Fast Food, Central Nervous System Insulin Resistance, and Obesity

Isganaitis, Elvira; Lustig, Robert H.

doi:10.1161/01.atv.0000186208.06964.91

Cited by 204 publications

(180 citation statements)

References 106 publications

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“…Leptin acts on neurons in the hypothalamus and arcuate nucleus, and appears to act in opposition to neuropeptide Y, and in concert with insulin and corticotropin-releasing hormone (CRH) to reduce food intake. Leptin and insulin are thought to influence the hedonic perception of food, both centrally (reviewed in Isganaitis and Lustig, 2005), and via taste receptors. Leptin modulates sweet taste sensation via actions on sweet taste receptor cells via the leptin receptor.…”

Section: A Role For Cephalic Phase Responses In Appetite and Satiety?mentioning

confidence: 99%

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

2008

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Anticipatory physiological regulation is an adaptive strategy that enables animals to respond faster to physiologic and metabolic challenges. The cephalic phase responses are anticipatory responses that prepare animals to digest, absorb and metabolize nutrients. They enable the sensory aspects of the food to interact with the metabolic state of the animal to influence feeding behavior. The anticipatory digestive secretions and metabolic adjustments in response to food cues are key adaptations that affect digestive and metabolic efficiency and aid in controlling the resulting elevation of metabolic fuels in the blood. Cephalic phase responses enable digestion, metabolism and appetite to be regulated in a coordinated fashion. These responses have significant effects on meal size. For example, if the cephalic phase insulin response is blocked the result is poor glucose control and smaller meals. Cephalic phase responses also are linked to motivation to feed, and may play a more direct role in regulating meal size beyond the permissive one of ameliorating negative consequences of feeding. For example, the orexigenic peptide ghrelin appears to display a cephalic phase response, rising before expected meal times. This anticipatory ghrelin response increases appetite; interestingly it also enhances fat absorption, linking appetite with digestion and metabolism.

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Section: A Role For Cephalic Phase Responses In Appetite and Satiety?mentioning

confidence: 99%

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

2008

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“…On the other hand, reward centers activation by high sugar and fat content palatable foods promotes desire 'to come back for more by upregulating of hunger signaling (orexin, AgRP, and MCH) in hypothalamic orexigenic networks and by blunting brain responses to the peripheral satiety hormones, insulin and leptin (ErlansonAlbertsson, 2005;Isganaitis and Lustig, 2005). Prefrontal cortex modulates these effects via reciprocal innervation with the hypothalamic-limbic areas (Berthoud, 2004a) by forming subjective hedonic perceptions and integrating them with metabolic signals and with intrapsychic and environmental contexts (Kringelbach, 2005).…”

