Hindbrain Control of Food Intake: Behavioral Evidence for Metabolic Sensing and Modulation of Orosensory Responsiveness

Emotions ◽  
2015 ◽  
pp. 137-148
Author(s):  
R. C. Ritter ◽  
G. E. Edwards ◽  
V. K. Nonavinakere
Keyword(s):  
Food Intake ◽  
Metabolic Sensing ◽  
Behavioral Evidence

scholarly journals Fatty acid-induced astrocyte ketone production and the control of food intake

2016 ◽  
Vol 310 (11) ◽  
pp. R1186-R1192 ◽  
Author(s):  
Christelle Le Foll ◽  
Barry E. Levin
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Ketone Bodies ◽  
Critical Role ◽  
Caloric Intake ◽  
Ventromedial Hypothalamus ◽  
Leptin Resistance ◽  
Metabolic Sensing ◽  
Total Fat ◽  
Metabolic Unit

Obesity and Type 2 diabetes are major worldwide public health issues today. A relationship between total fat intake and obesity has been found. In addition, the mechanisms of long-term and excessive high-fat diet (HFD) intake in the development of obesity still need to be elucidated. The ventromedial hypothalamus (VMH) is a major site involved in the regulation of glucose and energy homeostasis where “metabolic sensing neurons” integrate metabolic signals from the periphery. Among these signals, fatty acids (FA) modulate the activity of VMH neurons using the FA translocator/CD36, which plays a critical role in the regulation of energy and glucose homeostasis. During low-fat diet (LFD) intake, FA are oxidized by VMH astrocytes to fuel their ongoing metabolic needs. However, HFD intake causes VMH astrocytes to use FA to generate ketone bodies. We postulate that these astrocyte-derived ketone bodies are exported to neurons where they produce excess ATP and reactive oxygen species, which override CD36-mediated FA sensing and act as a signal to decrease short-term food intake. On a HFD, VMH astrocyte-produced ketones reduce elevated caloric intake to LFD levels after 3 days in rats genetically predisposed to resist (DR) diet-induced obesity (DIO), but not leptin-resistant DIO rats. This suggests that, while VMH ketone production on a HFD can contribute to protection from obesity, the inherent leptin resistance overrides this inhibitory action of ketone bodies on food intake. Thus, astrocytes and neurons form a tight metabolic unit that is able to monitor circulating nutrients to alter food intake and energy homeostasis.

Obesity and adiposity: the culprit of dietary protein efficacy

2020 ◽  
Vol 134 (4) ◽  
pp. 389-401
Author(s):  
Carla El-Mallah ◽  
Omar Obeid
Keyword(s):  
Food Intake ◽  
Behavioural Change ◽  
Physiological Mechanism ◽  
Short Term ◽  
The Past ◽  
Body Adiposity ◽  
Reduce Sugar ◽  
Eye Opening ◽  
Potential Strategy ◽  
Limitations And Exceptions

Abstract Obesity and increased body adiposity have been alarmingly increasing over the past decades and have been linked to a rise in food intake. Many dietary restrictive approaches aiming at reducing weight have resulted in contradictory results. Additionally, some policies to reduce sugar or fat intake were not able to decrease the surge of obesity. This suggests that food intake is controlled by a physiological mechanism and that any behavioural change only leads to a short-term success. Several hypotheses have been postulated, and many of them have been rejected due to some limitations and exceptions. The present review aims at presenting a new theory behind the regulation of energy intake, therefore providing an eye-opening field for energy balance and a potential strategy for obesity management.

