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Evidence for multiple inhibitory feeding signals in dehydration anorexia
Abstracts / Appetite 52 (2009) 815–868
Acute stress decreases food reward related brain activity LEMMENS 1,2 , A. NIEUWENHUIZEN 1,2 , E. J. BORN 1,2,∗ , S. FORMISANO 3 , R. GOEBEL 3 , M. WESTERTERP-PLANTENGA 1,2 1 Dept Human Biology, Maastricht University, Maastricht, Netherlands 2 TIFood and Nutrition, Wageningen, Netherlands 3 Dept Cognitive Neuroscience, Maastricht University, Maastricht, Netherlands Stress results in eating in the absence of hunger, likely due to changed food reward signaling. Our hypothesis: stress decreases central food reward signaling. To determine the effect of acute stress on food choice reward related brain activity, fasted women (n = 10, BMI = 21.5 ± 2.2 kg/m2 , Age = 24 ± 4 years) came 2× to randomly complete either the rest or stress (math test) condition. Per session, 2 fMRI scans were made, wherein subjects chose a meal (food images). The food’s rewarding value (liking & wanting), food characteristics (crispiness, FullnessOfTaste etc.), energy intake, plasma cortisol and VAS hunger & satiety were measured. Fasted state was confirmed by low satiety/high hunger (10.0 ± 10.3, 79.4 ± 15.3 m VAS). All conditions: Meal 1 energy intake (3 ± 1 MJ) and liking were equal, and food wanting was lower at meal 2 ( = −.3 items/category, p < .01). At rest: Meal 1 decreased hunger, increased satiety (−41.5, 50.6 mm VAS, p < .01), and energy intake and putamen activity was lower at meal 2 (−1.1 MJ/AUC =−.9%BOLD s, p < .05). The math-test led to stress (cortisol AUC = +2.2 × 104 nmol min/l, p < .05). Under stress: Satiety was lower after meal 1 (−8.0 mm VAS, p < .01), Meal 2 energy intake was similar to meal 1, crispiness and FullnessOfTaste were chosen more and brain activity was lower in relevant areas: putamen, amygdala and hippocampus (AUC = −1.0, −4.7, −2.5%BOLD s, p < .05). Our data suggest lower reward signaling and reward sensitivity under stress. doi:10.1016/j.appet.2009.04.028
Evidence for multiple inhibitory feeding signals in dehydration anorexia C.N. BOYLE ∗ , A.G. WATTS University of Southern California, Los Angeles, CA, USA Dehydrated (DE)-anorexic rats reliably begin eating within minutes of drinking water. Given the rapidity of this effect, we hypothesize that drinking water produces disinhibitory signals that release stimulatory networks to promote feeding. To investigate these inhibitory signals, we compared the ingestive behaviors of DE rats after the return of free access to water to the behavior exhibited by pair-fed (PF) rats after the return of free access to food. While both groups exhibit similar neuropeptidergic and hormonal profiles that are consistent with negative energy balance and usually promote feeding, DE rats exhibit hyperosmolality and voluntarily restrict food intake. We hypothesize that the rapid release (disinhibition) of stimulatory networks following the return of water is a distinct process that is dissociable from the slower suppression of inhibitory signals that impact central feeding networks. The components of feeding and drinking that constitute meal microstructure were analyzed for both groups in the minutes and days following the return of water or food. We found that DE but not PF rats maintain deficits in feeding behavior for some time, suggesting that some suppression of feeding networks persists in DE rats following water consumption. Our results show that although drinking water quickly disinhibits stimulatory feeding networks in DE rats, complete removal of all inhibitory signals requires additional time. Thus, hyperosmolality generates multiple inhibitory signals to inhibit feeding that are differentially disengaged and suppressed over time upon the return to euhydration. doi:10.1016/j.appet.2009.04.029
821
Effects of hunger and experience on portion size estimation by men N. BROGDEN ∗ , C. SINCLAIR, E. ALMIRON-ROIG Department of Biological Sciences, University of Chester, Chester, United Kingdom This study explores how hunger and experience influence portion size perception. Underestimation of food portion sizes, particularly in energy dense foods is associated with energy overconsumption; however its underlying mechanisms are poorly understood. Research suggests that postingestive consequences of food consumption may create links between foods and their ability to evoke fullness (Perceived Satiation, PS). Whether such links alter portion size perception is unclear. Twenty-seven men were tested in a 2 × 2 design on their estimate of portion sizes after an overnight fast (hungry) or after breakfast (full); and prompted or not with a PS cue (“how full would you be after consuming this amount of food”) before estimating portions. Foods included candy, cake, fruit, cereals, chips and caloric drinks. Estimates were compared with ADA, FDA, BDA