scholarly journals Kaleidoscope

2017 ◽  
Vol 210 (1) ◽  
pp. 87-88 ◽  
Author(s):  
Derek K. Tracy ◽  
Dan W. Joyce ◽  
Sukhwinder S. Shergill
Keyword(s):  
Weight Gain ◽  
Nucleus Accumbens ◽  
Food Addiction ◽  
Environmental Cues ◽  
Junk Food ◽  
Obesity Epidemic ◽  
Portion Sizes ◽  
Food Seeking ◽  
The Brain ◽  
Sensitive Group

Tapping into your New Year resolutions, we present some cautionary data to consider.Recent research on novel addiction types suggests that, in addition to hunger, the urge to eat is considerably influenced by environmental cues. Obese individuals have been shown to be more sensitive to these, with subsequent stronger craving and larger portion sizes. Neurobiologically, this has been linked with pathological alterations to cue-triggered motivational responses in the nucleus accumbens (NAc) parallel to those seen in drug addiction. Oginsky et al investigated the effects of a junk-food diet on obesity-susceptible and obesity-resistant rats. Glutamatergic calcium-permeable AMPA receptor (CP-AMPAR) functioning in the NAc showed more rapid and long-lasting (for weeks after cessation of junk-food consumption) increases in the obesity-sensitive group. CP-AMPARs mediate cue-triggered food seeking, and their changes in the brain occurred before weight gain. The data support the concept that ‘junk food addiction’ induced by the consumption of fatty and high-sugar foods may be contributing to the obesity epidemic.

scholarly journals Eating junk-food has opposite effects on intrinsic excitability of nucleus accumbens core medium spiny neurons in obesity-susceptible vs. -resistant rats

2019 ◽  
Author(s):  
Max F. Oginsky ◽  
Carrie R. Ferrario
Keyword(s):  
Nucleus Accumbens ◽  
Intrinsic Excitability ◽  
Medium Spiny Neurons ◽  
Junk Food ◽  
Nucleus Accumbens Core ◽  
Initial Finding ◽  
Spiny Neurons ◽  
Whole Cell Patch Clamp ◽  
Underlying Mechanisms ◽  
Food Seeking

AbstractThe nucleus accumbens (NAc) plays critical roles in motivated behaviors, including food-seeking and feeding. Differences in NAc function contribute to over-eating that drives obesity, but the underlying mechanisms are poorly understood. In addition, there is a fair degree of variation in individual susceptibility vs. resistance to obesity that is due in part to differences in NAc function. For example, using selectively bred obesity-prone and obesity-resistant rats, we have found that excitability of medium spiny neurons within the NAc core is enhanced in obesity-prone vs. resistant populations, prior to any diet manipulation. However, it is unknown whether consumption of sugary, fatty junk-food alters MSN excitability. Here, whole-cell patch clamp recordings were conducted to examine MSN intrinsic excitability in adult male obesity-prone and obesity-resistant rats with and without exposure to a sugary, fatty junk-food diet. We replicated our initial finding that basal excitability is enhanced in obesity-prone vs. obesity-resistant rats and determined that this is due to a lower IA in prone vs. resistant groups. In addition, the junk-food diet had opposite effects on excitability in obesity-prone vs. obesity-resistant rats. Specifically, junk-food enhanced excitability in MSNs of obesity-resistant rats; this was mediated by a reduction in IA. In contrast, junk-food reduced excitability in MSNs from obesity-prone rats; this was mediated by an increase in IKIR. Thus, individual differences in obesity-susceptibility influence both basal excitability and how MSN excitability adapts to junk-food consumption.