Modifications in food intake, leptin and CCK postprandial levels after Gastric Banding for morbid obesity

2001 ◽  
Vol 120 (5) ◽  
pp. A209-A209
Author(s):  
M LUCA ◽  
E CERVELLIN ◽  
F GALEAZZI ◽  
D LANARO ◽  
L BUSETTO ◽  
...  
Keyword(s):  
Morbid Obesity ◽  
Food Intake ◽  
Gastric Banding

Interaction of GLP-1 with gastric distension in regulating food intake and satiety in humans

2001 ◽  
Vol 120 (5) ◽  
pp. A208-A208
Author(s):  
L DEGEN ◽  
D MATZINGER ◽  
B FISCHER ◽  
F ZIMMERLI ◽  
M KNUPP ◽  
...  
Keyword(s):  
Food Intake ◽  
Gastric Distension

Dietary intake of tryptophan tied emotion-related impulsivity in humans

2019 ◽  
pp. 1-8 ◽  
Author(s):  
Florian Javelle ◽  
Descartes Li ◽  
Philipp Zimmer ◽  
Sheri L. Johnson
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Food Intake ◽  
Essential Amino Acid ◽  
Food Habits ◽  
Psychological Disorder ◽  
Serotonin Synthesis ◽  
Amino Acid Tryptophan ◽  
Pass Through ◽  
Three Factor

Abstract. Emotion-related impulsivity, defined as the tendency to say or do things that one later regret during periods of heightened emotion, has been tied to a broad range of psychopathologies. Previous work has suggested that emotion-related impulsivity is tied to an impaired function of the serotonergic system. Central serotonin synthesis relies on the intake of the essential amino acid, tryptophan and its ability to pass through the blood brain barrier. Objective: The aim of this study was to determine the association between emotion-related impulsivity and tryptophan intake. Methods: Undergraduate participants (N = 25, 16 women, 9 men) completed a self-rated measure of impulsivity (Three Factor Impulsivity Index, TFI) and daily logs of their food intake and exercise. These data were coded using the software NutriNote to evaluate intakes of tryptophan, large neutral amino acids, vitamins B6/B12, and exercise. Results: Correlational analyses indicated that higher tryptophan intake was associated with significantly lower scores on two out of three subscales of the TFI, Pervasive Influence of Feelings scores r =  –.502, p < . 010, and (lack-of) Follow-Through scores, r =  –.407, p < . 050. Conclusion: Findings provide further evidence that emotion-related impulsivity is correlated to serotonergic indices, even when considering only food habits. It also suggests the need for more research on whether tryptophan supplements might be beneficial for impulsive persons suffering from a psychological disorder.

Food-Evoked Changes in Humans

2010 ◽  
Vol 24 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Peter Walla ◽  
Maria Richter ◽  
Stella Färber ◽  
Ulrich Leodolter ◽  
Herbert Bauer
Keyword(s):  
Food Intake ◽  
Startle Response ◽  
Brain Activity ◽  
Soft Drink ◽  
Ice Cream ◽  
Response Amplitude ◽  
Response Modulation ◽  
Motivational States ◽  
Localization Analysis ◽  
Study Participants

Two experiments investigate effects related to food intake in humans. In Experiment 1, we measured startle response modulation while study participants ate ice cream, yoghurt, and chocolate. Statistical analysis revealed that ice cream intake resulted in the most robust startle inhibition compared to no food. Contrasting females and males, we found significant differences related to the conditions yoghurt and chocolate. In females, chocolate elicited the lowest response amplitude followed by yoghurt and ice cream. In males, chocolate produced the highest startle response amplitude even higher than eating nothing, whereas ice cream produced the lowest. Assuming that high response amplitudes reflect aversive motivation while low response amplitudes reflect appetitive motivational states, it is interpreted that eating ice cream is associated with the most appetitive state given the alternatives of chocolate and yoghurt across gender. However, in females alone eating chocolate, and in males alone eating ice cream, led to the most appetitive state. Experiment 2 was conducted to describe food intake-related brain activity by means of source localization analysis applied to electroencephalography data (EEG). Ice cream, yoghurt, a soft drink, and water were compared. Brain activity in rostral portions of the superior frontal gyrus was found in all conditions. No localization differences between conditions occurred. While EEG was found to be insensitive, startle response modulation seems to be a reliable method to objectively quantify motivational states related to the intake of different foods.

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