Evidence map›Paper›PMID 29789721›Full record

SynthesisInternational journal of obesity (2005)2018

Is leptin resistance the cause or the consequence of diet-induced obesity?

Kathy C G de Git, Céline Peterse, Sanne Beerens, Mieneke C M Luijendijk, Geoffrey van der Plasse, Susanne E la Fleur, Roger A H Adan

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in International journal of obesity (2005), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Cannabis and cannabinoid research · 2022
    Review
  6. Review
  7. Review
  8. TNF-Oxidative medicine and cellular longevity · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Obesity and COVID-19: A Fatal Alliance.Indian journal of clinical biochemistry : IJCB · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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.

Kathy C G de GitBrain Center Rudolf Magnus, Department of Translational Neuroscience, University Medical Center Utrecht, Utrecht University, Utrecht, 3584 CG, The Netherlands.
Céline PeterseBrain Center Rudolf Magnus, Department of Translational Neuroscience, University Medical Center Utrecht, Utrecht University, Utrecht, 3584 CG, The Netherlands.
Sanne BeerensBrain Center Rudolf Magnus, Department of Translational Neuroscience, University Medical Center Utrecht, Utrecht University, Utrecht, 3584 CG, The Netherlands.
Mieneke C M LuijendijkBrain Center Rudolf Magnus, Department of Translational Neuroscience, University Medical Center Utrecht, Utrecht University, Utrecht, 3584 CG, The Netherlands.
Geoffrey van der PlasseBrain Center Rudolf Magnus, Department of Translational Neuroscience, University Medical Center Utrecht, Utrecht University, Utrecht, 3584 CG, The Netherlands.
Susanne E la FleurDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, 1105 AZ, The Netherlands.ORCID http://orcid.org/0000-0002-4298-7451
Roger A H AdanBrain Center Rudolf Magnus, Department of Translational Neuroscience, University Medical Center Utrecht, Utrecht University, Utrecht, 3584 CG, The Netherlands. r.a.h.adan@umcutrecht.nl.ORCID http://orcid.org/0000-0001-8994-0661

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesObesity is strongly associated with leptin resistance. It is unclear whether leptin resistance results from the (over)consumption of energy-dense diets or if reduced leptin sensitivity is also a pre-existing factor in rodent models of diet-induced obesity (DIO). We here tested whether leptin sensitivity on a chow diet predicts subsequent weight gain and leptin sensitivity on a free choice high-fat high-sucrose (fcHFHS) diet.

methodsBased upon individual leptin sensitivity on chow diet, rats were grouped in leptin sensitive (LS, n = 22) and leptin resistant (LR, n = 19) rats (P = 0.000), and the development of DIO on a fcHFHS diet was compared. The time-course of leptin sensitivity was measured over weeks in individual rats.

resultsBoth on a chow and a fcHFHS diet, high variability in leptin sensitivity was observed between rats, but not over time per individual rat. Exposure to the fcHFHS diet revealed that LR rats were more prone to develop DIO (P = 0.013), which was independent of caloric intake (p ≥ 0.320) and the development of diet-induced leptin resistance (P = 0.769). Reduced leptin sensitivity in LR compared with LS rats before fcHFHS diet exposure, was associated with reduced leptin-induced phosphorylated signal transducer and activator of transcription 3 (pSTAT3) levels in the dorsomedial and ventromedial hypothalamus (P ≤ 0.049), but not the arcuate nucleus (P = 0.558).

conclusionsA pre-existing reduction in leptin sensitivity determines the susceptibility to develop excessive DIO after fcHFHS diet exposure. Rats with a pre-existing reduction in leptin sensitivity develop excessive DIO without eating more calories or altering their leptin sensitivity.

Indexed as

AnimalsDietDietary FatsLeptinMetabolic DiseasesObesityRatsSucroseDietary FatsLeptinSucrose

Identifiers

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.