Format

Send to

Choose Destination
See comment in PubMed Commons below
Am J Clin Nutr. 1998 Mar;67(3 Suppl):535S-541S.

Manipulation of dietary fat and energy density and subsequent effects on substrate flux and food intake.

Author information

  • 1MRC Dunn Clinical Nutrition Centre, Cambridge, United Kingdom. Andrew.Prentice@MRC-Dunn.cam.ac.uk

Abstract

Dietary fat has traditionally been viewed as being particularly lipogenic because of its high energy density, metabolic efficiency, and palatability. If these attributes of dietary fat were counteracted by a high satiating power, or if the body made autoregulatory adjustments in fat utilization in response to high fat intakes, energy balance would not necessarily be displaced. However, recent experiments have shown that neither of these hold true: human and animal trials consistently show that covert manipulation of dietary fat can induce hyperphagia, which can readily lead to spontaneous fat storage of 50-100 g/d in humans. Experiments with isoenergy-dense diets show that this high-fat hyperphagia (with diets of similar palatability) is caused by the high energy density of fatty foods rather than by their other attributes. Hyperphagia has therefore been termed passive overconsumption because it occurs unintentionally and without the consumption of excess bulk. When palatability is allowed to vary normally, high-fat foods may additionally induce active overconsumption in response to the enhanced organoleptic qualities of fats. In terms of substrate flux, fat is at the bottom of an oxidative hierarchy that determines fuel selection. Whereas alcohol, carbohydrates, and protein elicit powerful autoregulatory adjustments in their oxidation in response to changes in intake, fat fails to elicit such a response and fat balance is therefore easily displaced. These physiologic observations provide mechanistic support for secular-trend, cross-cultural, and cross-sectional epidemiologic studies investigating the role of energy-dense diets in the etiology of obesity.

PMID:
9497166
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center