Differential Effects of Fructose and Glucose on Cerebral Blood Flow—Reply

Page, Kathleen A.; Sinha, Rajita; Sherwin, Robert S.

doi:10.1001/jama.2013.3367

Cited by 4 publications

(2 citation statements)

References 6 publications

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“…This is in line with animal research showing central administration of glucose to inhibit food intake and fructose to stimulate feeding [34]. Further, in humans, fructose ingestion to lead to lower levels of serum glucose, insulin, and glucagon-like polypeptide 1 (GLP-1), a hormone associated with increased satiety relative to glucose ingestion [35]. …”

Section: Effects Of Sugars On “Homeostatic” Neural Systemssupporting

confidence: 72%

Recent studies of the effects of sugars on brain systems involved in energy balance and reward: Relevance to low calorie sweeteners

Murray

Tulloch

Criscitelli

et al. 2016

Physiology & Behavior

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The alarmingly high rates of overweight and obesity pose a serious global health threat. Numerous factors can result in weight gain, one of which is excess consumption of caloric sweeteners. In an effort to aid weight loss efforts, many people have switched from caloric sweeteners to low calorie sweeteners, which provide sweet taste without the accompanying calories. In this review, we present an overview of the animal literature produced in the last 5 years highlighting the effects of sugar consumption on neural pathways involved in energy balance regulation and reward processing. We also examine the latest evidence that is beginning to elucidate the effects of low calorie sweeteners on these neural pathways, as well as how homeostatic and hedonic systems interact in response to, or to influence, sugar consumption.

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Section: Effects Of Sugars On “Homeostatic” Neural Systemssupporting

confidence: 72%

Recent studies of the effects of sugars on brain systems involved in energy balance and reward: Relevance to low calorie sweeteners

Murray

Tulloch

Criscitelli

et al. 2016

Physiology & Behavior

View full text Add to dashboard Cite

show abstract

“…Interestingly, HPA axis adaptations with low cortisol awakening responses have been reported in higher BMI groups (Hillman, Dorn, Loucks, & Berga, 2012; Packard, Egan, & Ulrich-Lai, 2016; Sinha & Jastreboff, 2013; Tyrka, Walters, Price, Anderson, & Carpenter, 2012), and reduced dopamine activity has been associated with obesity (Wang et al, 2003). Finally, we have shown that in response to a standard glucose drink, healthy lean individuals showed increased connectivity between the hypothalamus and dopamine-rich regions of the ventral and dorsal striatum as well as the insula (Page, Sinha, & Sherwin, 2013), suggesting significant associations between the hypothalamic circuitry and extrahypothalamic striatal limbic circuits in response to food intake. In previous work, we also showed that experimentally reducing blood glucose to mild hypoglycemic levels relative to normal euglycemic levels, not only increases plasma cortisol but also increases wanting of HP foods and brain activation of reward-motivational (striatal) and emotion-stress (limbic) regions in response to high fat, high sugar HP versus low fat and non-food pictures.…”

Section: Overeating Of Hp Foods and Metabolic And Stress Hormone Respmentioning

confidence: 99%

Role of addiction and stress neurobiology on food intake and obesity

Sinha

2018

Biological Psychology

Self Cite

146

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The US remains at the forefront of a global obesity epidemic with a significant negative impact on public health. While it is well known that a balance between energy intake and expenditure is homeostatically regulated to control weight, growing evidence points to multifactorial social, neurobehavioral and metabolic determinants of food intake that influence obesity risk. This review presents factors such as the ubiquitous presence of rewarding foods in the environment and increased salience of such foods that stimulate brain reward motivation and stress circuits to influence eating behaviors. These rewarding foods via conditioned and reinforcing effects stimulate not only metabolic, but also stress hormones, that, in turn, hijack the brain emotional (limbic) and motivational (striatal) pathways, to promote food craving and excessive food intake. Furthermore, the impact of high levels of stress and trauma and altered metabolic environment (e.g. higher weight, altered insulin sensitivity) on prefrontal cortical self-control processes that regulate emotional, motivational and visceral homeostatic mechanisms of food intake and obesity risk are also discussed. A heuristic framework is presented in which the interactive dynamic effects of neurobehavioral adaptations in metabolic, motivation and stress neurobiology may further support food craving, excessive food intake and weight gain in a complex feed-forward manner. Implications of such adaptations in brain addictive-motivational and stress pathways and their effects on excessive food intake and weight gain are discussed to highlight key questions that requires future research attention in order to better understand and address the growing obesity epidemic.

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Additional Biological Mechanisms of Hedonic Eating

Wilcox

2021

Food Addiction, Obesity, and Disorders of Overeating

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Differential Effects of Fructose and Glucose on Cerebral Blood Flow—Reply

Cited by 4 publications

References 6 publications

Recent studies of the effects of sugars on brain systems involved in energy balance and reward: Relevance to low calorie sweeteners

Recent studies of the effects of sugars on brain systems involved in energy balance and reward: Relevance to low calorie sweeteners

Role of addiction and stress neurobiology on food intake and obesity

Additional Biological Mechanisms of Hedonic Eating

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