scholarly journals Vulnerability to diet-induced obesity is associated with greater food priming-induced reinstatement of palatable food seeking

2020 ◽  
Vol 213 ◽  
pp. 112730 ◽  
Author(s):  
Hannah Bodnar ◽  
Brianna Denyko ◽  
Paige Waenke ◽  
Kevin T. Ball
Keyword(s):  
Palatable Food ◽  
Diet Induced Obesity ◽  
Food Seeking

scholarly journals Metaplasticity in the ventral pallidum as a potential marker for the development of diet-induced obesity

2020 ◽  
Author(s):  
Shani Gendelis ◽  
Dorrit Inbar ◽  
Kineret Inbar ◽  
Shanee Mesner ◽  
Yonatan M. Kupchik
Keyword(s):  
Major Change ◽  
Normal Weight ◽  
Ventral Pallidum ◽  
Modern World ◽  
Inhibitory Input ◽  
Palatable Food ◽  
Diet Induced Obesity ◽  
Potential Marker ◽  
Unlimited Access ◽  
Patch Clamp Electrophysiology

AbstractA major driver of obesity is the increasing palatability of processed foods. Although reward circuits promote the consumption of palatable food their involvement in obesity remains unclear. The ventral pallidum (VP) is a key hub in the reward system that encodes the hedonic aspects of palatable food consumption and participates in various proposed feeding circuits. However, there is still no evidence for its involvement in developing diet-induced obesity. Here we examine, using male C57bl6/J mice and patch-clamp electrophysiology, how chronic high-fat-high-sugar (HFHS) diet changes the physiology of the VP and whether mice that gain the most weight differ in their VP physiology from others. We found that 10-12 weeks of HFHS diet hyperpolarized and decreased the firing rate of VP neurons without a major change in synaptic inhibitory input. Within the HFHS group, obesity-prone (OP, top 33% weight gainers) mice had a more hyperpolarized VP with longer latency to fire action potentials upon depolarization compared to obesity-resistant (OR, bottom 33% weight gainers) mice. OP mice also showed synaptic potentiation of inhibitory inputs both at the millisecond and minute ranges. Moreover, we found that the tendency to potentiate the inhibitory inputs to the VP might exist in overeating mice even before exposure to HFHS, thus making it a potential property of being an overeater. These data point to the VP as a critical player in obesity and suggest that hyperpolarized membrane potential of, and potentiated inhibitory inputs to, VP neurons may play a significant role in promoting overeating of palatable food.Significance statementIn modern world, where highly-palatable food is readily available, overeating is often driven by motivational, rather than metabolic, needs. It is thus conceivable that reward circuits differ between obese and normal-weight individuals. But is such difference, if it exists, innate or develops with overeating? Here we reveal synaptic properties in the ventral pallidum, a central hub of reward circuits, that differ between mice that gain the most and the least weight when given unlimited access to highly-palatable food. We show that these synaptic differences exist also without exposure to palatable food, potentially making them innate properties that render some more susceptible than others to overeat. Thus, the propensity to overeat may have a strong innate component embedded in reward circuits.

scholarly journals Effects of chronic stress on reinstatement of palatable food seeking: Sex differences and relationship to trait anxiety

2020 ◽  
Vol 221 ◽  
pp. 112900
Author(s):  
Kevin T. Ball ◽  
Olivia Best ◽  
Erin Hagan ◽  
Claire Pressimone ◽  
Lindsay Tosh
Keyword(s):  
Sex Differences ◽  
Chronic Stress ◽  
Trait Anxiety ◽  
Palatable Food ◽  
Food Seeking

scholarly journals The use of the reinstatement model to study relapse to palatable food seeking during dieting

2014 ◽  
Vol 76 ◽  
pp. 395-406 ◽  
Author(s):  
Donna J. Calu ◽  
Yu-Wei Chen ◽  
Alex B. Kawa ◽  
Sunila G. Nair ◽  
Yavin Shaham
Keyword(s):  
Palatable Food ◽  
Food Seeking

scholarly journals The Orexigenic Force of Olfactory Palatable Food Cues in Rats

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3101
Author(s):  
Fiona Peris-Sampedro ◽  
Iris Stoltenborg ◽  
Marie V. Le May ◽  
Pol Sole-Navais ◽  
Roger A. H. Adan ◽  
...  
Keyword(s):  
Risk Taking ◽  
Neural Substrates ◽  
Male Rats ◽  
Palatable Food ◽  
Food Cues ◽  
Ghrelin Receptor ◽  
Hypothalamic Arcuate Nucleus ◽  
Olfactory Detection ◽  
Food Seeking ◽  
External Stimuli

