Meal size of high-fat food is reliably greater than high-carbohydrate food across externally-evoked single-meal tests and long-term spontaneous feeding in rat

doi:10.1016/j.appet.2005.02.004

Appetite

Volume 45, Issue 2, October 2005, Pages 191-194

https://doi.org/10.1016/j.appet.2005.02.004 Get rights and content

Abstract

A series of studies in rat using isoenergetic (kcal/ml) liquid diets differing in fat content has previously found dietary fat to dose-dependently increase daily caloric intake. In single-meal tests in which meal initiation was externally evoked in feeding-associated environments, the behavioral expression of this overeating was found to be larger meal intake. The present studies confirmed the ecological validity of this larger meal size of high-fat diet (HF) relative to high-carbohydrate diet (HC): meal size of HF>HC in home-cage testing (Experiment 1), and during undisturbed, spontaneous feeding in which ingestive behavior was continuously monitored (Experiments 2 and 3). These findings demonstrate that single-meal paradigms yield results consistent with spontaneous feeding of high-fat and high-carbohydrate liquid diets, thus supporting the use of single-meal studies to better understand the physiological bases of elevated caloric intake associated with chronic consumption of a high-fat diet.

Section snippets

Experiment 1: meal size in home cage

A larger meal size of HF relative to HC has been observed in paradigms in which animals were removed from the home cage, placed in an experimental chamber, and offered food shortly thereafter (Warwick et al., 2000, Warwick and Synowski, 1999). After a few repetitions of this ritutal, rats clearly associate the chamber with eating as evidenced by nose-pokes and licks in the food area prior to food presentation. The present study investigated whether differential meal size of HF and HC would

Experiment 2: meal size during spontaneous feeding

When consumed ad libitum, HF elicits greater daily energy intake than HC; however, there is an initial period of hypophagia and weight loss probably attributable to neophobia (Warwick & Weingarten, 1995). Since atypical meal patterning would be expected during this initial phase, a period of diet acclimation took place prior measurement of spontaneous intake of HF and HC. Twenty-three new rats were housed in Plexiglas experimental chambers (MedAssociates, Inc., St Albans VT) equipped with

Experiment 3: spontaneous feeding following acclimation to mid-fat diet

To prevent neophobia from influencing measurement of spontaneous meal size, rats in Experiment 2 had been acclimated to either HF or HC prior to recording of feeding behavior. However, this acclimation produced diet-specific differences in body weight gain prior to collection of meal size data. To reduce the novelty of the HF and HC diets while still permitting the formation of weight-matched diet groups, a mixture of HF and HC was fed during the acclimation phase to all animals.

For 14 days, 11

General discussion

A liquid high-fat food (HF) was found to elicit larger meal size than an isocaloric (kcal/ml) high-carbohydrate food (HC) during ad lib spontaneous feeding, as well as in single-meal test paradigms in which meal initiation was externally evoked as observed previously (Warwick and Synowski, 1999, Warwick et al., 2000). These consistent results support the use of single-meal methods to investigate biological mechanisms underlying diet-related differences in daily energy intake.

Furthermore, the

Acknowledgements

Rosie Mills is thanked for outstanding technical assistance. Supported by NIDDK 55367 (to Z. Warwick).

References (13)

G.A. Bray et al.
Dietary fat does affect obesity!
American Journal of Clinical Nutrition
(1998)
B.J. Rolls et al.
Fat, carbohydrate, and the regulation of energy intake
American Journal of Clinical Nutrition
(1995)
Z.S. Warwick
Probing the causes of high-fat diet hyperphagia: A mechanistic and behavioral dissection
Neuroscience and Biobehavioral Reviews
(1996)
Z.S. Warwick et al.
Role of dietary fat in calorie intake and weight gain
Neuroscience and Biobehavioral Reviews
(1992)
Z.S. Warwick et al.
Effect of food deprivation and maintenance diet composition on fat preference and acceptance in rats
Physiology and Behavior
(1999)
Z.S. Warwick et al.
Dietary fat content affects energy intake and weight gain independent of diet caloric density in rats
Physiology & Behavior
(2002)

There are more references available in the full text version of this article.

Cited by (17)

