Evidence map›Paper›PMID 20943754›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2011

Somatostatin and its receptors contribute in a tissue-specific manner to the sex-dependent metabolic (fed/fasting) control of growth hormone axis in mice.

José Córdoba-Chacón, Manuel D Gahete, Justo P Castaño, Rhonda D Kineman, Raul M Luque

Abstract readComparative Study
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

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  13. Association between a polymorphic poly-T repeat sequence in the promoter of the somatostatin gene and hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2016
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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

5 authors at 4 institutions in 2 countries.

José Córdoba-ChacónDepartment of Cell Biology, Physiology, and Immunology, University of Cordoba, Instituto Maimónides de Investigación Biomédica de Córdoba, and Centro de Investigacion Biomedica en Red Fisiopatología de la Obesidad y Nutrición, Cordoba, Spain.
Manuel D Gahete
Justo P Castaño
Rhonda D Kineman
Raul M Luque
University of Córdoba · ESCentro de Investigación Biomédica en Red · ESInstituto Maimónides de Investigación Biomédica de Córdoba · ESUniversity of Illinois Chicago · US

Funding

Growth hormone and adult physiologyR01DK088133 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KINEMAN, RHONDA D · 2010 to 2013
$1.0M
NIDDK NIH HHS R01 DK088133PHS HHS NIDDK 30677
6 · The paper itself

Abstract

Somatostatin (SST) inhibits growth hormone (GH) secretion and regulates multiple processes by signaling through its receptors sst1-5. Differential expression of SST/ssts may contribute to sex-specific GH pattern and fasting-induced GH rise. To further delineate the tissue-specific roles of SST and sst1-5 in these processes, their expression patterns were evaluated in hypothalamus, pituitary, and stomach of male and female mice under fed/fasted conditions in the presence (wild type) or absence (SST-knockout) of endogenous SST. Under fed conditions, hypothalamic/stomach SST/ssts expression did not differ between sexes, whereas male pituitary expressed more SST and sst2A/2B/3/5A/5TMD2/5TMD1 and less sst1, and male pituitary cell cultures were more responsive to SST inhibitory actions on GH release compared with females. This suggests that local pituitary SST/ssts can contribute to the sexually dimorphic pattern of GH release. Fasting (48 h) reduced stomach sst2A/B and hypothalamic SST/sst2A expression in both sexes, whereas it caused a generalized downregulation of pituitary sst subtypes in male and of sst2A only in females. Thus, fasting can reduce SST sensitivity across tissues and SST input to the pituitary, thereby jointly contributing to enhance GH release. In SST-knockout mice, lack of SST differentially altered sst subtype expression levels in both sexes, supporting an important role for SST in sex-dependent control of GH axis. Evaluation of SST, IGF-I, and glucocorticoid effects on hypothalamic and pituitary cell cultures revealed that these hormones could directly account for alterations in sst2/5 expression in the physiological states examined. Taken together, these results indicate that changes in SST output and sensitivity can contribute critically to precisely define, in a tissue-dependent manner, the sex-specific metabolic regulation of the GH axis.

Indexed as

Amino Acid MotifsAnimalsCell LineCells, CulturedCorticosteroneFastingFemaleGastric MucosaGene Expression RegulationGrowth HormoneHypothalamusInsulin-Like Growth Factor IMaleMiceMice, Inbred C57BLMice, KnockoutCorticosteroneGrowth Hormoneinsulin-like growth factor-1, mouseInsulin-Like Growth Factor IProtein IsoformsReceptors, SomatostatinRNA, MessengerSomatostatin

Identifiers

PMID20943754
PMCPMC3023207
OpenAlexW2145126598

What OpenQuestion 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 OpenQuestion graph.