Peripheral control of meal size in the rat: Effect of sham feeding on meal size and drinking rate.

Davis, John D.; Campbell, Constance S.

doi:10.1037/h0034667

Cited by 197 publications

(69 citation statements)

References 17 publications

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“…Inhibitory postingestive signaling decreases licking rates, meal duration, and burst number (13)(14)(15); decreases in the latter two measures were evident when comparing lick microstructure during 10% vs. 1% Intralipid intake (Figs. 1C and 2C).…”

Section: Discussionmentioning

confidence: 96%

μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals

Katsuura

Heckmann

Taha

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Katsuura Y, Heckmann JA, Taha SA. -Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals. Am J Physiol Regul Integr Comp Physiol 301: R244 -R254, 2011. First published May 4, 2011 doi:10.1152/ajpregu.00406.2010.-Infusion of a -opioid receptor (MOR) agonist into the nucleus accumbens (NAcc) drives voracious food intake, an effect hypothesized to occur through increased tastant palatability. While intake of many palatable foods is elevated by MOR stimulation, this manipulation has a preferential effect on fatty food ingestion. Consumption of high-fat foods is increased by NAcc MOR stimulation even in rats that prefer a carbohydrate-rich alternative under baseline conditions. This suggests that NAcc MOR stimulation may not simply potentiate palatability signals and raises the possibility that mechanisms mediating fat intake may be distinct from those underlying intake of other tastants. The present study was conducted to investigate the physiological mechanisms underlying the effects of NAcc MOR stimulation on fatty food intake. In experiment 1, we analyzed lick microstructure in rats ingesting Intralipid to identify the changes underlying feeding induced by infusion of a MOR-specific agonist into the NAcc. MOR stimulation in the NAcc core, but not shell, increased burst duration and first-minute licks, while simultaneously increasing the rate and duration of Intralipid ingestion. These results suggest that MOR activation in the core increases Intralipid palatability and attenuates inhibitory postingestive feedback. In experiment 2, we measured the effects of MOR stimulation in the NAcc core on consumption of nonnutritive olestra. A MOR-specific agonist dose dependently increased olestra intake, demonstrating that caloric signaling is not required for hyperphagia induced by NAcc MOR stimulation. Feeding induced by drug infusion in both experiments 1 and 2 was blocked by a MOR antagonist. In experiment 3, we determined whether MOR activation in the NAcc core could attenuate satiety-related signaling caused by infusion of the melanocortin agonist MTII into the third ventricle. Suppression of intake caused by MTII was reversed by MOR stimulation. Together, our results suggest that MOR stimulation in the NAcc core elevates fatty food intake through palatability mechanisms dependent on orosensory cues and suppression of satiety signals inhibiting food intake. nucleus accumbens; food reward UNDERSTANDING THE NEURAL MECHANISMS that promote food intake exceeding metabolic need is a fundamentally important step in addressing the growing health problem of overweight and obesity. While food intake is determined by the convergence of many neural signaling pathways (31), central opioid signaling acting in motivation/reward circuits may be particularly important in driving excessive food consumption, as these brain circuits are involved in determining the reinforcing value of tastants (3, 24, 28).Activation of -opioid receptors (MORs) in th...

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Section: Discussionmentioning

confidence: 96%

μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals

Katsuura

Heckmann

Taha

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The defect in satiety mechanisms in BN, aggravated by postprandial vomiting or purging, can be modeled in the sham-feeding rat (Davis and Campbell 1973;Mook 1963). A gastric fistula is placed to have the ingested liquid food drain from the stomach, thereby minimizing contact of food with the gastric and intestinal mucosa, producing a reversible, acquired defect in satiation.…”

