Short-term Regulation Of Food Intake Research Articles

Evidence for Constitutive Microbiota-Dependent Short-Term Control of Food Intake in Mice: Is There a Link with Inflammation, Oxidative Stress, Endotoxemia, and GLP-1?

Aims: Although prebiotics, probiotics, and fecal transplantation can alter the sensation of hunger and/or feeding behavior, the role of the constitutive gut microbiota in the short-term regulation of food intake during normal physiology is still unclear. Results: An antibiotic-induced microbiota depletion study was designed to compare feeding behavior in conventional and microbiota-depleted mice. Tissues were sampled to characterize the time profile of microbiota-derived signals in mice during consumption of either standard or high-fat food for 1 h. Pharmacological and genetic tools were used to evaluate the contribution of postprandial endotoxemia and inflammatory responses in the short-term regulation of food intake. We observed constitutive microbial and macronutrient-dependent control of food intake at the time scale of a meal; that is, within 1 h of food introduction. Specifically, microbiota depletion increased food intake, and the microbiota-derived anorectic effect became significant during the consumption of high-fat but not standard food. This anorectic effect correlated with a specific postprandial microbial metabolic signature, and did not require postprandial endotoxemia or an NOD-, LRR-, and Pyrin domain-containing protein 3-inflammasome-mediated inflammatory response. Innovation and Conclusion: These findings show that the gut microbiota controls host appetite at the time scale of a meal under normal physiology. Interestingly, a microbiota-derived anorectic effect develops specifically with a high-fat meal, indicating that gut microbiota activity is involved in the satietogenic properties of foods. Antioxid. Redox Signal. 37, 349-369.

Activation of the ARCPOMC→MeA Projection Reduces Food Intake.

Proopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARC) plays an essential role in the control of food intake and energy expenditure. Melanocortin-4 receptors (MC4Rs) are expressed in key areas that are implicated in regulating energy homeostasis. Although the importance of MC4Rs in the paraventricular hypothalamus (PVH) has been well documented, the role of MC4Rs in the medial amygdala (MeA) on feeding remains controversial. In this study, we specifically examine the role of a novel ARCPOMC→MeA neural circuit in the regulation of short-term food intake. To map a local melanocortinergic neural circuit, we use monosynaptic anterograde as well as retrograde viral tracers and perform double immunohistochemistry to determine the identity of the neurons receiving synaptic input from POMC neurons in the ARC. To investigate the role of the ARCPOMC→MeA projection on feeding, we optogenetically stimulate channelrhodopsin-2 (ChR2)-expressing POMC fibers in the MeA. Anterograde viral tracing studies reveal that ARC POMC neurons send axonal projections to estrogen receptor-α (ER-α)- and MC4R-expressing neurons in the MeA. Retrograde viral tracing experiments show that the neurons projecting to the MeA is located mainly in the lateral part of the ARC. Optogenetic stimulation of the ARCPOMC→MeA pathway reduces short-term food intake. This anorectic effect is blocked by treatment with the MC4R antagonist SHU9119. In addition to the melanocortinergic local circuits within the hypothalamus, this extrahypothalamic ARCPOMC→MeA neural circuit would play a role in regulating short-term food intake.

Intestinal NAPE-PLD contributes to short-term regulation of food intake via gut-to-brain axis.

Our objective was to explore the physiological role of the intestinal endocannabinoids in the regulation of appetite upon short-term exposure to high-fat-diet (HFD) and understand the mechanisms responsible for aberrant gut-brain signaling leading to hyperphagia in mice lacking Napepld in the intestinal epithelial cells (IECs). We generated a murine model harboring an inducible NAPE-PLD deletion in IECs (NapepldΔIEC). After an overnight fast, we exposed wild-type (WT) and NapepldΔIEC mice to different forms of lipid challenge (HFD or gavage), and we compared the modification occurring in the hypothalamus, in the vagus nerve, and at endocrine level 30 and 60 min after the stimulation. NapepldΔIEC mice displayed lower hypothalamic levels of N-oleoylethanolamine (OEA) in response to HFD. Lower mRNA expression of anorexigenic Pomc occurred in the hypothalamus of NapepldΔIEC mice after lipid challenge. This early hypothalamic alteration was not the consequence of impaired vagal signaling in NapepldΔIEC mice. Following lipid administration, WT and NapepldΔIEC mice had similar portal levels of glucagon-like peptide-1 (GLP-1) and similar rates of GLP-1 inactivation. Administration of exendin-4, a full agonist of GLP-1 receptor (GLP-1R), prevented the hyperphagia of NapepldΔIEC mice upon HFD. We conclude that in response to lipid, NapepldΔIEC mice displayed reduced OEA in brain and intestine, suggesting an impairment of the gut-brain axis in this model. We speculated that decreased levels of OEA likely contributes to reduce GLP-1R activation, explaining the observed hyperphagia in this model. Altogether, we elucidated novel physiological mechanisms regarding the gut-brain axis by which intestinal NAPE-PLD regulates appetite rapidly after lipid exposure.

