Evidence map›Paper›PMID 30393997›Full record

Trial reportDiabetes, obesity & metabolism2019

Follistatins in glucose regulation in healthy and obese individuals.

Nikolaos Perakakis, Alexander Kokkinos, Natia Peradze, Nicholas Tentolouris, Wael Ghaly, Dimitrios Tsilingiris, Andreas Alexandrou, Christos S Mantzoros

Abstract readClinical Trial
In one paragraph

Trial report in Diabetes, obesity & metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 52 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

8 authors at 2 institutions in 3 countries.

Nikolaos PerakakisDivision of Endocrinology, Diabetes and Metabolism, Harvard Medical School, Harvard University, Boston, Massachusetts.ORCID 0000-0002-2319-6603
Alexander KokkinosFirst Department of Propaedeutic Medicine, Medical School, National and Kapodistrian University of Athens, Laiko General Hospital, Athens, Greece.
Natia PeradzeDivision of Endocrinology, Diabetes and Metabolism, Harvard Medical School, Harvard University, Boston, Massachusetts.
Nicholas TentolourisFirst Department of Propaedeutic Medicine, Medical School, National and Kapodistrian University of Athens, Laiko General Hospital, Athens, Greece.
Wael GhalyDivision of Endocrinology, Diabetes and Metabolism, Harvard Medical School, Harvard University, Boston, Massachusetts.
Dimitrios TsilingirisFirst Department of Propaedeutic Medicine, Medical School, National and Kapodistrian University of Athens, Laiko General Hospital, Athens, Greece.
Andreas AlexandrouFirst Department of Surgery, Medical School, National and Kapodistrian University of Athens, Laiko General Hospital, Athens, Greece.
Christos S MantzorosDivision of Endocrinology, Diabetes and Metabolism, Harvard Medical School, Harvard University, Boston, Massachusetts.ORCID 0000-0003-3755-8158
Joslin Diabetes Center · USNational and Kapodistrian University of Athens · GR

Funding

Harvard Clinical and Translational Science CenterUL1TR001102 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$106.2M
Leptin and Adipokine PhysiologyK24DK081913 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MANTZOROS, CHRISTOS S · 2008 to 2020
$1.5M
NCATS NIH HHS UL1 TR001102NIDDK NIH HHS K24 DK081913
6 · The paper itself

Abstract

aimsIt has been suggested recently that follistatin (FST) and its homologous protein, follistatin-like 3 (FSTL3), may be a therapeutic target in the treatment of type 2 diabetes because of their glucose-regulatory effects in rodents. MATERIALS AND

methodsWe investigated this hypothesis in humans by studying the physiology of a possible glycaemia-follistatin feedback loop, that is, whether glucose, but not lipid intake (oral or intravenous), can regulate circulating FST and FSTL3 in healthy humans (n = 32), whether the levels of follistatins change in response to various types of bariatric operation in morbidly obese individuals, with or without type 2 diabetes (n = 41), and whether such changes are associated prospectively with improvement of glucose homeostasis/insulin sensitivity.

resultsIn healthy individuals, circulating FST decreases after intravenous or oral glucose intake compared to controls, indicating the presence of a negative feedback mechanism. In morbid obesity, insulin resistance, glycaemia, circulating FST and FSTL3 are all reduced (by 22%-33%) after Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy. Importantly, the changes in circulating FST 3 months after bariatric surgery are associated prospectively with the changes in glucose, insulin, HOMA-IR and HbA1c observed 6 months postoperatively in individuals with and without type 2 diabetes.

conclusionsOur findings provide evidence of an important role of FST in glucose homeostasis in healthy individuals as well as in severely obese individuals with insulin resistance and type 2 diabetes. Our data extend recent results from animal studies to humans and support the need for further evaluation of FST inactivation strategies for targeting hyperglycaemia and insulin resistance.

Indexed as

AdultBariatric SurgeryBlood GlucoseCase-Control StudiesCohort StudiesEmulsionsFemaleFollistatinFollistatin-Related ProteinsGastrectomyGlucoseHumansMaleMiddle AgedObesityObesity, MorbidBlood GlucoseEmulsionsFollistatinFollistatin-Related ProteinsFstl3 protein, humanGlucosePhospholipidsSoybean Oilsoybean oil, phospholipid emulsionactivindiabeteshumaninsulinobesityweight

Identifiers

PMID30393997
PMCPMC6368471
OpenAlexW2900161728

What OpenQuestion holds

Textmetadata
LicenceTDM
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.