and FSA portion standards. Portion size estimates for all foods/drinks were significantly smaller under hungry than under full conditions (p < 0.01). The PS cue had no effect. Error of estimates increased with increasing ED (r = 0.42, p < 0.05). Except for the banana, estimates were significantly smaller than actual amounts displayed, irrespective of appetite status (p < 0.001). This study confirms that hunger, a physiological cue, alters perception of food amounts. Higher ED foods and caloric beverages were worse estimated than other foods, in agreement with their reported obesity-inducing nature. There were large discrepancies between subjects’ perceptions of a portion and recommendations from governments/health professionals. doi:10.1016/j.appet.2009.04.030
Proestrus rats on a high-fat diet have less central inflammation than male rats L.M. BROWN 1,∗ , P.T. COONEY 1 , C.N. MILLER 1 , D.J. CLEGG 2 1 Department of Nutrition, University of North Carolina at Greensboro, Greensboro, NC, USA 2 University of Texas Southwestern Medical Center, Department of Internal Medicine, Dallas, TX, USA There is evidence that obesity is characterized by chronic activation of inflammatory pathways. The neuroprotective effects of ovarian hormones may be a result of the anti-inflammatory effects of estrogen and progesterone in adipose and cardiovascular tissue. In the present study we sought to extend these findings to the CNS. Three-month-old male and female Long-Evans rats (age matched) were given a HF or a low-fat (LF) diet for 72 h (n = 22) and sacrificed. Females were phased daily and started on the HF diet on the day of estrus so that 72 h later they would be in proestrus which is the peak of estradiol and progesterone. The medial basal hypothalamus was extracted and processed to determine if females were protected from HF-diet induced increased expression of inflammatory markers. Real-time quantitative PCR was performed for IL-6, SOCS3 and TNF␣. Males on the HF diet had increased hypothalamic expression of IL-6 and SOCS3 when compared to the LF diet while TNF␣ mRNA was unchanged. In contrast, females on the HF diet had reduced hypothalamic expression of IL-6 when compared to the LF diet while mRNA for SOCS3 and TNF␣ were unchanged. These data provide evidence that estradiol, previously demonstrated to be anti-inflammatory, may protect females from the metabolic syndrome or the diseases associated with obesity because exposure to a HF diet results in less CNS inflammation. doi:10.1016/j.appet.2009.04.031
Acute stress decreases food reward related brain activity LEMMENS 1,2 , A. NIEUWENHUIZEN 1,2 , E. J. BORN 1,2,∗ , S. FORMISANO 3 , R. GOEBEL 3 , M. WESTERTERP-PLANTENGA 1,2 1 Dept Human Biology, Maastricht University, Maastricht, Netherlands 2 TIFood and Nutrition, Wageningen, Netherlands 3 Dept Cognitive Neuroscience, Maastricht University, Maastricht, Netherlands Stress results in eating in the absence of hunger, likely due to changed food reward signaling. Our hypothesis: stress decreases central food reward signaling. To determine the effect of acute stress on food choice reward related brain activity, fasted women (n = 10, BMI = 21.5 ± 2.2 kg/m2 , Age = 24 ± 4 years) came 2× to randomly complete either the rest or stress (math test) condition. Per session, 2 fMRI scans were made, wherein subjects chose a meal (food images). The food’s rewarding value (liking & wanting), food characteristics (crispiness, FullnessOfTaste etc.), energy intake, plasma cortisol and VAS hunger & satiety were measured. Fasted state was confirmed by low satiety/high hunger (10.0 ± 10.3, 79.4 ± 15.3 m VAS). All conditions: Meal 1 energy intake (3 ± 1 MJ) and liking were equal, and food wanting was lower at meal 2 ( = −.3 items/category, p < .01). At rest: Meal 1 decreased hunger, increased satiety (−41.5, 50.6 mm VAS, p < .01), and energy intake and putamen activity was lower at meal 2 (−1.1 MJ/AUC =−.9%BOLD s, p < .05). The math-test led to stress (cortisol AUC = +2.2 × 104 nmol min/l, p < .05). Under stress: Satiety was lower after meal 1 (−8.0 mm VAS, p < .01), Meal 2 energy intake was similar to meal 1, crispiness and FullnessOfTaste were chosen more and brain activity was lower in relevant areas: putamen, amygdala and hippocampus (AUC = −1.0, −4.7, −2.5%BOLD s, p < .05). Our data suggest lower reward signaling and reward sensitivity under stress. doi:10.1016/j.appet.2009.04.028
