Obesity and dietary fat influence dopamine neurotransmission: exploring the convergence of metabolic state, physiological stress, and inflammation on dopaminergic control of food intake

Wallace, Conner; Fordahl, Steve C.

doi:10.1017/s0954422421000196

Cited by 31 publications

(18 citation statements)

References 191 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Just as the CNS controls feeding and energy expenditure, diet and nutrients can affect CNS function. Diet-induced obesity and high-fat diets reduce dopamine release and reuptake, leading to disruption of the satiety circuits between nucleus accumbens (NAc) dopamine terminals and projections to the hypothalamus [68,69]. Long-term feeding of high-fat diets in mice depletes dopamine in the NAc, which may contribute to the development of obesity [70].…”

Section: Discussionmentioning

confidence: 99%

Methylmercury-Induced Metabolic Alterations in Caenorhabditis elegans Are Diet-Dependent

Crawford

Martell

Nielsen

et al. 2021

Toxics

View full text Add to dashboard Cite

Methylmercury (MeHg) is a well-known neurotoxicant; however, its role in metabolic diseases has been gaining wider attention. Chronic exposure to MeHg in human populations shows an association with diabetes mellitus and metabolic syndrome (MS). As the incidences of both obesity and MS are on the rise globally, it is important to understand the potential role of MeHg in the development of the disease. There is a dearth of information on dietary interactions between MeHg and lipids, which play an important role in developing MS. We have previously shown that MeHg increases food seeking behaviors, lipid levels, fat storage, and pro-adipogenic gene expression in C. elegans fed the standard OP50 Escherichia coli diet. However, we hypothesized that these metabolic changes could be prevented if the worms were fed a bacterial diet lower in lipid content. We tested whether C. elegans developed metabolic alterations in response to MeHg if they were fed two alternative E. coli strains (HT115 and HB101) that are known absorb significantly less lipids from their media. Additionally, to explore the effect of a high-lipid and high-cholesterol diet on MeHg-induced metabolic dysfunction, we supplemented the OP50 strain with twice the standard concentration of cholesterol in the nematode growth media. Wild-type worms fed either the HB101 or HT115 diet were more resistant to MeHg than the worms fed the OP50 diet, showing a significant right-hand shift in the dose–response survival curve. Worms fed the OP50 diet supplemented with cholesterol were more sensitive to MeHg, showing a significant left-hand shift in the dose–response survival curve. Changes in sensitivity to MeHg by differential diet were not due to altered MeHg intake in the worms as measured by inductively coupled mass spectrometry. Worms fed the low-fat diets showed protection from MeHg-induced metabolic changes, including decreased food consumption, lower triglyceride content, and lower fat storage than the worms fed either of the higher-fat diets. Oxidative stress is a common characteristic of both MeHg exposure and high-fat diets. Worms fed either OP50 or OP50 supplemented with cholesterol and treated with MeHg had significantly higher levels of reactive oxygen species, carbonylated proteins, and loss of glutathione than the worms fed the HT115 or HB101 low-lipid diets. Taken together, our data suggest a synergistic effect of MeHg and dietary lipid levels on MeHg toxicity and fat metabolism in C. elegans, which may affect the ability of MeHg to cause metabolic dysfunction.

show abstract

Section: Discussionmentioning

confidence: 99%

Methylmercury-Induced Metabolic Alterations in Caenorhabditis elegans Are Diet-Dependent