Food Addiction

2018 ◽  
Author(s):  
Edison de Mello
Keyword(s):  
United States ◽  
Food Industry ◽  
Food Addiction ◽  
The United States ◽  
Pharmacological Intervention ◽  
Addiction Recovery ◽  
Physiological Factors ◽  
Obesity Epidemic ◽  
High Glycemic Index ◽  
The Brain

Although an impressive and increasing amount of research has shown how particular foods affect brain chemistry and can lead to food addictions, the idea of food addiction as an actual disease is still controversial. The alarming growth in the obesity epidemic in the United States, however, is quickly eating away at this controversy. Research now shows that genetics, the nucleus accumbens, the gut bacteria (microbiota), and other physiological factors have a vast effect on obesity, cravings, binge eating, and food addiction. Speculation that the food industry has utilized the effects of the high glycemic index foods, such as refined starches, sugars, and fat have on the brain to engineer foods for taste, not nutrition and to get people “hooked” is also discussed. Integrative treatment approaches to food addiction that can synergically help with food addiction recovery are presented. These include biochemical restoration, IV nutrient therapy, meditation practices, pharmacological intervention, and more.

scholarly journals The Role of Neuropeptide Y in the Nucleus Accumbens

2021 ◽  
Vol 22 (14) ◽  
pp. 7287
Author(s):  
Masaki Tanaka ◽  
Shunji Yamada ◽  
Yoshihisa Watanabe
Keyword(s):  
Nervous System ◽  
Nucleus Accumbens ◽  
Neuropeptide Y ◽  
Emotional Behavior ◽  
Characteristic Functions ◽  
Receptor Subtypes ◽  
Neuroendocrine Mechanisms ◽  
Fear And Anxiety ◽  
The Brain

Neuropeptide Y (NPY), an abundant peptide in the central nervous system, is expressed in neurons of various regions throughout the brain. The physiological and behavioral effects of NPY are mainly mediated through Y1, Y2, and Y5 receptor subtypes, which are expressed in regions regulating food intake, fear and anxiety, learning and memory, depression, and posttraumatic stress. In particular, the nucleus accumbens (NAc) has one of the highest NPY concentrations in the brain. In this review, we summarize the role of NPY in the NAc. NPY is expressed principally in medium-sized aspiny neurons, and numerous NPY immunoreactive fibers are observed in the NAc. Alterations in NPY expression under certain conditions through intra-NAc injections of NPY or receptor agonists/antagonists revealed NPY to be involved in the characteristic functions of the NAc, such as alcohol intake and drug addiction. In addition, control of mesolimbic dopaminergic release via NPY receptors may take part in these functions. NPY in the NAc also participates in fat intake and emotional behavior. Accumbal NPY neurons and fibers may exert physiological and pathophysiological actions partly through neuroendocrine mechanisms and the autonomic nervous system.

Changes in Health Behaviors Associated With Weight Gain by Weight Classification During the COVID-19 Pandemic

2021 ◽  
pp. 089011712110229
Author(s):  
Kristie Rupp ◽  
Ciarán P. Friel
Keyword(s):  
Weight Gain ◽  
Health Behaviors ◽  
Weight Status ◽  
Vegetable Consumption ◽  
Caloric Intake ◽  
Healthy Weight ◽  
Cross Sectional ◽  
Obesity Epidemic ◽  
Logistic Regression Models ◽  
Online Panels

Purpose: To determine whether perceived changes (i.e. perception of engagement during the pandemic relative to pre-pandemic) in specific health behaviors differ by weight status (i.e. healthy weight, overweight, obese). Design: Cross-sectional. Recruitment took place between June-August 2020, via social media posts and Qualtrics online panels. Setting: Participants completed the survey online through the Qualtrics platform. Sample: Analyses included N = 502 participants (≥18 years); 45.2% healthy weight (n = 227), 28.5% overweight (n = 143), and 26.3% obese (n = 132). Measures: Study-specific survey items included questions about demographics and perceived changes in health behaviors. Analysis: Logistic regression models, adjusted for age, race, ethnicity, gender, education, and COVID-19 diagnosis, assessed the odds of perceiving changes in health behaviors considered a risk for weight gain. Results: Participants with obesity, but not overweight, were significantly more likely to report deleterious changes to health behaviors compared to healthy weight peers, including: (1) decreased fruit/vegetable consumption [adjusted odds ratio (AOR) = 1.92; 95% confidence interval (CI): (1.13, 3.26)]; (2) increased processed food consumption [AOR = 1.85; 95%CI: (1.15, 3.00)]; (3) increased caloric intake [AOR = 1.66; 95% CI: (1.06, 2.61)]; (4) decreased physical activity [AOR = 2.07; 95%CI: (1.31, 3.28)]; and (5) deterioration in sleep quality [AOR = 2.07; 95%CI: (1.32, 3.25)]. Conclusion: Our findings suggest that adults with obesity may be at greater risk for unhealthy behaviors during a period of prolonged social distancing, potentially exacerbating the obesity epidemic.

