Behavioral components of high-fat diet hyperphagia:  meal size and postprandial satiety

Warwick, Zoe S.; McGuire, Colleen M.; Bowen, Kathleen J.; Synowski, Stephen J.

doi:10.1152/ajpregu.2000.278.1.r196

Cited by 38 publications

(34 citation statements)

References 16 publications

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“…There was no overall change in the total daily food intake, however, the daily pattern of ingestion was markedly altered. There was a significant decrease in meal size and an increase in meal duration in CCK 1 R +/+ mice ingesting the HF diet compared to the isocaloric LF diet; which is consistent with previous observations in rodents and humans [19,20]. In addition, there was a concomitant decrease in meal frequency in CCK 1 R +/+ mice fed the HF diet compared to the isocaloric LF diet.…”

Section: Discussionsupporting

confidence: 91%

CCK1 receptor is essential for normal meal patterning in mice fed high fat diet

Donovan

Paulino

Raybould

2007

Physiology & Behavior

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Cholecystokinin (CCK), released by lipid in the intestine, initiates satiety by acting at cholecystokinin type 1 receptors (CCK 1 Rs) located on vagal afferent nerve terminals located in the wall of the gastrointestinal tract. In the present study, we determined the role of the CCK 1 R in the short term effects of a high fat diet on daily food intake and meal patterns using mice in which the CCK 1 R gene is deleted. CCK 1 R -/-and CCK 1 R +/+ mice were fed isocaloric high fat (HF) or low fat (LF) diets ad libitum for 18 hours each day and meal size, meal frequency, intermeal interval, and meal duration were determined. Daily food intake was unaltered by diet in the CCK 1 R -/-compared to CCK 1 R +/+ mice. However, meal size was larger in the CCK 1 R -/-mice compared to CCK 1 R +/+ mice when fed a HF diet, with a concomitant decrease in meal frequency. Meal duration was increased in mice fed HF diet regardless of phenotype. In addition, CCK 1 R -/-mice fed a HF diet had a 75% decrease in the time to 1 st meal compared to CCK 1 R +/+ mice following a 6 hr fast. These data suggest that lack of the CCK 1 R results in diminished satiation, causing altered meal patterns including larger, less frequent meals when fed a high fat diet. These results suggest that the CCK 1 R is involved in regulating caloric intake on a meal to meal basis, but that other factors are responsible for regulation of daily food intake.

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Section: Discussionsupporting

confidence: 91%

CCK1 receptor is essential for normal meal patterning in mice fed high fat diet

Donovan

Paulino

Raybould

2007

Physiology & Behavior

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“…Chronic consumption of a high-fat diet has long been known to enhance total caloric intake as well as raise circulating levels of TG (36,69). Also, a small high-fat meal (15 kcal) or injection of a fat emulsion (10 kcal), both of which elevate TG levels, stimulates food intake in subsequent meals (12,42,50,69,70). The present findings help to elucidate possible mechanisms underlying this phenomenon of fat-induced hyperphagia.…”

