Evidence map›Paper›PMID 26900642›Full record

ArticleThe Journal of clinical endocrinology and metabolism2016

Effect of Leptin Administration on Circulating Apolipoprotein CIII levels in Patients With Lipodystrophy.

Andrea Kassai, Ranganath Muniyappa, Amy E Levenson, Mary F Walter, Brent S Abel, Michael Ring, Simeon I Taylor, Sudha B Biddinger, Monica C Skarulis, Phillip Gorden and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 14 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

11 authors at 3 institutions in 1 country.

Andrea KassaiDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Ranganath MuniyappaDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Amy E LevensonDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Mary F WalterDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Brent S AbelDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Michael RingDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Simeon I TaylorDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Sudha B BiddingerDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Monica C SkarulisDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Phillip GordenDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Rebecca J BrownDiabetes, Endocrinology and Obesity Branch (A.K., R.M., B.S.A., M.R., M.C.S., P.G., R.J.B.), Clinical Core Laboratory (M.F.W.), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; Division of Endocrinology (A.E.L., S.B.B.), Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115; and Division of Endocrinology, Diabetes, and Nutrition (S.I.T.), University of Maryland School of Medicine, Baltimore, Maryland 21201.
Boston Children's Hospital · USNational Institute of Diabetes and Digestive and Kidney Diseases · USUniversity of Maryland, Baltimore · US

Funding

Biobehavioral Studies of Obesity, Weight loss and RecidivismZIADK075007 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MUNIYAPPA, RANGANATH · 2009 to 2025
$13.8M
CAREER DEVELOPMENT IN DIABETES RESEARCH FOR PEDIATRIC ENDOCRINOLOGISTSK12DK094721 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI LAFFEL, LORI M, WHITE, MORRIS F. · 2011 to 2021
$6.3M
Molecular and Clinical Studies of Insulin ResistanceZIADK047050 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI BROWN, REBECCA · 2009 to 2025
$6.1M
Clinical utility of leptin therapy in syndromic forms of insulin resistance.ZIADK047052 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI BROWN, REBECCA · 2009 to 2025
$5.5M
Control of lipid metabolism in insulin resistant statesR01DK094162 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI BIDDINGER, SUDHA B · 2012 to 2015
$1.5M
NIDDK NIH HHS K12 DK094721NIDDK NIH HHS L40 DK065607NIDDK NIH HHS R01 DK094162
6 · The paper itself

Abstract

contextApolipoprotein CIII (apoCIII), an inhibitor of lipoprotein lipase, plays an important role in triglyceride metabolism. However, the role of apoCIII in hypertriglyceridemia in lipodystrophy and the effects of leptin replacement on apoCIII levels are unknown.

objectiveThe objective of the study was to test the hypotheses that apoCIII is elevated in hypertriglyceridemic patients with lipodystrophy and that leptin replacement in these patients lowers circulating apoCIII. DESIGN, SETTING, STUDY PARTICIPANTS, INTERVENTION, AND OUTCOME MEASURES: Using a post hoc cross-sectional case-control design, we compared serum apoCIII levels from patients with lipodystrophy not associated with HIV (n = 60) and age-, gender-, race-, and ethnicity-matched controls (n = 54) participating in ongoing studies at the National Institutes of Health. In a prospective, open-label, ongoing study, we studied the effects of 6–12 months of leptin replacement on apoCIII in lipodystrophy patients as an exploratory outcome.

resultsApoCIII was higher in lipodystrophy patients (geometric mean [25th and 75th percentiles]) (23.9 mg/dL [14.6, 40.3]) compared with controls (14.9 mg/dL [12.3, 17.7]) (P < .0001). ApoCIII and triglyceride levels were positively correlated in patients with lipodystrophy (R = 0.72, P < .0001) and healthy controls (R = 0.6, P < .0001). Leptin replacement (6–12 mo) did not significantly alter apoCIII (before leptin: 23.4 mg/dL [14.5, 40.1]; after leptin: 21.4 mg/dL [16.7, 28.3]; P = .34).

conclusionsLeptin replacement in lipodystrophy did not alter serum apoCIII levels. Elevated apoCIII may play a role in the hypertriglyceridemia of lipodystrophy independent of leptin deficiency and replacement.

Indexed as

AdultAnimalsApolipoprotein C-IIICase-Control StudiesCross-Sectional StudiesFemaleHumansLeptinLipodystrophyMaleMiceMiddle AgedYoung AdultApolipoprotein C-IIILeptin

Identifiers

PMID26900642
PMCPMC4880162
OpenAlexW2283817678

What OpenQuestion holds

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Registered trials

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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.