scholarly journals Wireless logging of extracellular neuronal activity in the telencephalon of free-swimming salmonids

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Susumu Takahashi ◽  
Takumi Hombe ◽  
Riku Takahashi ◽  
Kaoru Ide ◽  
Shinichiro Okamoto ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Environmental Cues ◽  
Fish Movement ◽  
Water Tank ◽  
Head Direction ◽  
Free Swimming ◽  
Rodent Brain ◽  
River Migration ◽  
Spike Waveforms ◽  
The Brain

Abstract Background Salmonids return to the river where they were born in a phenomenon known as mother-river migration. The underpinning of migration has been extensively examined, particularly regarding the behavioral correlations of external environmental cues such as the scent of the mother-river and geomagnetic compass. However, neuronal underpinning remains elusive, as there have been no biologging techniques suited to monitor neuronal activity in the brain of large free-swimming fish. In this study, we developed a wireless biologging system to record extracellular neuronal activity in the brains of free-swimming salmonids. Results Using this system, we recorded multiple neuronal activities from the telencephalon of trout swimming in a rectangular water tank. As proof of principle, we examined the activity statistics for extracellular spike waveforms and timing. We found cells firing maximally in response to a specific head direction, similar to the head direction cells found in the rodent brain. The results of our study suggest that the recorded signals originate from neurons. Conclusions We anticipate that our biologging system will facilitate a more detailed investigation into the neural underpinning of fish movement using internally generated information, including responses to external cues.

scholarly journals Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance

2016 ◽  
Vol 48 (7) ◽  
pp. 491-501 ◽  
Author(s):  
Madeliene Stump ◽  
Deng-Fu Guo ◽  
Ko-Ting Lu ◽  
Masashi Mukohda ◽  
Xuebo Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
High Fat Diet ◽  
Control Diet ◽  
Cre Recombinase ◽  
Dominant Negative ◽  
High Fat ◽  
Pparγ Agonist ◽  
The Brain

Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

scholarly journals The Gut Microbiome Derived From Anorexia Nervosa Patients Impairs Weight Gain and Behavioral Performance in Female Mice

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2441-2452 ◽  
Author(s):  
Tomokazu Hata ◽  
Noriyuki Miyata ◽  
Shu Takakura ◽  
Kazufumi Yoshihara ◽  
Yasunari Asano ◽  
...  
Keyword(s):  
Body Weight ◽  
Anorexia Nervosa ◽  
Weight Gain ◽  
Food Intake ◽  
Brain Stem ◽  
Body Weight Gain ◽  
Field Tests ◽  
Compulsive Behavior ◽  
The Brain ◽  
Poor Weight Gain

Abstract Anorexia nervosa (AN) results in gut dysbiosis, but whether the dysbiosis contributes to AN-specific pathologies such as poor weight gain and neuropsychiatric abnormalities remains unclear. To address this, germ-free mice were reconstituted with the microbiota of four patients with restricting-type AN (gAN mice) and four healthy control individuals (gHC mice). The effects of gut microbes on weight gain and behavioral characteristics were examined. Fecal microbial profiles in recipient gnotobiotic mice were clustered with those of the human donors. Compared with gHC mice, gAN mice showed a decrease in body weight gain, concomitant with reduced food intake. Food efficiency ratio (body weight gain/food intake) was also significantly lower in gAN mice than in gHC mice, suggesting that decreased appetite as well as the capacity to convert ingested food to unit of body substance may contribute to poor weight gain. Both anxiety-related behavior measured by open-field tests and compulsive behavior measured by a marble-burying test were increased only in gAN mice but not in gHC mice. Serotonin levels in the brain stem of gAN mice were lower than those in the brain stem of gHC mice. Moreover, the genus Bacteroides showed the highest correlation with the number of buried marbles among all genera identified. Administration of Bacteroides vulgatus reversed compulsive behavior but failed to exert any substantial effect on body weight. Collectively, these results indicate that AN-specific dysbiosis may contribute to both poor weight gain and mental disorders in patients with AN.

scholarly journals Enhanced food motivation in obese mice is controlled by D1R expressing spiny projection neurons in the nucleus accumbens.

