Evidence map›Paper›PMID 25279500›Full record

ArticleThe Journal of clinical endocrinology and metabolism2014

Leptin therapy alters appetite and neural responses to food stimuli in brain areas of leptin-sensitive subjects without altering brain structure.

Olivia M Farr, Christina Fiorenza, Panagiotis Papageorgiou, Mary Brinkoetter, Florencia Ziemke, Bang-Bon Koo, Rafael Rojas, Christos S Mantzoros

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  11. Leptin in Leanness and Obesity: JACC State-of-the-Art Review.Journal of the American College of Cardiology · 2021
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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 4 institutions in 1 country.

Olivia M FarrDivision of Endocrinology (O.M.F., C.F., P.P., M.B., F.Z., C.S.M.), VA Boston Healthcare System and Beth-Israel Deaconess Medical Center/Harvard Medical School, Boston, Massachusetts 02215; Department of Anatomy and Neurobiology (B.-B.K.), Boston University School of Medicine, Boston, Massachusetts 02215; and Division of Radiology (R.R.), Beth-Israel Deaconess Medical Center/Harvard Medical School, Boston, Massachusetts 02215.
Christina Fiorenza
Panagiotis Papageorgiou
Mary Brinkoetter
Florencia Ziemke
Bang-Bon Koo
Rafael Rojas
Christos S Mantzoros
VA Boston Healthcare System · USBeth Israel Deaconess Medical Center · USBoston University · USHarvard University · US

Funding

ZINC STATUS AND T CELL DISORDER IN MILD HUMAN ZINC DEFICIENCYM01RR001032 · NCRR · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MANTZOROS, CHRISTOS S · 1985 to 2008
$32.3M
Leptin Signaling in HumansI01CX000422 · VA · VA BOSTON HEALTH CARE SYSTEM · PI MANTZOROS, CHRISTOS S · 2011 to 2014
–
CSRD VA I01 CX000422NCRR NIH HHS M01 RR001032NCRR NIH HHS M01-RR-01032PHS HHS 58785PHS HHS 79929PHS HHS 81913
6 · The paper itself

Abstract

contextLeptin is a key regulator of energy intake and expenditure. Individuals with congenital leptin deficiency demonstrate structural and functional brain changes when given leptin. However, whether acquired leptin deficiency may operate similarly is unclear.

objectiveWe set out to determine whether the brains of individuals with acquired leptin deficiency may react to leptin in a similar manner.

designWe used functional magnetic resonance imaging before and after short- and long-term metreleptin treatment in three leptin-sensitive patients with acquired hypoleptinemia. Nine healthy women were scanned as normoleptinemic controls.

settingThe setting was an academic medical center. PATIENTS OR OTHER

participantsThe participants were 3 hypoleptinemic women and nine normoleptinemic, matched women.

interventionsWe used metreleptin, recombinant leptin, therapy for 24 weeks in hypoleptinemic women only.

main outcome measureWe measured neural changes in response to viewing food as compared to nonfood images. We hypothesized that metreleptin treatment would increase brain activity in areas related to cognitive control and inhibition and would decrease brain activity in areas related to reward processing, as compared to the normoleptinemic counterparts.

resultsUnlike patients with congenital leptin deficiency, hypoleptinemic patients demonstrated no structural brain differences from healthy controls and/or structural changes in response to treatment. Short-term metreleptin treatment in leptin-sensitive hypoleptinemic subjects enhances areas involved in detecting the salience and rewarding value of food during fasting, whereas long-term treatment decreases attention to food and the rewarding value of food after feeding. Furthermore, hypothalamic activity is modulated by metreleptin treatment, and leptin decreases functional connectivity of the hypothalamus to key feeding-related areas in these hypoleptinemic subjects.

conclusionsLeptin replacement in acutely hypoleptinemic women did not alter brain structure but did alter functional cortical activity to food cues in key feeding and reward-related areas.

Indexed as

AdolescentAdultAppetiteBrainEatingFemaleFoodHormone Replacement TherapyHumansHypothalamusInhibition, PsychologicalLeptinMagnetic Resonance ImagingPhotic StimulationTreatment OutcomeYoung AdultLeptinmetreleptin

Identifiers

PMID25279500
PMCPMC4255115
OpenAlexW1973543642

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.