Evidence map›Paper›PMID 24342176›Full record

ArticleAppetite2014

Analyses of meal patterns across dietary shifts.

Yada Treesukosol, Timothy H Moran

Abstract read
In one paragraph

Article in Appetite, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
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  14. A predictive model of rat calorie intake as a function of diet energy density.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  15. Article
  16. Acute high-fat diet upregulates glutamatergic signaling in the dorsal motor nucleus of the vagus.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. High-Fat Diet-Induced Obesity Ablates Gastric Vagal Afferent Circadian Rhythms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
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.

Yada TreesukosolDepartment of Psychiatry and Behavioral Sciences, School of Medicine, Johns Hopkins University, Ross 615, 720 Rutland Ave, Baltimore, MD 21205, USA. Electronic address: yadatree@jhmi.edu.
Timothy H MoranDepartment of Psychiatry and Behavioral Sciences, School of Medicine, Johns Hopkins University, Ross 615, 720 Rutland Ave, Baltimore, MD 21205, USA. Electronic address: tmoran@jhmi.edu.

Funding

JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Gastrointestional Integration and FeedingR01DK019302 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI MORAN, TIMOTHY H · 1986 to 2019
$7.1M
Gastrointestional Integration and FeedingR56DK019302 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI MORAN, TIMOTHY H · 2010 to 2010
$720k
NIDDK NIH HHS DK019302NIDDK NIH HHS P30 DK079637NIDDK NIH HHS R01 DK019302NIDDK NIH HHS R56 DK019302
6 · The paper itself

Abstract

The direct controls of meal size can be categorized into positive signals such as those from the oral cavity and negative signals such as postoral inhibitory cues. It follows that the relative contribution of these signals, and in turn meal pattern parameters, change across periods of high-energy diet exposure. Here, we compared daily intake and meal pattern analysis in male Sprague-Dawley rats presented a high-energy diet for 6weeks then standard chow for ∼1week (HE), with those of standard chow fed controls (CHOW). These measures allow for evaluation of (1) whether there are distinct dynamic and static phases of DIO and if so, how they are characterized, (2) how meal patterns change across short and long term HE experience, and (3) ingestive behavioral changes when HE-fed animals are returned to standard chow. The HE animals showed significantly higher intake primarily driven by an increase in meal size compared to CHOW controls. This was most pronounced during the first several days of high-energy diet exposure thus characterizing the dynamic phase. Intake and meal size decreased with longer exposure to the diet but remained significantly higher than those of CHOW. Increased meal size could be driven by enhanced orosensory stimulation and/or reduced sensitivity to postoral inhibitory feedback. Distribution curves derived from histogram plots of meal size revealed both larger average meal size (right shift) and spread (standard deviation) thus it is tempting to speculate that more than one type of mechanism influences increased meal size. Meal number decreased suggesting post meal inhibitory signaling is relatively intact. However, this increase was insufficient to compensate for the increased meal size. When HE animals were switched to standard chow, daily intake and meal size decreased and eventually returned to values comparable to those of the CHOW rats. Meal number remained lower suggesting altered physiological mechanism(s) that underlie the control of ingestive behavior as a function of previous high-energy diet exposure.

Indexed as

DietFeeding BehaviorMealsAnimal FeedAnimalsBody WeightEatingEnergy IntakeMalePortion SizeRatsRats, Sprague-DawleyHigh fatMeal numberMeal sizeOralPalatabilityPostingestive

Identifiers

PMID24342176
PMCPMC3944059

What OpenQuestion holds

Textmetadata
LicenceTDM
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.