2022 ◽  
Author(s):  
Bridget A Matikainen-Ankney ◽  
Alex A Legaria ◽  
Yvan M Vachez ◽  
Caitlin A Murphy ◽  
Yiyan A Pan ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Food Reward ◽  
Ex Vivo ◽  
D1 Receptor ◽  
Physical Work ◽  
Projection Neurons ◽  
Food Motivation ◽  
Obese Mice ◽  
Food Seeking

Obesity is a chronic relapsing disorder that is caused by an excess of caloric intake relative to energy expenditure. In addition to homeostatic feeding mechanisms, there is growing recognition of the involvement of food reward and motivation in the development of obesity. However, it remains unclear how brain circuits that control food reward and motivation are altered in obese animals. Here, we tested the hypothesis that signaling through pro-motivational circuits in the core of the nucleus accumbens (NAc) is enhanced in the obese state, leading to invigoration of food seeking. Using a novel behavioral assay that quantifies physical work during food seeking, we confirmed that obese mice work harder than lean mice to obtain food, consistent with an increase in the relative reinforcing value of food in the obese state. To explain this behavioral finding, we recorded neural activity in the NAc core with both in vivo electrophysiology and cell-type specific calcium fiber photometry. Here we observed greater activation of D1-receptor expressing NAc spiny projection neurons (NAc D1SPNs) during food seeking in obese mice relative to lean mice. With ex vivo slice physiology we identified both pre- and post-synaptic mechanisms that contribute to this enhancement in NAc D1SPN activity in obese mice. Finally, blocking synaptic transmission from D1SPNs decreased physical work during food seeking and attenuated high-fat diet-induced weight gain. These experiments demonstrate that obesity is associated with a selective increase in the activity of D1SPNs during food seeking, which enhances the vigor of food seeking. This work also establishes the necessity of D1SPNs in the development of diet-induced obesity, identifying a novel potential therapeutic target.

scholarly journals You aren't what you eat, you become what you eat

2021 ◽  
Author(s):  
Christopher R Stephens ◽  
Jonathan F Easton ◽  
Heriberto Roman Sicilia
Keyword(s):  
Weight Gain ◽  
Energy Intake ◽  
Energy Gap ◽  
Age Groups ◽  
Population Level ◽  
Energy Imbalance ◽  
Obesity Epidemic ◽  
Daily Energy ◽  
Large Populations ◽  
Energy Excess

Obesity (and the consequent obesity epidemic) is a complex, adaptive process, taking place over a time span of many years. Energy intake is recognized as a potentially important driver of obesity, especially in the context of an identifiable energy imbalance which, it is surmised, must lead to weight gain. Similarly, energy expenditure must play an important role. However, both show an enormous degree of individual variation. Therefore, measuring them is an exceedingly difficult task, especially in the context of large populations and long time periods. It has been argued that population-level observed weight gain can be traced back to very small daily energy imbalances while, at the same time, positing that a much larger maintenance energy gap is responsible for maintaining the energy requirements of the increased weight population. In this paper we examine the relation between BMI and energy intake as functions of age. The convexity of the BMI curves as a function of age and gender demonstrate the enhanced obesity risk apparent in young adults and women, and imply that no settling points exist at the population level. Consistent with other studies, overall weight increases are consistent with a very small daily energy imbalance, about 7 cal. Consumption as a function of age shows a small, steady, linear decrease of about 8 cal per year, and can be associated with a maximal energy excess/deficit of about 250cal for the youngest and oldest age groups. By examining weight differences between age groups as a function of age, we argue that this excess/deficit is an important motor for the observed weight differences, and argue that the apparent energy imbalance of 250 cal, due to excess consumption, leads to an effective imbalance of only 7 cal due to the existence of various physiological and behavioral mechanisms that enhance weight homeostasis and effectively reduce the energy excess from 250 cal to 7 cal. We discuss several possibilities for such mechanisms.

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