Section: Central Mechanisms For Energy Balance and For Food Reward Acmentioning

confidence: 99%

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Elman

Borsook

Lukas

2006

Neuropsychopharmacol

138

142

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Obesity is highly prevalent among patients with schizophrenia and is associated with detrimental health consequences. Although excessive consumption of fast food and pharmacotherapy with such second-generation antipsychotic agents (SGAs) as clozapine and olanzapine has been implicated in the schizophrenia/obesity comorbidity, the pathophysiology of this link remains unclear. Here, we propose a mechanism based on brain reward function, a relevant etiologic factor in both schizophrenia and overeating. A comprehensive literature search on neurobiology of schizophrenia and of eating behavior was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) energy homeostasis, (2) food reward and hedonics, (3) reward function in schizophrenia, and (4) metabolic effects of the SGAs. A mesolimbic hyperdopaminergic state may render motivational/incentive reward system insensitive to low salience/palatability food. This, together with poor cognitive control from hypofunctional prefrontal cortex and enhanced hedonic impact of food, owing to exaggerated opioidergic drive (clinically manifested as pain insensitivity), may underlie unhealthy eating habits in patients with schizophrenia. Treatment with SGAs purportedly improves dopamine-mediated reward aspects, but at the cost of increased appetite and worsened or at least not improved opiodergic capacity. These effects can further deteriorate eating patterns. Pathophysiological and therapeutic implications of these insights need further validation via prospective clinical trials and neuroimaging studies. INTRODUCTIONObesity has reached pandemic proportions and it is rapidly surpassing smoking as a number one killer in the industrialized world (Sturm, 2002;Skidmore and Yarnell, 2004). Its annual cost to the American society is staggering, and is estimated to be around $117 billion owing to related illnesses and loss of productivity (National Institute of Diabetes and Digestive and Kidney Diseases, 2005).In schizophrenia, obesity is twice as prevalent as in the general public, afflicting over half this patient population (Allison et al, 1999a;Dixon et al, 2000; American Diabetes Association, 2004;Marder et al, 2004;Wirshing, 2004). Besides negative psychosocial impacts (distorted selfesteem and societal stigmatization) and medications noncompliance, schizophrenics appear to be particularly susceptible to the detrimental medical sequelae of obesity such as the 'Metabolic Syndrome', which is a cluster of cardiovascular risk factors, including abdominal adiposity, insulin resistance, impaired, glucose tolerance, dyslipidemia, and hypertension (McKee et al, 1986;Mukherjee et al, 1996;Brown et al, 2000;Haupt and Newcomer, 2002;Ryan and Thakore, 2002;Ryan et al, 2003;Holt et al, 2004;Kohen, 2004;Marder et al, 2004;Lieberman et al, 2005).Excessive body weight gain (BWG) could be attributed to a constellation of endocrine, molecular, genetic, demographic, and lifestyle-related factors. Provided that a common tra...

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“…At the same time, other studies suggest that solid energy-dense foods cause CNS insulin resistance (Isganaitis and Lustig, 2005); fail to trigger satiety mechanisms, and also lead to overeating. As a result, solid fast foods (Isganaitis and Lustig, 2005;Prentice and Jebb, 2003) and liquid, energy-dilute beverages (Bray et al, 2004) have been blamed, separately and together, for the obesity epidemic.…”

Section: Introductionmentioning

confidence: 99%

“…Not only has sugar content of the diet increased, but much of the sugar is consumed in liquid form (Bray et al, 2004). Current research on sugars and body weight has focused on the interactions of physiological systems with sugar content of the food supply (Elliott et al, 2002;Bray et al, 2004;Gross et al, 2004;Isganaitis and Lustig, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…Energydense diets cause insulin and leptin resistance in the central nervous system (CNS) (Schwartz, 2006) and blunt responses to physiological signals of satiety (Erlanson-Albertsson, 2005). Diet-induced CNS insulin resistance is the suggested reason why pleasure response to energy-dense foods does not diminish even in the face of caloric repletion (Lustig, 2001;Isganaitis and Lustig, 2005). Sweetness may also affect cortisol reactivity and compensate for feelings of stress (Epel et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Intense sweeteners, energy intake and the control of body weight

2007

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Replacing sugar with low-calorie sweeteners is a common strategy for facilitating weight control. By providing sweet taste without calories, intense sweeteners help lower energy density of beverages and some foods. Reduced dietary energy density should result in lower energy intakes -but are the energy reduction goals, in fact, achieved? The uncoupling of sweetness and energy, afforded by intense sweeteners, has been the focus of numerous studies over the past two decades. There are recurring arguments that intense sweeteners increase appetite for sweet foods, promote overeating, and may even lead to weight gain. Does reducing energy density of sweet beverages and foods have a measurable impact on appetite and energy intakes, as examined both in short-term studies and over a longer period? Can reductions in dietary energy density achieved with intense sweeteners really affect body weight control? This paper reviews evidence from laboratory, clinical and epidemiological studies in the context of current research on energy density, satiety and the control of food intake.

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Fast Food, Central Nervous System Insulin Resistance, and Obesity

Cited by 204 publications

References 106 publications

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Intense sweeteners, energy intake and the control of body weight

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