Crawford

Martell

Nielsen

et al. 2021

Toxics

View full text Add to dashboard Cite

show abstract

“…Indeed research on ASR-related behaviors, characteristics, traits and processes has expanded considerably in recent years and there is now a growing set of possibilities for inclusion in research about ASR phenotypes in childhood including: temperament (such as impulsivity and effortful control) ( 90 ), Executive function (such as inhibitory control), genetic susceptibility, reward sensitivity, hedonic responses to food, cognitive function ( 91 ), cognitive control and negative affect ( 92 ), state and/or trait food cue reactivity ( 93 ), brain reward sensitivity to food cues ( 94 ), dietary measures, such as dietary fat or carbohydrates ( 95 , 96 ), fructose consumption ( 97 ), intake of processed food ( 98 ), sensory sensitivity ( 99 ), neuroimaging functional connectivity ( 100 ), metabolomics and analysis of the gut microbiome ( 101 , 102 ), measures of the social facilitation of eating ( 103 ), susceptibility to modeling ( 104 ), effects of portion size cues ( 105 ) and attachment security ( 106 ), behavioral and neural measures of appetitive traits such as through neuroimaging measures ( 107 , 108 ). A helpful broadening of work on ASR phenotypes is also suggested by attention to endophenotypes where genetic predisposition and neural substrates as well as behavioral measures are included ( 107 , 109 – 112 ).…”

Section: Discussionmentioning

confidence: 99%

Conceptualizing and Measuring Appetite Self-Regulation Phenotypes and Trajectories in Childhood: A Review of Person-Centered Strategies

2021

View full text Add to dashboard Cite

This review uses person-centered research and data analysis strategies to discuss the conceptualization and measurement of appetite self-regulation (ASR) phenotypes and trajectories in childhood (from infancy to about ages 6 or 7 years). Research that is person-centered provides strategies that increase the possibilities for investigating ASR phenotypes. We first examine the utility of examining underlying phenotypes using latent profile/class analysis drawing on cross-sectional data. The use of trajectory analysis to investigate developmental change is then discussed, with attention to phenotypes using trajectories of individual behaviors as well as phenotypes based on multi-trajectory modeling. Data analysis strategies and measurement approaches from recent examples of these person-centered approaches to the conceptualization and investigation of appetite self-regulation and its development in childhood are examined. Where relevant, examples from older children as well as developmental, clinical and educational psychology are drawn on to discuss when and how person-centered approaches can be used. We argue that there is scope to incorporate recent advances in biological and psychoneurological knowledge about appetite self-regulation as well as fundamental processes in the development of general self-regulation to enhance the examination of phenotypes and their trajectories across childhood (and beyond). The discussion and conclusion suggest directions for future research and highlight the potential of person-centered approaches to progress knowledge about the development of appetite self-regulation in childhood.

show abstract

“…What influences can the indoor environment, circulating factors (triglycerides, inflammatory factors, etc. ), hormones and the contents of the digestive tract or even the gut microbiota and genetic factors have on the reward system, the cognitive system and the taste/mouthfeel of fat in obesity [163,[222][223][224][225][226][227]? Do endocrine disruptors (bisphenol-A) alter the reward system in the prenatal and neonatal periods as observed in mice [228]?…”

Section: Taste/mouthfeel Of Fat and Obesity Cause Or Consequence?mentioning

confidence: 99%

Taste of Fat and Obesity: Different Hypotheses and Our Point of View

et al. 2022

View full text Add to dashboard Cite

Obesity results from a temporary or prolonged positive energy balance due to an alteration in the homeostatic feedback of energy balance. Food, with its discriminative and hedonic qualities, is a key element of reward-based energy intake. An alteration in the brain reward system for highly palatable energy-rich foods, comprised of fat and carbohydrates, could be one of the main factors involved in the development of obesity by increasing the attractiveness and consumption of fat-rich foods. This would induce, in turn, a decrease in the taste of fat. A better understanding of the altered reward system in obesity may open the door to a new era for the diagnosis, management and treatment of this disease.

show abstract

Obesity and dietary fat influence dopamine neurotransmission: exploring the convergence of metabolic state, physiological stress, and inflammation on dopaminergic control of food intake

Cited by 31 publications

References 191 publications

Methylmercury-Induced Metabolic Alterations in Caenorhabditis elegans Are Diet-Dependent

Methylmercury-Induced Metabolic Alterations in Caenorhabditis elegans Are Diet-Dependent

Conceptualizing and Measuring Appetite Self-Regulation Phenotypes and Trajectories in Childhood: A Review of Person-Centered Strategies

Taste of Fat and Obesity: Different Hypotheses and Our Point of View

Contact Info

Product

Resources

About