Section: Hyperphagia Due To Impaired Satietymentioning

confidence: 99%

Relevance of animal models to human eating disorders and obesity

2008

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Background and rationale This review addresses the role animal models play in contributing to our knowledge about the eating disorders anorexia nervosa (AN) and bulimia nervosa (BN) and obesity. Objectives Explore the usefulness of animal models in complex biobehavioral familial conditions, such as AN, BN, and obesity, that involve interactions among genetic, physiologic, psychological, and cultural factors. Results and conclusionsThe most promising animal model to mimic AN is the activity-based anorexia rodent model leading to pathological weight loss. The paradigm incorporates reward elements of the drive for activity in the presence of an appetite and allows the use of genetically modified animals. For BN, the sham-feeding preparation in rodents equipped with a gastric fistula appears to be best suited to reproduce the postprandial emesis and the defects in satiety. Animal models that incorporate genes linked to behavior and mood may clarify biobehavioral processes underlying AN and BN. By contrast, a relative abundance of animal models has contributed to our understanding of human obesity. Both environmental and genetic determinants of obesity have been modeled in rodents. Here, we consider single gene mutant obesity models, along with models of obesigenic environmental conditions. The contributions of animal models to obesity research are illustrated by their utility for identifying genes linked to human obesity, for elucidating the pathways that regulate body weight and for the identification of potential therapeutic targets. The utility of these models may be further improved by exploring the impact of experimental manipulations on the behavioral determinants of energy balance.

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“…Whereas the hypothalamic model incorporates a behavior-integrative function, these findings show that contained within the caudal brainstem are integrative mechanisms capable of translating feeding-relevant sensory information into adaptive responses reminiscent of those obtained in the neurologically intact rat. The decerebrate's response to gastrointestinal and gustatory feedback, the primary controls of ingestive behavior over the short term (e.g., 15,30,40,125,207), endows it with a semblance of normal meal size control. Most intriguing, it has also become clear in recent years that within the brainstem are interoceptor mechanisms that provide the kind of information underlying control of energy balance over the longer term.…”

Section: Introductionmentioning

confidence: 99%

The Neuroanatomical Axis for Control of Energy Balance

Grill

Kaplan

2002

Frontiers in Neuroendocrinology

351

219

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The hypothalamic feeding-center model, articulated in the 1950s, held that the hypothalamus contains the interoceptors sensitive to blood-borne correlates of available or stored fuels as well as the integrative substrates that process metabolic and visceral afferent signals and issue commands to brainstem mechanisms for the production of ingestive behavior. A number of findings reviewed here, however, indicate that sensory and integrative functions are distributed across a central control axis that includes critical substrates in the basal forebrain as well as in the caudal brainstem. First, the interoceptors relevant to energy balance are distributed more widely than had been previously thought, with a prominent brainstem complement of leptin and insulin receptors, glucose-sensing mechanisms, and neuropeptide mediators. The physiological relevance of this multiple representation is suggested by the demonstration that similar behavioral effects can be obtained independently by stimulation of respective forebrain and brainstem subpopulations of the same receptor types (e.g., leptin, CRH, and melanocortin). The classical hypothalamic model is also challenged by the integrative achievements of the chronically maintained, supracollicular decerebrate rat. Decerebrate and neurologically intact rats show similar discriminative responses to taste stimuli and are similarly sensitive to intake-inhibitory feedback from the gut. Thus, the caudal brainstem, in neural isolation from forebrain influence, is sufficient to mediate ingestive responses to a range of visceral afferent signals. The decerebrate rat, however, does not show a hyperphagic response to food deprivation, suggesting that interactions between forebrain and brainstem are necessary for the behavioral response to systemic/ metabolic correlates of deprivation in the neurologically intact rat. At the same time, however, there is evidence suggesting that hypothalamic-neuroendocrine responses to fasting depend on pathways ascending from brainstem. Results reviewed are consistent with a distributionist (as opposed to hierarchical) model for the control of energy balance that emphasizes: (i) control mechanisms endemic to hypothalamus and brainstem that drive their unique effector systems on the basis of local interoceptive, and in the brainstem case, visceral, afferent inputs and (ii) a set of uni-and bidirectional interactions that coordinate adaptive neuroendocrine, autonomic, and behavioral responses to changes in metabolic status. KEY WORDS: feeding behavior; leptin; glucose sensing; decerebrate; neuropeptide; hypothalamic model; caudal brainstem; energy balance.

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Peripheral control of meal size in the rat: Effect of sham feeding on meal size and drinking rate.

Cited by 197 publications

References 17 publications

μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals

μ-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing palatability and suppressing satiety signals

Relevance of animal models to human eating disorders and obesity

The Neuroanatomical Axis for Control of Energy Balance

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