Effect of video game playing and a glucose preload on subjective appetite, subjective emotions, and food intake in overweight and obese boys.

Video game playing (VGP) is associated with overweight/obesity (OW/OB). VGP and caloric preloads in the pre-meal environment influence short-term food intake (FI) in healthy-weight children. Therefore, the purpose of the present study was to examine the effect of pre-meal VGP and a glucose preload on subjective emotions, subjective appetite, and FI in boys with OW/OB. On 4 separate mornings, boys with OW/OB (n = 22; mean ± SD: age = 11.9 ± 1.6 years; body mass index percentile = 94.3 ± 3.9) participated in 4 test conditions. Two hours after a standardized breakfast, boys consumed equally sweetened preloads (250 mL) of sucralose (0 kcal) or glucose (200 kcal), with or without 30 min of subsequent VGP. Immediately after each test condition, FI was evaluated during an ad libitum pizza meal. Subjective appetite was measured at 0 (baseline), 15, and 30 min. Subjective emotions (aggression, anger, excitement, disappointment, happiness, upset, and frustration) were measured at 0 and 30 min. VGP did not affect FI, but the glucose preload decreased FI compared with the sucralose control (Δ = -103 ± 48 kcal, p < 0.01). However, cumulative FI (preload kcal + meal kcal) was 9% higher after the glucose preload (p < 0.01). Subjective appetite increased with time (p < 0.05) but was not influenced by preload or VGP. Frustration was the only subjective emotion that increased following VGP (p < 0.01). A glucose preload, but not VGP, suppressed FI in boys with OW/OB, suggesting a primary role of physiological factors in short-term FI regulation.

Protein Digestion-Derived Peptides and the Peripheral Regulation of Food Intake.

The gut plays a central role in energy homeostasis. Food intake regulation strongly relies on the gut–brain axis, and numerous studies have pointed out the significant role played by gut hormones released from enteroendocrine cells. It is well known that digestive products of dietary protein possess a high satiating effect compared to carbohydrates and fat. Nevertheless, the processes occurring in the gut during protein digestion involved in the short-term regulation of food intake are still not totally unraveled. This review provides a concise overview of the current data concerning the implication of food-derived peptides in the peripheral regulation of food intake with a focus on the gut hormones cholecystokinin and glucagon-like peptide 1 regulation and the relationship with some aspects of glucose homeostasis.

Loss of Vagal Sensitivity to Cholecystokinin in Rats Born with Intrauterine Growth Retardation and Consequence on Food Intake.

Perinatal malnutrition is associated with low birth weight and an increased risk of developing metabolic syndrome in adulthood. Modification of food intake (FI) regulation was observed in adult rats born with intrauterine growth retardation induced by maternal dietary protein restriction during gestation and maintained restricted until weaning. Gastrointestinal peptides and particularly cholecystokinin (CCK) play a major role in short-term regulation of FI by relaying digestive signals to the hindbrain via the vagal afferent nerve (VAN). We hypothesized that vagal sensitivity to CCK could be affected in rats suffering from undernutrition [low protein (LP)] during fetal and postnatal life, leading to an altered gut–brain communication and impacting satiation. Our aim was to study short-term FI along with signals of appetite and satiation in adult LP rats compared to control rats. The dose–response to CCK injection was investigated on FI as well as the associated signaling pathways activated in nodose ganglia. We showed that LP rats have a reduced first-meal satiety ratio after a fasting period associated to a higher postprandial plasmatic CCK release, a reduced sensitivity to CCK when injected at low concentration and a reduced presence of CCK-1 receptor in nodose ganglia. Accordingly, the lower basal and CCK-induced phosphorylation of calcium/calmodulin-dependent protein kinase in nodose ganglia of LP rats could reflect an under-expressed vanilloid family of transient receptor potential cation channels on VAN. Altogether, the present data demonstrated a reduced vagal sensitivity to CCK in LP rats at adulthood, which could contribute to deregulation of FI reported in this model.

