Obesity-Related Differences between Women and Men in Brain Structure and Goal-Directed Behavior

Horstmann, Annette; Busse, Franziska P.; Mathar, David; Müller, Karsten; Lepsien, Jöran; Schlögl, Haiko; Kabisch, Stefan; Kratzsch, Jürgen; Neumann, Jane; Stümvoll, Michael; Villringer, Arno; Pleger, Burkhard

doi:10.3389/fnhum.2011.00058

Cited by 147 publications

(177 citation statements)

References 59 publications

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“…However, the neuroenergetic rigidity in obese individuals was accompanied by reduced gray matter volumes within frontotemporal brain structures, anterior cingulum, putamen, insula, and cerebellum compared with normal-weight control subjects, which is consistent with previous data providing evidence of obesity-related structural changes within the prefrontal cortex and the ventral striatum (19,20). Again, the question arises as to which mechanism might be behind the obesity-related brain morphology changes.…”

Section: Discussionsupporting

confidence: 89%

Blunted Brain Energy Consumption Relates to Insula Atrophy and Impaired Glucose Tolerance in Obesity

et al. 2015

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Brain energy consumption induced by electrical stimulation increases systemic glucose tolerance in normalweight men. In obesity, fundamental reductions in brain energy levels, gray matter density, and cortical metabolism, as well as chronically impaired glucose tolerance, suggest that disturbed neuroenergetic regulation may be involved in the development of overweight and obesity. Here, we induced neuronal excitation by anodal transcranial direct current stimulation versus sham, examined cerebral energy consumption with 31 P magnetic resonance spectroscopy, and determined systemic glucose uptake by euglycemic-hyperinsulinemic glucose clamp in 15 normal-weight and 15 obese participants. We demonstrate blunted brain energy consumption and impaired systemic glucose uptake in obese compared with normal-weight volunteers, indicating neuroenergetic dysregulation in obese humans. Broadening our understanding of reduced multifocal gray matter volumes in obesity, our findings show that reduced appetite-and taste-processing area morphometry is associated with decreased brain energy levels. Specifically, gray matter volumes of the insula relate to brain energy content in obese participants. Overall, our results imply that a diminished cerebral energy supply may underlie the decline in brain areas assigned to food intake regulation and therefore the development of obesity.The incidence and prevalence of obesity have been escalating worldwide, and obesity has already reached epidemic proportions (1,2). This frightening development, in conjunction with the urgent need to replace more-or-less inefficient treatment strategies, has resulted in the development of new pathophysiological concepts of obesity. There is currently a growing consensus that this disease involves dysregulation within brain areas assigned to control food intake behavior and systemic energy homeostasis (3,4). Data show that complex neuronal pathways with reciprocal connections between the hypothalamus, brainstem, and higher cortical centers control appetite and food intake behavior (5), whereas afferent inputs from the periphery as well as efferent signals to peripheral organs regulate energy homeostasis (6). At large, appetite perception, food intake behavior, and energy homeostasis are synchronized in the hypothalamus as the cerebral "appetite center" (3,4). In this context, lower levels of high-energy phosphates (i.e., ATP and phosphocreatine [PCr]), have been detected in obese compared with normal-weight humans (7), which suggests a relationship between brain energy supply and body weight regulation. Supporting this view is the finding that cerebral ATP and PCr levels predict the amount of calories subsequently consumed (8). Moreover, brain energy consumption by electrical stimulation increases glucose tolerance in normal-weight men (9). On this basis, we aimed to test

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Section: Discussionsupporting

confidence: 89%

Blunted Brain Energy Consumption Relates to Insula Atrophy and Impaired Glucose Tolerance in Obesity

et al. 2015

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“…Obese women showed greater response to immediate reward (even in the face of delayed negative consequences) as opposed to lean women, and this differential response was not observed in obese men. 53 Another important imaging study demonstrated that youth who are at risk for obesity (defined as having both parents overweight/obese) showed an increased activation of the reward circuitry in response to food or monetary rewards, 54 suggesting that parental obesity can contribute to the child's risk for obesity. This same research group has also shown that reduced responding of the striatum to palatable food consumption can develop with weight gain, as opposed to existing prior to weight gain.…”

