Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Promotion of adipogenesis by neuropeptide Y during the later stages of chicken preadipocyte differentiation

Shipp SL., Cline MA., Gilbert ER.

Animal Study, published in Physiol Rep (2016) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Physiol Rep (2016)
Reported sample size
—
Source database
Europe PMC
PMID
27803314
PMCID
PMC5112489
DOI
10.14814/phy2.13006
Citations
12

Abstract (original English)

Neuropeptide Y (NPY) promotes adipogenesis in both birds and mammals, although mechanisms in avians remain unclear. The objective of this study was thus to evaluate effects of NPY on chick preadipocyte proliferation and differentiation. Preadipocytes were treated with 0, 1, 10, or 100 nmol/L NPY and gene expression and cellular proliferation were evaluated at 12, 24, and 48 h. At 12 h posttreatment, mRNA abundance of topoisomerase II alpha (TOP2A), and thioredoxin-dependent peroxidase 2 was upregulated and NPY was downregulated in response to NPY (0 vs. 100 nmol/L) in preadipocytes. Cells were also treated with NPY during differentiation and harvested at 8, 10, and 12 days postinduction of differentiation. At day 8 postinduction of differentiation, there was increased lipid accumulation (0 vs. 10 and 100 nmol/L), expression of CCAAT/enhancer binding protein β and fatty acid binding protein 4 (FABP4) (0 vs. 100 nmol/L), and sterol regulatory element-binding protein (0 vs. 10 and 100 nmol/L) mRNA in NPY-treated cells. The number of proliferating cells decreased on day 8 in response to NPY (0 vs. 10 nmol/L). At day 10, FABP4 and Kruppel-like factor 7 mRNAs were downregulated (0 vs. 10 and 100 nmol/L, and 100 nmol/L, respectively), and at day 12, TOP2A mRNA was down-regulated (0 vs. 100 nmol/L) in response to NPY treatment. Activity of glycerol-3-phosphate dehydrogenase (G3PDH) was

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Cells, CulturedAdipocytesAnimalsChickensNeuropeptide YRNA, MessengerCell DifferentiationCell ProliferationDown-RegulationMale

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.