Effect of Macronutrient Composition on Short-Term Food Intake and Weight Loss

AbstractThe purpose of this review is to describe the role of macronutrient composition on the suppression of short-term food intake (FI) and weight loss. The effects of macronutrient composition on short-term FI will be reviewed first, followed by a brief examination of longer-term clinical trials that vary in effects of dietary macronutrient composition on weight loss. The objectives were: 1) to examine the effect of macronutrient composition on the suppression of short-term FI, 2) to determine whether some macronutrient sources suppress FI beyond their provision of energy, 3) to assess the combined effects of macronutrients on FI and glycemic response, and 4) to determine whether knowledge of the effect of macronutrients on short-term FI has led to greater success in spontaneous weight loss, adherence to energy-restricted diets, and better weight maintenance after weight loss. Although knowledge of macronutrient composition on short-term FI regulation has advanced our understanding of the role of diet composition on energy balance, it has yet to lead to greater success in long-term weight loss and weight maintenance. It is clear from this review that many approaches based on manipulating dietary macronutrient composition can help people lose weight as long as they follow the diets. However, only by evaluating the interaction between the physiologic systems that govern FI and body weight may the benefits of dietary macronutrient composition be fully realized.

Pre-meal video game playing and a glucose preload suppress food intake in normal weight boys

Increased food intake (FI) during television viewing has been reported in children, but it is unknown if this occurs following pre-meal video game playing (VGP). The objective was to determine the effect of pre-meal VGP for 30 min on subjective appetite and emotions, and FI in normal weight (NW) boys after a glucose or control preload. On four test mornings, NW boys (n = 19) received equally sweetened preloads of a non-caloric sucralose control or 50 g glucose in 250 mL of water, with or without VGP for 30 min. Food intake from an ad libitum pizza meal was measured immediately after. Subjective appetite was measured at 0, 15, 30, and 60 min. Subjective emotions were determined by visual analog scale at baseline and immediately before lunch. Both VGP (p = 0.023) and glucose (p < 0.001) suppressed FI. Pre-meal VGP compared with no-VGP, and glucose compared with the non-caloric control, decreased FI by 59 and 170 kcal, respectively. Subjective average appetite increased to 30 min (p = 0.003), but was lower after glucose (p = 0.01) in both the VGP and no-VGP conditions compared with the control. Frustration and aggression scores increased after VGP (p < 0.05), but did not correlate with FI. However, baseline and pre-meal happiness and excitement scores were inversely associated with FI. In conclusion, both pre-meal VGP and the glucose preload suppressed FI, supporting the roles of both physiologic and environmental factors in the regulation of short-term FI in 9- to 14-year-old NW boys.

A pre‐meal glucose drink, but not video game playing, suppresses food intake in overweight and obese boys (1040.8)

We previously reported decreased food intake (FI) after a glucose drink and 30 min of video game playing (VGP) in normal weight boys, but the effect on FI in boys with increased adiposity is unknown. Therefore, we examined the effect of 30 min of pre‐meal VGP on subjective appetite, emotions and FI in overweight/obese (&gt;85th BMI percentile) boys after a glucose drink. On four mornings, in random order and one‐week apart, boys (n = 22; age = 11.9 ± 0.3 y) consumed equally sweetened drinks (250 mL) of sucralose (0 kcal) or 50 g (200 kcal) glucose, with or without 30 min of subsequent VGP, 2 h after a standardized breakfast. Immediately after all test conditions FI (mean ± SEM kcal) from an ad libitum pizza meal was measured. Subjective appetite was measured at baseline (0 min), 20, 35, and 65 min (post‐meal). While glucose (p &lt; 0.01) decreased FI (∆ = ‐103 ± 48 kcal) compared with the sucralose control, cumulative FI (drink kcal + meal kcal) was higher (p &lt; 0.01). Fullness (p &lt; 0.05) was lower, and subjective aggressiveness (p &lt; 0.01), excitement (p &lt; 0.01), upset (p = 0.05), and frustration (p &lt; 0.05) higher after VGP; however, subjective emotions did not correlate with FI. In conclusion, the stronger effect of glucose compared with VGP on FI is indicative of the primary role of physiologic factors in the short‐term regulation of FI in overweight/obese boys.Grant Funding Source: Supported by The Danone Institute of Canada, Grant‐in‐aid program

Involvement of orexin-A neurons but not melanin-concentrating hormone neurons in the short-term regulation of food intake in rats