Section: Postnatal Effects Of a High-fat Dietmentioning

confidence: 99%

High-fat diet alters the dopamine and opioid systems: effects across development

Reyes

2012

Int J Obes Supp

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Consumption of a high-fat diet has been linked to obesity, dyslipidemia and cardiovascular disease. Less well appreciated are adverse effects on the brain and behavior. Recent research has shown that consumption of a high-fat diet can alter gene expression within the brain, and the dopamine and opioid neurotransmitter systems appear to be vulnerable to dysregulation. This review will focus on recent reports in both humans and animal models that describe adverse effects of high-fat diet consumption on the central reward circuitry. In addition, the importance of different development windows will be discussed, with effects observed in both the prenatal/perinatal time period and with chronic high-fat diet consumption in adulthood.

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“…Furthermore, structural differences in NAcc volume have been positively associated with body mass index (BMI) in adults (5,6). Because the development of the NAcc precedes the development of prefrontal control systems (7), this structure is suggested to play a key role in motivating and establishing unhealthy eating behaviors early in the lifespan.…”

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confidence: 99%

Genetic risk for obesity predicts nucleus accumbens size and responsivity to real-world food cues

Rapuano

Zieselman

Kelley

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Obesity is a major public health concern that involves an interaction between genetic susceptibility and exposure to environmental cues (e.g., food marketing); however, the mechanisms that link these factors and contribute to unhealthy eating are unclear. Using a well-known obesity risk polymorphism (FTO rs9939609) in a sample of 78 children (ages 9-12 y), we observed that children at risk for obesity exhibited stronger responses to food commercials in the nucleus accumbens (NAcc) than children not at risk. Similarly, children at a higher genetic risk for obesity demonstrated larger NAcc volumes. Although a recessive model of this polymorphism best predicted body mass and adiposity, a dominant model was most predictive of NAcc size and responsivity to food cues. These findings suggest that children genetically at risk for obesity are predisposed to represent reward signals more strongly, which, in turn, may contribute to unhealthy eating behaviors later in life.T he relationship between genes and sensitivity to environmental cues is elusive, yet it is paramount to understanding the development of potentially maladaptive human behaviors. The rising prevalence of obesity is a major public health concern that has been attributed to various factors, such as genetic susceptibility (1), and increases in the availability and marketing of calorie-dense foods (2). However, little is known about how genetic predisposition to obesity influences sensitivity to real-world food cues and contributes to the development of unhealthy eating behaviors.Previous neuroimaging studies have demonstrated that responses to food cues in reward-related regions of the brain, such as the nucleus accumbens (NAcc), predict weight gain in adulthood (3) and giving in to food temptations in daily life (4). Furthermore, structural differences in NAcc volume have been positively associated with body mass index (BMI) in adults (5, 6). Because the development of the NAcc precedes the development of prefrontal control systems (7), this structure is suggested to play a key role in motivating and establishing unhealthy eating behaviors early in the lifespan. Importantly, genetic factors are a known contributor to brain development (8) and may influence risky behaviors during childhood and adolescence by biasing the early development of anatomical structures underlying reward-related brain function.In addition, the notion that genes contribute to obesity has recently gained much attention. More specifically, the fat-mass and obesity-associated (FTO) rs9939609 polymorphism has been strongly related to increased BMI and adiposity across the lifespan, and is suggested to influence food intake and food choice, rather than energy expenditure (9-11). Those with two high-risk "A" alleles (AA) are at an enhanced risk for obesity compared with those with two low-risk "T" alleles (TT) or those who are heterozygous (AT) for the FTO rs9939609 polymorphism. Although the FTO gene is highly expressed in the brain (1), the mechanism by which this gene promotes unhealthy...

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Obesity-Related Differences between Women and Men in Brain Structure and Goal-Directed Behavior

Cited by 147 publications

References 59 publications

Blunted Brain Energy Consumption Relates to Insula Atrophy and Impaired Glucose Tolerance in Obesity

Blunted Brain Energy Consumption Relates to Insula Atrophy and Impaired Glucose Tolerance in Obesity

High-fat diet alters the dopamine and opioid systems: effects across development

Genetic risk for obesity predicts nucleus accumbens size and responsivity to real-world food cues

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