Evidence map›Paper›PMID 25319187›Full record

Trial reportJournal of the American Heart Association2014

Role of dietary fats in modulating cardiometabolic risk during moderate weight gain: a randomized double-blind overfeeding trial (LIPOGAIN study).

David Iggman, Fredrik Rosqvist, Anders Larsson, Johan Arnlöv, Lena Beckman, Mats Rudling, Ulf Risérus

Registry-linked trialOpen access · goldAbstract readComparative StudyRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01427140 (Metabolic Consequences of Moderate Weight Gain - Role of Dietary Fat Composition), which is not on this map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.5field-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.

NCT01427140 nacompletednot on this map

Metabolic Consequences of Moderate Weight Gain - Role of Dietary Fat Composition (LIPOGAIN): a Randomized Double-Blind Controlled Study

TypeinterventionalSponsorUppsala UniversityRan2011 to 2011Enrolled41ConditionsHealthyArmsPolyunsaturated fatty acid group, Saturated fatty acid group
3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  10. Review
  11. Review
  12. Dietary Fatty Acids and Inflammation: Focus on the n-6 Series.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Linoleic acid, glycemic control and Type 2 diabetes.Prostaglandins, leukotrienes, and essential fatty acids · 2018
    Review
  20. Pediatric Age Palm Oil Consumption.International journal of environmental research and public health · 2018
    Review
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

7 authors at 3 institutions in 1 country.

David IggmanUnit for Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden (D.I., F.R., U.R.) Center for Clinical Research Dalarna, Falun, Sweden (D.I.).
Fredrik RosqvistUnit for Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden (D.I., F.R., U.R.).
Anders LarssonSection of Clinical Chemistry, Department of Medical Sciences, Uppsala University, Uppsala, Sweden (A.L.).
Johan ArnlövDepartment of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden (J.) School of Health and Social Studies, Dalarna University, Falun, Sweden (J.).
Lena BeckmanMetabolism Unit, Department of Endocrinology, Metabolism and Diabetes, Karolinska Institutet, Stockholm, Sweden (L.B., M.R.) Molecular Nutrition Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden (L.B., M.R.) Center for Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden (L.B., M.R.).
Mats RudlingMetabolism Unit, Department of Endocrinology, Metabolism and Diabetes, Karolinska Institutet, Stockholm, Sweden (L.B., M.R.) Molecular Nutrition Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden (L.B., M.R.) Center for Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden (L.B., M.R.).
Ulf RisérusUnit for Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden (D.I., F.R., U.R.).
Uppsala University · SEKarolinska Institutet · SEScience for Life Laboratory · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhether the type of dietary fat could alter cardiometabolic responses to a hypercaloric diet is unknown. In addition, subclinical cardiometabolic consequences of moderate weight gain require further study. METHODS AND

resultsIn a 7-week, double-blind, parallel-group, randomized controlled trial, 39 healthy, lean individuals (mean age of 27±4) consumed muffins (51% of energy [%E] from fat and 44%E refined carbohydrates) providing 750 kcal/day added to their habitual diets. All muffins had identical contents, except for type of fat; sunflower oil rich in polyunsaturated fatty acids (PUFA diet) or palm oil rich in saturated fatty acids (SFA diet). Despite comparable weight gain in the 2 groups, total: high-density lipoprotein (HDL) cholesterol, low-density lipoprotein:HDL cholesterol, and apolipoprotein B:AI ratios decreased during the PUFA versus the SFA diet (-0.37±0.59 versus +0.07±0.29, -0.31±0.49 versus +0.05±0.28, and -0.07±0.11 versus +0.01±0.07, P=0.003, P=0.007, and P=0.01 for between-group differences), whereas no significant differences were observed for other cardiometabolic risk markers. In the whole group (ie, independently of fat type), body weight increased (+2.2%, P<0.001) together with increased plasma proinsulin (+21%, P=0.007), insulin (+17%, P=0.003), proprotein convertase subtilisin/kexin type 9, (+9%, P=0.008) fibroblast growth factor-21 (+31%, P=0.04), endothelial markers vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and E-selectin (+9, +5, and +10%, respectively, P<0.01 for all), whereas nonesterified fatty acids decreased (-28%, P=0.001).

conclusionsExcess energy from PUFA versus SFA reduces atherogenic lipoproteins. Modest weight gain in young individuals induces hyperproinsulinemia and increases biomarkers of endothelial dysfunction, effects that may be partly outweighed by the lipid-lowering effects of PUFA. CLINICAL TRIAL REGISTRATION URL: http://ClinicalTrials.gov. Unique identifier: NCT01427140.

Indexed as

Weight GainAdultAtherosclerosisBlood Chemical AnalysisBlood GlucoseBody WeightCardiovascular DiseasesCholesterolDietary FatsDiet, High-FatFemaleHealthy VolunteersHumansInsulin ResistanceLipidsLipoproteinsBlood GlucoseCholesterolDietary FatsLipidsLipoproteinsPalm OilPlant OilsSunflower OilAtherosclerosislipidslipoproteinnutritionobesity

Identifiers

PMID25319187
PMCPMC4323808
OpenAlexW2138571140

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.