In order to elucidate the involvement of melanin-concentrating hormone (MCH) and orexin-A (ORX-A) neurons of the perifornical/lateral hypothalamic areas (PF/LH) in the regulation of food intake induced by acutely reduced glucose availability, we examined the food intake response and c-Fos expression in the MCH and ORX-A neurons in the PF/LH during 2-deoxy-D-glucose (2DG)-induced glucoprivation (400 mg/kg; i.v.) and systemic insulin-induced hypoglycemia (5 U/kg; s.c.) in male Wistar rats. The administration of both 2DG and insulin stimulated food intake and induced c-Fos expression in the ORX-A neurons corresponding to food intake, but not in the MCH neurons. These data indicate that ORX-A neurons, but not MCH neurons, play a role in the short-term regulation of food intake, and that the input signals for the neurons containing MCH and ORX-A are different, and these neurons play different roles in the regulation of feeding behavior.

Role of oleoylethanolamide as a feeding regulator in goldfish.

Oleoylethanolamide (OEA) is a bioactive lipid mediator, produced in the intestine and other tissues, which is involved in energy balance regulation in mammals, modulating feeding and lipid metabolism. The purpose of the present study was to investigate the presence and possible role of OEA in feeding regulation in goldfish (Carassius auratus). We assessed whether goldfish peripheral tissues and brain contain OEA and their regulation by nutritional status. OEA was detected in all studied tissues (liver, intestinal bulb, proximal intestine, muscle, hypothalamus, telencephalon and brainstem). Food deprivation (48 h) reduced intestinal OEA levels and levels increased upon re-feeding, suggesting that this compound may be involved in the short-term regulation of food intake in goldfish, as a satiety factor. Next, the effects of acute intraperitoneal administration of OEA on feeding, swimming and plasma levels of glucose and triglycerides were analysed. Food intake, swimming activity and circulating triglyceride levels were reduced by OEA 2 h post-injection. Finally, the possible interplay among OEA and other feeding regulators (leptin, cholecystokinin, ghrelin, neuropeptide Y, orexin and monoamines) was investigated. OEA actions on energy homeostasis in goldfish could be mediated, at least in part, through interactions with ghrelin and the serotonergic system, as OEA treatment reduced ghrelin expression in the intestinal bulb, and increased serotonergic activity in the telencephalon. In summary, our results indicate for the first time in fish that OEA could be involved in the regulation of feeding, swimming and lipid metabolism, suggesting a high conservation of OEA actions in energy balance throughout vertebrate evolution.

Ghrelin for regulating appetite and energy balance: A systematic review

Gut hormones play a significant role in regulating feeding and energy balance. Almost all the gut hormones are responsible for reducing appetite i.e. they are anorectic, except for ghrelin which is responsible for increasing the appetite i.e. it has an orexigenic effect. Ghrelin is a 28-amino acid bioactive peptide hormone that was isolated from the stomach in 1999 by Kojima et al. A natural endogenous ligand of the growth hormone (GH) secretagogue receptor, it helps in the regulation of glucose and fat metabolism and regulation of energy balance. It also plays an essential role in regulation of appetite and bodyweight as well as modulation of gastrointestinal functions. The electronic databases, like CENTRAL, DARE, CDSR, Cochrane Methodology Reviews, MEDLINE, PUBMED and other resources. hard copies and unpublished works were searched. Pubmed keyword strategy was tailored to the other databases. The previous studies points out that Ghrelin is a hormone and the only known circulating orexigen produced in response to hunger. Although many substances play a role in the control of appetite, ghrelin is the only known peptide which increases appetite by sending signals of starvation from a stomach to the central nervous system. Besides playing a role in short-term regulation of food intake, ghrelin might also play a role in long-term regulation of energy balance. It also shows effects on the reward and motivation centers in the brain regions. Ghrelin has diverse roles. It also plays an essential role in regulation of appetite and bodyweight as well as modulation of gastrointestinal functions. As ghrelin is disturbed in obesity, it is important to reveal the mechanism of action for the purpose of developing novel therapeutic interventions.

