Evidence map›Paper›PMID 23493533›Full record

ReviewAdvances in nutrition (Bethesda, Md.)2013

Dietary components in the development of leptin resistance.

Joseph R Vasselli, Philip J Scarpace, Ruth B S Harris, William A Banks

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in nutrition (Bethesda, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  9. A nexus of lipid andFrontiers in endocrinology · 2022
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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

4 authors at 4 institutions in 1 country.

Joseph R VasselliNutrition Obesity Research Center, Department of Medicine, St. Luke's-Roosevelt Hospital, and Columbia University Institute of Human Nutrition, New York, NY, USA. jrv1@columbia.edu
Philip J Scarpace
Ruth B S Harris
William A Banks
Augusta University · USSt. Luke's-Roosevelt Hospital Center · USUniversity of Florida · USUniversity of Washington · US

Funding

RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
LEPTIN AND PERIPHERAL GLUCOSE METABOLISMR01DK053903 · NIDDK · UNIVERSITY OF GEORGIA (UGA) · PI HARRIS, RUTH B · 1999 to 2018
$4.6M
TRAINING IN THE NEUROBIOLOGY OF AGINGT32AG000196 · NIA · UNIVERSITY OF FLORIDA · PI SCARPACE, PHILIP J · 1989 to 2011
$2.0M
Leptin resistance: 1 mechanism underlying age-related obesityR01AG026159 · NIA · UNIVERSITY OF FLORIDA · PI SCARPACE, PHILIP J · 2004 to 2008
$1.7M
Mechanisms of diet-induced leptin resistance in ARC and VTAR01DK091710 · NIDDK · UNIVERSITY OF FLORIDA · PI SCARPACE, PHILIP J, TUMER, NIHAL · 2012 to 2015
$1.5M
NIA NIH HHS AG-26159NIA NIH HHS T32AG00196NIDDK NIH HHS DK053903NIDDK NIH HHS DK-26687NIDDK NIH HHS P30 DK026687NIDDK NIH HHS R01 DK053903NIDDK NIH HHS R01 DK091710
6 · The paper itself

Abstract

Classically, leptin resistance has been associated with increased body fat and circulating leptin levels, and the condition is believed to contribute to the onset and/or maintenance of obesity. Although a great deal is known about the central nervous system mechanisms mediating leptin resistance, considerably less is known about the role of diet in establishing and maintaining this altered hormonal state. An exciting new finding has recently been published demonstrating the existence of leptin resistance in normal-weight rats with lean leptin levels by feeding them a high-concentration-fructose diet. This finding has opened the possibility that specific macronutrients may be capable of inducing leptin resistance, independently of the amount of body fat or circulating leptin present in the treated animals. This review describes several lines of research that have recently emerged indicating that specific types of dietary sugars and fats are capable of inducing leptin resistance in experimental rodent models. The results further show that diet-induced leptin resistance is capable of increasing energy intake and elevating body weight gain under appropriate dietary challenges. It appears that biological mechanisms on multiple levels may underlie the dietary induction of leptin resistance, including alterations in the leptin blood-to-brain transport system, in peripheral glucose metabolism, and in central leptin receptor signaling pathways. What is clear from the findings reviewed here is that diet-induced leptin resistance can occur in the absence of elevated circulating leptin levels and body weight, rendering it a potential cause and/or predisposing factor to excess body weight gain and obesity.

Indexed as

Energy IntakeWeight GainAdipose TissueAnimalsBrainDietDietary FatsDietary SucroseGlucoseHumansLeptinMetabolic DiseasesObesityDietary FatsDietary SucroseGlucoseLeptin

Identifiers

PMID23493533
PMCPMC3649097
OpenAlexW2130252057

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.