Evidence for multiple inhibitory feeding signals in dehydration anorexia C.N. BOYLE ∗ , A.G. WATTS University of Southern California, Los Angeles, CA, USA Dehydrated (DE)-anorexic rats reliably begin eating within minutes of drinking water. Given the rapidity of this effect, we hypothesize that drinking water produces disinhibitory signals that release stimulatory networks to promote feeding. To investigate these inhibitory signals, we compared the ingestive behaviors of DE rats after the return of free access to water to the behavior exhibited by pair-fed (PF) rats after the return of free access to food. While both groups exhibit similar neuropeptidergic and hormonal profiles that are consistent with negative energy balance and usually promote feeding, DE rats exhibit hyperosmolality and voluntarily restrict food intake. We hypothesize that the rapid release (disinhibition) of stimulatory networks following the return of water is a distinct process that is dissociable from the slower suppression of inhibitory signals that impact central feeding networks. The components of feeding and drinking that constitute meal microstructure were analyzed for both groups in the minutes and days following the return of water or food. We found that DE but not PF rats maintain deficits in feeding behavior for some time, suggesting that some suppression of feeding networks persists in DE rats following water consumption. Our results show that although drinking water quickly disinhibits stimulatory feeding networks in DE rats, complete removal of all inhibitory signals requires additional time. Thus, hyperosmolality generates multiple inhibitory signals to inhibit feeding that are differentially disengaged and suppressed over time upon the return to euhydration. doi:10.1016/j.appet.2009.04.029
821
Effects of hunger and experience on portion size estimation by men N. BROGDEN ∗ , C. SINCLAIR, E. ALMIRON-ROIG Department of Biological Sciences, University of Chester, Chester, United Kingdom This study explores how hunger and experience influence portion size perception. Underestimation of food portion sizes, particularly in energy dense foods is associated with energy overconsumption; however its underlying mechanisms are poorly understood. Research suggests that postingestive consequences of food consumption may create links between foods and their ability to evoke fullness (Perceived Satiation, PS). Whether such links alter portion size perception is unclear. Twenty-seven men were tested in a 2 × 2 design on their estimate of portion sizes after an overnight fast (hungry) or after breakfast (full); and prompted or not with a PS cue (“how full would you be after consuming this amount of food”) before estimating portions. Foods included candy, cake, fruit, cereals, chips and caloric drinks. Estimates were compared with ADA, FDA, BDA and FSA portion standards. Portion size estimates for all foods/drinks were significantly smaller under hungry than under full conditions (p < 0.01). The PS cue had no effect. Error of estimates increased with increasing ED (r = 0.42, p < 0.05). Except for the banana, estimates were significantly smaller than actual amounts displayed, irrespective of appetite status (p < 0.001). This study confirms that hunger, a physiological cue, alters perception of food amounts. Higher ED foods and caloric beverages were worse estimated than other foods, in agreement with their reported obesity-inducing nature. There were large discrepancies between subjects’ perceptions of a portion and recommendations from governments/health professionals. doi:10.1016/j.appet.2009.04.030
Proestrus rats on a high-fat diet have less central inflammation than male rats L.M. BROWN 1,∗ , P.T. COONEY 1 , C.N. MILLER 1 , D.J. CLEGG 2 1 Department of Nutrition, University of North Carolina at Greensboro, Greensboro, NC, USA 2 University of Texas Southwestern Medical Center, Department of Internal Medicine, Dallas, TX, USA There is evidence that obesity is characterized by chronic activation of inflammatory pathways. The neuroprotective effects of ovarian hormones may be a result of the anti-inflammatory effects of estrogen and progesterone in adipose and cardiovascular tissue. In the present study we sought to extend these findings to the CNS. Three-month-old male and female Long-Evans rats (age matched) were given a HF or a low-fat (LF) diet for 72 h (n = 22) and sacrificed. Females were phased daily and started on the HF diet on the day of estrus so that 72 h later they would be in proestrus which is the peak of estradiol and progesterone. The medial basal hypothalamus was extracted and processed to determine if females were protected from HF-diet induced increased expression of inflammatory markers. Real-time quantitative PCR was performed for IL-6, SOCS3 and TNF␣. Males on the HF diet had increased hypothalamic expression of IL-6 and SOCS3 when compared to the LF diet while TNF␣ mRNA was unchanged. In contrast, females on the HF diet had reduced hypothalamic expression of IL-6 when compared to the LF diet while mRNA for SOCS3 and TNF␣ were unchanged. These data provide evidence that estradiol, previously demonstrated to be anti-inflammatory, may protect females from the metabolic syndrome or the diseases associated with obesity because exposure to a HF diet results in less CNS inflammation. doi:10.1016/j.appet.2009.04.031