Section: Stimulatory Effect Of Dietary Fat On Opioid Peptides In the mentioning

confidence: 56%

Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides

Chang

Karatayev²,

Ahsan³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Chang GQ, Karatayev O, Ahsan R, Gaysinskaya V, Marwil Z, Leibowitz SF. Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides. Am J Physiol Endocrinol Metab 292: E561-E570, 2007; doi:10.1152/ajpendo.00087.2006.-The opioid peptides enkephalin (ENK) and dynorphin (DYN), when injected into the hypothalamus, are known to stimulate feeding behavior and preferentially increase the ingestion of a high-fat diet. Studies of another peptide, galanin (GAL), with similar effects on feeding demonstrate that a high-fat diet, in turn, can stimulate the expression of this peptide in the hypothalamus. The present study tested different diets and variable periods of high-vs. low-fat diet consumption to determine whether the opioid peptides respond in a similar manner as GAL. In six experiments, the effects of dietary fat on ENK and DYN were examined in three hypothalamic areas: the paraventricular nucleus (PVN), perifornical hypothalamus (PFH), and arcuate nucleus (ARC). The results demonstrated that the ingestion of a high-fat diet increases gene expression and peptide levels of both ENK and DYN in the hypothalamus. The strongest and most consistent effect is seen in the PVN. In this nucleus, ENK and DYN are increased by 50 -100% after 1 wk, 1 day, 60 min, and even 15 min of high-fat diet consumption. While showing some effect in the PFH, these peptides in the ARC are considerably less responsive, exhibiting no change in response to the briefer periods of diet intake. This effect of dietary fat on PVN opioids can be observed with diets equal in caloric density and palatability and without a change in caloric intake, body weight, fat pad weight, or levels of insulin or leptin. The data reveal a strong and consistent association between these peptides and a rise in circulating levels of triglycerides, supporting a role for these lipids in the fat-induced stimulation of opioid peptides in the PVN, similar to GAL. galanin; opioid peptides; arcuate nucleus; feeding behavior; lipids RECENT EVIDENCE has demonstrated a close relationship between the orexigenic peptide galanin (GAL) and the consumption of a fat-rich diet. When injected into the paraventricular nucleus (PVN), this peptide stimulates feeding behavior in rats, and while having no specific effect on macronutrient preferences, GAL produces its strongest response in animals that prefer fat or are maintained on a fat-rich diet (34,41,65). Moreover, measurements of endogenous GAL reveal a stimulatory effect of acute or chronic high-fat diet consumption on gene expression and peptide levels specifically in the PVN (13,36,52). This supports the existence of a positive feedback loop, whereby a peptide stimulates intake of a diet that, in turn, increases production of this same peptide.The focus of this study is on the endogenous opioid peptides, enkephalin (ENK) and dynorphin (DYN). These peptides, like GAL, are known to increase feeding in a dose-dependent manner, and this response is observed with injection in...

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“…This fat-induced hyperphagia is evident in chronic feeding paradigms, with total daily intake and meal size rising in direct proportion to the amount of fat in the diet. It is also seen in acute feeding paradigms, with a small high-fat meal (10-15 Kcals) compared to an equal calorie low-fat meal being followed by a shorter post-meal interval and increased food intake in subsequent meals [25,[95][96][97][98]. This acute hyperphagia occurs whether the fat-rich meal is presented in solid or liquid form, infused intragastrically, injected as a fat emulsion, or given in a sham-feeding paradigm.…”

Section: Pathophysiological Consequences Of Dietary Fat Tg and Oreximentioning

confidence: 99%

Overconsumption of dietary fat and alcohol: Mechanisms involving lipids and hypothalamic peptides

Leibowitz

2007

Physiology & Behavior

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The studies described in this report provide interesting animal models for exploring some of the metabolic and neural antecedents to the over-consumption of fat and alcohol. The results provide strong support for the existence of positive feedback loops that involve a close relation between circulating lipids and orexigenic peptides in dorsal regions of the hypothalamus. The peptides involved in these circuits include galanin, enkephalin, dynorphin and orexin. These peptides are expressed in the paraventricular nucleus and perifornical lateral hypothalamus, and they have very different functions from peptides expressed in the arcuate nucleus. Through mechanisms involving circulating lipids that rise on energy-dense diets, these peptides in the dorsal hypothalamus are each increased by the consumption of fat and ethanol; these nutrients, in turn, stimulate further production of these same peptides that promote overeating and excess drinking. These mechanisms involving non-homeostatic, positive feedback circuits may be required under conditions when food supplies are scarce and periods of gorging are essential to survival. However, they have pathological and sometimes life-threatening consequences in modern society, where fat-rich foods and alcoholic drinks are abundantly available and are contributing to the marked rise over the past 25 years in obesity and diabetes in both children and adults.

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Behavioral components of high-fat diet hyperphagia: meal size and postprandial satiety

Cited by 38 publications

References 16 publications

CCK1 receptor is essential for normal meal patterning in mice fed high fat diet

CCK1 receptor is essential for normal meal patterning in mice fed high fat diet

Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides

Overconsumption of dietary fat and alcohol: Mechanisms involving lipids and hypothalamic peptides

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