Analyses of meal patterns across dietary shifts
2014, Appetite
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 6 weeks then standard chow for ∼1 week (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.
Intermittent access to sweet high-fat liquid induces increased palatability and motivation to consume in a rat model of binge consumption
2013, Physiology and Behavior
Binge eating disorders are characterized by discrete episodes of rapid and excessive food consumption. In rats, giving intermittent access to sweet fat food mimics this aspect of binge eating. These models typically employ solid food; however, the total amount consumed depends on motivation, palatability and satiety, which are difficult to dissociate with solid food. In contrast, lick microstructure analysis can be used to dissociate these parameters when the ingestant is a liquid. Therefore, we developed a binge model using a liquid emulsion composed of corn oil, heavy cream and sugar. We show that rats given intermittent access to this high-fat emulsion develop binge-like behavior comparable to that previously observed with solid high-fat food. One feature of this behavior was a gradual escalation in consumption across 2.5 weeks of intermittent access, which was not apparent in rats given lower-fat liquid on the same access schedule. Lick microstructure analysis suggests that this escalation was due at least in part to increases in both motivation to consume and palatability-driven consumption.
Animal Models of Dietary-Induced Obesity
2013, Animal Models for the Study of Human Disease
This chapter aims to review literature on different aspects of obesity from fat-rich diets in non-human species. Usefulness of using small rodents in animal models to infer aspects of human obesity is discussed in terms of similarities and differences and how obesity is defined. The paradigm of using fat-rich diets in animal models of human obesity is explored according to its adequacy and dietary characteristics related to fatty acid composition. Physiological factors and mechanisms that can play a role in the development of obesity induced by a diet rich in fat are examined, namely the efficiency of nutrient utilization and the possible lack of inhibitory effect of fat on intake. The role of hormones such as leptin, ghrelin and insulin is discussed. Bevavioural mechanisms related to sensory-specific facilitation of eating with fat rich diets, altered feeding rhythmicity and learned eating are considered. The possible reversal of fat-rich diet induced obesity in animal models is explored. This chapter concludes with comments on appropriate design of animal studies and suggestions for future research.
Acute exposure to a high-fat diet alters meal patterns and body composition
2010, Physiology and Behavior
Weight gain and adiposity are often attributed to the overconsumption of unbalanced, high-fat diets however, the pattern of consumption can also contribute to associated body weight and compositional changes. The present study explored the rapid alterations in meal patterns of normal-weight rats given continuous access to high-fat diet and examined body weight and composition changes compared to chow fed controls. Ten Long–Evans rats were implanted with subcutaneous microchips for meal pattern analysis. Animals were body weight matched and separated into two groups: high-fat or chow fed. Each group was maintained on their assigned diet for nine days and monitored for 22 h each day for meal pattern behavior. Body weight was evaluated every other day, and body composition measures were taken prior and following diet exposure. High-fat fed animals gained more weight and adipose tissue than chow fed controls and displayed a reduced meal frequency and increased meal size. Furthermore, meal size was significantly correlated with the gain of adipose tissue. Together, these results suggest that consumption of a high-fat diet can rapidly alter meal patterns, which in turn contribute to the development of adiposity.
Circulating triglycerides after a high-fat meal: Predictor of increased caloric intake, orexigenic peptide expression, and dietary obesity
2009, Brain Research
Recent studies in normal-weight rats have linked circulating triglycerides (TG), when elevated by a high-fat (HF) compared to equicaloric low-fat (LF) meal, to an increase in subsequent food intake and hypothalamic expression of orexigenic peptides. The present study tested whether natural variations between rats in their TG levels after a small HF meal can also be related to their individual patterns of eating and peptide expression. In tail vein blood collected on three separate days 60 min after a HF meal, levels of TG were found to be strongly, positively correlated within rats from day to day but were highly variable between rats (75–365 mg/dl), allowing distinct subgroups (33% lowest or highest) to be formed. Compared to “Low-TG responders” with post-meal levels averaging 109 mg/dl, “High-TG responders” with 240 mg/dl showed in two separate experiments a significant increase in caloric intake in a subsequent laboratory chow meal. Before this larger meal, these rats with elevated TG consistently exhibited higher expression levels and synthesis of the orexigenic peptides, enkephalin, orexin and melanin-concentrating hormone, as revealed using real-time quantitative PCR, radiolabeled in situ hybridization, and immunofluorescence histochemistry. Over the long-term, the High-TG responders also showed an increased propensity to overeat, gain weight and accumulate excess body fat on a chronic HF diet. This simple measure of TG levels after a HF meal may offer a useful tool for identifying subpopulations with increased risk for overeating and dietary obesity and detecting early signs of brain disturbances that may contribute to this high-risk phenotype.
Anti-obesity drugs and neural circuits of feeding
2008, Trends in Pharmacological Sciences
Most of the drugs that have entered the market for treating obesity were originally developed to treat psychiatric diseases. During the past decade, understanding of the neural circuits that underlie food intake has increased considerably. Different aspects of ingestive behavior such as meal termination, meal initiation and overconsumption of highly rewarding and palatable foods are modulated by different neuroanatomical structures. Integration of the action of many signaling molecules (e.g. hormones, neurotransmitters and neuropeptides) in these structures results in a response that, ultimately, modulates food intake. Thus, the type of drug required by an obese patient might depend on the individual cause of obesity. In this article, we summarize the neural circuits that regulate food intake and we provide a framework for understanding how obesity drugs function. Several potential drug targets are expressed in different neural circuits, implying that current and future obesity drugs act on partially overlapping systems that control food intake.

View all citing articles on Scopus

View full text

Brief CommunicationMeal size of high-fat food is reliably greater than high-carbohydrate food across externally-evoked single-meal tests and long-term spontaneous feeding in rat

Abstract

Section snippets

Experiment 1: meal size in home cage

Experiment 2: meal size during spontaneous feeding

Experiment 3: spontaneous feeding following acclimation to mid-fat diet

General discussion

Acknowledgements

American Journal of Clinical Nutrition

American Journal of Clinical Nutrition

Neuroscience and Biobehavioral Reviews

Neuroscience and Biobehavioral Reviews

Physiology and Behavior

Physiology & Behavior

Brief Communication
Meal size of high-fat food is reliably greater than high-carbohydrate food across externally-evoked single-meal tests and long-term spontaneous feeding in rat