therefore, newborn Wistar rats were treated with enalapril (10 mg/kg of body mass) or saline, starting at the first day of life until the age of 16 days. Between days ninetieth and hundred and eightieth, a group of these animals received high fat diet (HFD). Molecular, biochemical, histological, and physiological data were collected. Enalapril treated animals presented hyperphagia, overweight, and increased serum level of triglycerides, total cholesterol and leptin, in adult life. Body composition analyses revealed higher fat mass with increased adipocyte size in these animals. Molecular analyses revealed that enalapril treatment increases neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) gene expression in hypothalamus, fatty acid synthase (FAS), and hormone-sensitive lipase (HSL) gene expression in retroperitoneal WAT, and decreases peroxixome proliferators-activated receptor (PPAR)γ, PPARα, uncoupling protein (UCP)2, and UCP3 gene expression in WAT. The results of the current study indicate that enalapril administration during early postnatal development increases body mass, adiposity and serum lipids in adulthood associated with enhanced food intake and decreased metabolic activity in WAT, predisposing to obesity in adulthood.

Indexed as

hyperphagiaNPYoverweightPPARrenin-angiotensin systemUCP

Identifiers

PMID25926796
PMCPMC4396349
OpenAlexW2016871464

What OpenQuestion 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 OpenQuestion graph.