Effects of Long- and Short-Chain Fatty Acids on the Release of Gastrointestinal Hormones using an ex Vivo Porcine Intestinal Tissue Model

Gastrointestinal (GI) peptide hormones play an important role in short-term regulation of food intake and blood glucose levels. Modulating their release is of potential relevance for weight management and possibly diabetes. As currently available models are hard to extrapolate to the human situation, the use of porcine intestinal tissue, collected from slaughter pigs, was investigated for this purpose. Intestinal tissue disks showed a predicted regional release pattern of GI peptides. Various long-chain fatty acids differentially stimulated release of glucagon-like peptide 1 (GLP-1) (up to 500%) and glucagon-like peptide 2 (GLP-2) (up to 200%) from ileal tissue disks, but effects on peptide YY (PYY) did not reach significance. Short-chain fatty acids had no effects on the release of GLP-1, GLP-2, and PYY in either the ileum or colon. In conclusion, this porcine tissue model shows to be of advantageous use in a tiered approach to study the potential of satiety-inducing compounds to be selected for studies in humans.

Ghrelin and feeding behaviour in preterm infants

The importance of early life events in the development of metabolic diseases is well recognized. Early postnatal environment, including nutrition, is key to future health, and this is particularly true for preterm infants. It is important that these infants receive sufficient nutrients to prevent growth restriction and promote neurodevelopment, while minimizing predisposition to metabolic diseases later in life. Feeding habits are the fundamental elements of nutrition and are influenced by many factors, including personal and familial habits, socioeconomic status, and cultural environment. In the last decades, there has been an important scientific interest toward the comprehension of the molecular and neural mechanisms regulating appetite. In these networks, act many peptide hormones produced in brain or gut, among which ghrelin is important because of its action in the short-term regulation of food intake and the long-term regulation of body weight. Ghrelin stimulates appetite and plays a role in regulating feeding behaviour. Ghrelin levels vary from fetal life through to early adulthood, with the highest levels observed in the very early years. Cord ghrelin levels have been evaluated in term and preterm newborns and high ghrelin levels have been observed in small-for-gestational age newborns and in newborns with intrauterine growth restriction. Moreover, ghrelin has been detected in term and preterm human breast milk, suggesting that it may play a role in the development of neuroendocrine pathways regulating appetite and energy homeostasis in early life. However, more research is required to better define ghrelin's role in breast milk and on feeding behaviour.

The Relationship between Substrate Metabolism, Exercise and Appetite Control

The way in which metabolic fuels are utilized can alter the expression of behaviour in the interests of regulating energy balance and fuel availability. This is consistent with the notion that the regulation of appetite is a psychobiological process, in which physiological mediators act as drivers of behaviour. The glycogenostatic theory suggests that glycogen availability is central in eliciting negative feedback signals to restore energy homeostasis. Due to its limited storage capacity, carbohydrate availability is tightly regulated and its restoration is a high metabolic priority following depletion. It has been proposed that such depletion may act as a biological cue to stimulate compensatory energy intake in an effort to restore availability. Due to the increased energy demand, aerobic exercise may act as a biological cue to trigger compensatory eating as a result of perturbations to muscle and liver glycogen stores. However, studies manipulating glycogen availability over short-term periods (1-3 days) using exercise, diet or both have often produced equivocal findings. There is limited but growing evidence to suggest that carbohydrate balance is involved in the short-term regulation of food intake, with a negative carbohydrate balance having been shown to predict greater ad libitum feeding. Furthermore, a negative carbohydrate balance has been shown to be predictive of weight gain. However, further research is needed to support these findings as the current research in this area is limited. In addition, the specific neural or hormonal signal through which carbohydrate availability could regulate energy intake is at present unknown. Identification of this signal or pathway is imperative if a casual relationship is to be established. Without this, the possibility remains that the associations found between carbohydrate balance and food intake are incidental.

Gastrin releasing peptide-29 evokes feeding responses in the rat

In mammals, gastrin releasing peptide (GRP) 10 and 27 reduce food intake. In the current work, we test the hypothesis that GRP-29, the large molecular form of GRP in the rat, also evokes feeding responses consistent with a possible role in satiety. Here, we measured three feeding responses, size of first meal, intermeal interval (IMI, time between first and second meal) and satiety ratio (SR, satiation period for every unit of food consumed in the first meal), in overnight food deprived rats following GRP-10, 27 or 29 (0, 0.3, 1.0, 2.1, 4.1, 10.3, 17.2 nmol/kg) intraperitoneally and presentation of a 10% sucrose test diet. GRP-29 and GRP-27 reduced the size of the first meal, prolonged IMI and increased SR, but GRP-10 failed to exhibit similar feeding responses. The order of potency was GRP-29 = GRP-27 > GRP-10. The current data support a role for GRP-29 in the short-term regulation of food intake.