Environmental cues recalling palatable foods motivate eating beyond metabolic need, yet the timing of this response and whether it can develop towards a less palatable but readily available food remain elusive. Increasing evidence indicates that external stimuli in the olfactory modality communicate with the major hub in the feeding neurocircuitry, namely the hypothalamic arcuate nucleus (Arc), but the neural substrates involved have been only partially uncovered. By means of a home-cage hidden palatable food paradigm, aiming to mimic ubiquitous exposure to olfactory food cues in Western societies, we investigated whether the latter could drive the overeating of plain chow in non-food-deprived male rats and explored the neural mechanisms involved, including the possible engagement of the orexigenic ghrelin system. The olfactory detection of a familiar, palatable food impacted upon meal patterns, by increasing meal frequency, to cause the persistent overconsumption of chow. In line with the orexigenic response observed, sensing the palatable food in the environment stimulated food-seeking and risk-taking behavior, which are intrinsic components of food acquisition, and caused active ghrelin release. Our results suggest that olfactory food cues recruited intermingled populations of cells embedded within the feeding circuitry within the Arc, including, notably, those containing the ghrelin receptor. These data demonstrate the leverage of ubiquitous food cues, not only for palatable food searching, but also to powerfully drive food consumption in ways that resonate with heightened hunger, for which the orexigenic ghrelin system is implicated.

scholarly journals Neurotensin neurons in the central extended amygdala control energy balance

2021 ◽  
Author(s):  
Alessandro Furlan ◽  
Alberto Corona ◽  
Sara Boyle ◽  
Radhashree Sharma ◽  
Rachel Rubino ◽  
...  
Keyword(s):  
Physical Activity ◽  
Energy Balance ◽  
Food Intake ◽  
Neuronal Population ◽  
Dependent Manner ◽  
Palatable Food ◽  
Extended Amygdala ◽  
Diet Induced Obesity ◽  
Sedentary Life Style ◽  
Metabolic Dysfunctions

Overeating and a sedentary life style are major causes of obesity and related metabolic disorders. Identification of the neurobiological processes that regulate energy balance will facilitate development of interventions for these disorders. Here we show that the Neurotensin-expressing neurons in the mouse IPAC (IPACNts), a nucleus of the central extended amygdala, bidirectionally coordinate hedonic feeding and physical activity, thereby regulating energy balance, metabolic processes and bodyweight. IPACNts are preferentially activated by consumption of highly palatable food or exposure to its taste and smell. Activating IPACNts promotes food intake in a palatability-dependent manner and decreases locomotion. Conversely, inhibiting IPACNts selectively reduces palatable food intake and dramatically enhances physical activity and energy expenditure, and in parallel stimulates physiological responses that oppose diet-induced obesity and metabolic dysfunctions. Thus, a single neuronal population, Neurotensin-expressing neurons in the IPAC, acts to control obesogenic and leptogenic processes by synergistically coordinating energy intake and expenditure with metabolism.

scholarly journals The Anxiogenic Drug Yohimbine Reinstates Palatable Food Seeking in a Rat Relapse Model: a Role of CRF1 Receptors

2005 ◽  
Vol 31 (10) ◽  
pp. 2188-2196 ◽  
Author(s):  
Udi E Ghitza ◽  
Sarah M Gray ◽  
David H Epstein ◽  
Kenner C Rice ◽  
Yavin Shaham
Keyword(s):  
Palatable Food ◽  
Food Seeking

scholarly journals Cannabinoid CB1 Receptors in the Intestinal Epithelium Are Required for Acute Western-Diet Preferences in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2874
Author(s):  
Bryant Avalos ◽  
Donovan A. Argueta ◽  
Pedro A. Perez ◽  
Mark Wiley ◽  
Courtney Wood ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
Endocannabinoid System ◽  
Dietary Fats ◽  
Treatment Preferences ◽  
Palatable Food ◽  
High Fat ◽  
Small Intestinal Epithelium ◽  
Diet Induced Obesity ◽  
Small Intestinal ◽  
Deficient Mice

The endocannabinoid system plays an important role in the intake of palatable food. For example, endocannabinoid signaling in the upper small-intestinal epithelium is increased (i) in rats after tasting dietary fats, which promotes intake of fats, and (ii) in a mouse model of diet-induced obesity, which promotes overeating via impaired nutrient-induced gut–brain satiation signaling. We now utilized a combination of genetic, pharmacological, and behavioral approaches to identify roles for cannabinoid CB1Rs in upper small-intestinal epithelium in preferences for a western-style diet (WD, high-fat/sucrose) versus a standard rodent diet (SD, low-fat/no sucrose). Mice were maintained on SD in automated feeding chambers. During testing, mice were given simultaneous access to SD and WD, and intakes were recorded. Mice displayed large preferences for the WD, which were inhibited by systemic pretreatment with the cannabinoid CB1R antagonist/inverse agonist, AM251, for up to 3 h. We next used our novel intestinal epithelium-specific conditional cannabinoid CB1R-deficient mice (IntCB1−/−) to investigate if intestinal CB1Rs are necessary for WD preferences. Similar to AM251 treatment, preferences for WD were largely absent in IntCB1−/− mice when compared to control mice for up to 6 h. Together, these data suggest that CB1Rs in the murine intestinal epithelium are required for acute WD preferences.

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