Evidence map›Paper›PMID 27533078›Full record

ArticleAutophagy2016

Hypothalamic AMPK-induced autophagy increases food intake by regulating NPY and POMC expression.

Tae Seok Oh, Hanchae Cho, Jae Hyun Cho, Seong-Woon Yu, Eun-Kyoung Kim

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 115 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

5 authors at 1 institution in 1 country.

Tae Seok Oha Department of Brain & Cognitive Sciences , Daegu Gyeongbuk Institute of Science & Technology , Dalseong-gun , Daegu , Korea.
Hanchae Choa Department of Brain & Cognitive Sciences , Daegu Gyeongbuk Institute of Science & Technology , Dalseong-gun , Daegu , Korea.
Jae Hyun Choa Department of Brain & Cognitive Sciences , Daegu Gyeongbuk Institute of Science & Technology , Dalseong-gun , Daegu , Korea.
Seong-Woon Yua Department of Brain & Cognitive Sciences , Daegu Gyeongbuk Institute of Science & Technology , Dalseong-gun , Daegu , Korea.
Eun-Kyoung Kima Department of Brain & Cognitive Sciences , Daegu Gyeongbuk Institute of Science & Technology , Dalseong-gun , Daegu , Korea.
Daegu Gyeongbuk Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypothalamic AMP-activated protein kinase (AMPK) plays important roles in the regulation of food intake by altering the expression of orexigenic or anorexigenic neuropeptides. However, little is known about the mechanisms of this regulation. Here, we report that hypothalamic AMPK modulates the expression of NPY (neuropeptide Y), an orexigenic neuropeptide, and POMC (pro-opiomelanocortin-α), an anorexigenic neuropeptide, by regulating autophagic activity in vitro and in vivo. In hypothalamic cell lines subjected to low glucose availability such as 2-deoxy-d-glucose (2DG)-induced glucoprivation or glucose deprivation, autophagy was induced via the activation of AMPK, which regulates ULK1 and MTOR complex 1 followed by increased Npy and decreased Pomc expression. Pharmacological or genetic inhibition of autophagy diminished the effect of AMPK on neuropeptide expression in hypothalamic cell lines. Moreover, AMPK knockdown in the arcuate nucleus of the hypothalamus decreased autophagic activity and changed Npy and Pomc expression, leading to a reduction in food intake and body weight. AMPK knockdown abolished the orexigenic effects of intraperitoneal 2DG injection by decreasing autophagy and changing Npy and Pomc expression in mice fed a high-fat diet. We suggest that the induction of autophagy is a possible mechanism of AMPK-mediated regulation of neuropeptide expression and control of feeding in response to low glucose availability.

Indexed as

AutophagyEatingGene Expression RegulationAMP-Activated Protein KinasesAnimalsArcuate Nucleus of HypothalamusAutophagy-Related Protein-1 HomologAutophagy-Related Protein 5Body WeightCell LineDeoxyglucoseDown-RegulationEnzyme ActivationGene Knockdown TechniquesHyperphagiaHypothalamusAMP-Activated Protein KinasesAtg5 protein, mouseAutophagy-Related Protein-1 HomologAutophagy-Related Protein 5DeoxyglucoseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesNeuropeptide YPro-OpiomelanocortinRNA, MessengerSirolimusTOR Serine-Threonine KinasesUlk1 protein, mouseappetiteautophagyglucoprivationglucose deprivationhypothalamic AMPKneuropeptide

Identifiers

PMID27533078
PMCPMC5103348
OpenAlexW2507223877

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.