Foods and nutrients modulates the release of anorexigenic gastrointestinal hormones

The short-term regulation of food intake controls what, how much and when we eat during one day or a single meal. When ingested, the nutrients produce satiety by means of mechanic stimulation and hormonal release. Many of these hormones also inhibit gastric empting and increase the gastric mechanoreceptor stimulation. The present review of the literature focuses on the effect of different food and nutrients on the release of anorexigenic regulators of food intake, as polypeptide insulinotropic glucose dependent, oxyntomodulin, peptide YY, cholecystokinin, and glucagon-like peptide 1.

Leptin (the ob gene product), ob-receptor and ghrelin immunolocalizations in fasted and fed swine gastrointestinal mucosa

Leptin and ghrelin are hormones, which affect food intake and energy balance. Leptin is secreted, among other tissues, by the mammalian white adipose tissue and can prevent feeding. Ghrelin, which is mainly secreted by the stomach, elicits the opposite effect. Considering that leptin has been extracted from the gastric mucosa too, this study was performed to investigate gastric immunolocalizations of leptin, leptin-receptor (OB-R) and ghrelin in 18 h-fasted and 2 h-fed adult pigs. Leptin was detected in the gastric fundus, where cells on the lower half of the gastric glands were positive for either OB or pepsinogen in fasted animals, and both immunoreactivities were detected all along the gastric glands in the fed ones. OB-R-immunoreactivity was present in duodenal and jejunal enterocytes, as already seen in other species. Ghrelin-positive endocrine cells were detected in all the three glandular regions of gastric mucosa, although labeled cells were most numerous in the oxyntic mucosa, without difference in relation with fasting and feeding. We suggest that leptin is involved in the peripheral short-term regulation of food intake, possibly acting as an endocrine and paracrine regulating factor.

Reduced energy intake at breakfast is not compensated for at lunch if a high-insoluble-fiber cereal replaces a low-fiber cereal

BackgroundIn cohort studies, insoluble fiber has been associated with a reduced risk of obesity and diabetes; however, compared with soluble fiber, its role in the regulation of short-term food intake (FI) and satiety has received little attention. Objective:Our aim was to compare the effects of a high-insoluble-fiber (HF) cereal with a low-fiber (LF) cereal on FI, subjective appetite (SA), and plasma glucose (PG) in healthy individuals. Design:Males and females (n = 32) were randomly assigned to consume 60 g of either HF (26 g insoluble fiber, 120 kcal) or LF (1 g fiber, 217 kcal) breakfast cereal. Pre- and postlunch SA and PG were measured regularly for 4 h, and ad libitum FI was measured at 3 h. Results:The prelunch SA area under the curve did not differ between the 2 cereals, but when expressed as change in appetite per kilocalorie of cereal, HF suppressed SA more than did LF (−17.6 ± 1.8 compared with −10.0 ± 1.1 mm · min · kcal−1, respectively; P < 0.01). Lunchtime FI did not differ between cereals, but cumulative energy intake (cereal + lunch) was lower after the HF than after the LF cereal (1330 ± 57 compared with 1422 ± 66 kcal, respectively; P = 0.01). The prelunch PG area under the curve (P < 0.0001) and the immediate postlunch PG (P = 0.01) were lower after HF cereal consumption. Conclusions:An HF breakfast cereal contributes to a cumulative reduction in breakfast and lunch energy intake, possibly due to its high satiety value per kilocalorie. A short-term benefit of the HF cereal, compared with LF cereal, was lower PG concentration before and immediately after lunch.

Increased expression of receptors for orexigenic factors in nodose ganglion of diet-induced obese rats

The vagal afferent pathway is important in short-term regulation of food intake, and decreased activation of this neural pathway with long-term ingestion of a high-fat diet may contribute to hyperphagic weight gain. We tested the hypothesis that expression of genes encoding receptors for orexigenic factors in vagal afferent neurons are increased by long-term ingestion of a high-fat diet, thus supporting orexigenic signals from the gut. Obesity-prone (DIO-P) rats fed a high-fat diet showed increased body weight and hyperleptinemia compared with low-fat diet-fed controls and high-fat diet-induced obesity-resistant (DIO-R) rats. Expression of the type I cannabinoid receptor and growth hormone secretagogue receptor 1a in the nodose ganglia was increased in DIO-P compared with low-fat diet-fed controls or DIO-R rats. Shifts in the balance between orexigenic and anorexigenic signals within the vagal afferent pathway may influence food intake and body weight gain induced by high fat diets.