Evidence map›Paper›PMID 9114043›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Direct antidiabetic effect of leptin through triglyceride depletion of tissues.

M Shimabukuro, K Koyama, G Chen, M Y Wang, F Trieu, Y Lee, C B Newgard, R H Unger

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
14.9field-weighted citation impact, top 1% 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

133 citing papers in PubMed, 653 citations in OpenAlex.

  1. Leptin-Mediated Changes in the Human Metabolome.The Journal of clinical endocrinology and metabolism · 2020
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  16. Metabolic and Energy Imbalance in Dysglycemia-Based Chronic Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
    Review
  17. Role of Leptin in the Digestive System.Frontiers in pharmacology · 2021
    Review
  18. Review
  19. Article
  20. Article

73 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

M ShimabukuroGifford Laboratories for Diabetes Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235, USA.
K Koyama
G Chen
M Y Wang
F Trieu
Y Lee
C B Newgard
R H Unger
The University of Texas Southwestern Medical Center · US

Funding

The Glucoregulatory and Liporegulatory Peptide HormonesR01DK002700 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI UNGER, ROGER HAROLD · 1994 to 2008
$2.5M
REGULATION OF THE HEPATIC NEGATIVE ACUTE PHASE RESPONSEK08DK002700 · NIDDK · YALE UNIVERSITY · PI DENSON, LEE ARMISTEAD · 2000 to 2004
$658k
THE GLUCOREGULATORY PEPTIDE HORMONESR37DK002700 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI UNGER, ROGER H. · 1986 to 1993
–
NIDDK NIH HHS DK02700-37NIDDK NIH HHS K08 DK002700NIDDK NIH HHS R01 DK002700
6 · The paper itself

Abstract

Leptin is currently believed to control body composition largely, if not entirely, via hypothalamic receptors that regulate food intake and thermogenesis. Here we demonstrate direct extraneural effects of leptin to deplete fat content of both adipocytes and nonadipocytes to levels far below those of pairfed controls. In cultured pancreatic islets, leptin lowered triglyceride (TG) content by preventing TG formation from free fatty acids (FFA) and by increasing FFA oxidation. In vivo hyperleptinemia, induced in normal rats by adenovirus gene transfer, depleted TG content in liver, skeletal muscle, and pancreas without increasing plasma FFA or ketones, suggesting intracellular oxidation. In islets of obese Zucker Diabetic Fatty rats with leptin receptor mutations, leptin had no effect in vivo or in vitro. The TG content was approximately 20 times normal, and esterification capacity was increased 3- to 4-fold. Thus, in rats with normal leptin receptors but not in Zucker Diabetic Fatty rats, nonadipocytes and adipocytes esterify FFA, store them as TG, and later oxidize them intracellularly via an "indirect pathway" of intracellular fatty acid metabolism controlled by leptin. By maintaining insulin sensitivity and preventing islet lipotoxicity, this activity of leptin may prevent adipogenic diabetes.

Indexed as

Receptors, Cell Surface3-Hydroxybutyric AcidAnimalsCarrier ProteinsCulture TechniquesDiabetes Mellitus, ExperimentalEsterificationFatty Acids, NonesterifiedGenotypeHydroxybutyratesHypoglycemic AgentsIslets of LangerhansLeptinLiverMaleMuscle, Skeletal3-Hydroxybutyric AcidCarrier ProteinsFatty Acids, NonesterifiedHydroxybutyratesHypoglycemic AgentsLeptinProteinsReceptors, Cell SurfaceReceptors, LeptinRecombinant Fusion ProteinsTriglycerides

Identifiers

PMID9114043
PMCPMC20776
OpenAlexW2053965920

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.