Evidence map›Paper›PMID 18196982›Full record

ReviewCurrent opinion in lipidology2008

Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance.

Kimber L Stanhope, Peter J Havel

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in lipidology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
10.9field-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

102 citing papers in PubMed, 263 citations in OpenAlex.

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  8. A dual sugar challenge test for lipogenic sensitivity to dietary fructose.The Journal of clinical endocrinology and metabolism · 2011
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42 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Kimber L StanhopeDepartment of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California 95616, USA.
Peter J Havel
University of California, Davis · US

Funding

UC DAVIS CLINICAL AND TRANSLATIONAL SCIENCE CENTER: BPCAUL1RR024146 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2006 to 2011
$27.0M
Effects of 2wk fructose & HFCS consumption on lipid dysregulation & insulin resisR01HL091333 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HAVEL, PETER J · 2008 to 2012
$2.0M
Dietary Fructose: Hormones &TG/Lipoprotein MetabolismR01HL075675 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI HAVEL, PETER J · 2004 to 2008
$1.8M
Fatty acid sources of fructose and HFCS-induced postprandial hypertriglyceridemiaR01HL107256 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HAVEL, PETER J, SCHWARZ, JEAN-MARC · 2011 to 2014
$1.5M
Effects of Chromium on Progression of Insulin ResistanceR21AT002599 · NCCIH · UNIVERSITY OF CALIFORNIA DAVIS · PI HAVEL, PETER J · 2004 to 2006
$598k
Effects of fish oil and alpha lipoic on the progression of insulin resistanceR21AT003645 · NCCIH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HAVEL, PETER J · 2006 to 2008
$591k
Prevention of Diabetes with Nutritional SupplementsR21AT002993 · NCCIH · UNIVERSITY OF CALIFORNIA DAVIS · PI HAVEL, PETER J · 2005 to 2007
$584k
NCCIH NIH HHS AT-002599NCCIH NIH HHS AT-002993NCCIH NIH HHS AT-003645NCCIH NIH HHS R21 AT002599NCCIH NIH HHS R21 AT002993NCCIH NIH HHS R21 AT003645NCRR NIH HHS UL1 RR024146NHLBI NIH HHS HL-075675NHLBI NIH HHS R01 HL075675NHLBI NIH HHS R01 HL091333NHLBI NIH HHS R01 HL107256
6 · The paper itself

Abstract

purpose of reviewBased on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome. RECENT

findingsThe earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance. SUMMARY: Our investigation and future studies of the effects of fructose consumption may help to clarify the sequence of events leading to development of metabolic syndrome.

Indexed as

Insulin ResistanceDyslipidemiasFatty Acids, NonesterifiedFructoseHumansIntra-Abdominal FatSweetening AgentsFatty Acids, NonesterifiedFructoseSweetening Agents

Identifiers

PMID18196982
PMCPMC4151171
OpenAlexW1967008598

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.