Overeating of palatable food is associated with blunted leptin and ghrelin responses

Lindqvist, Andreas; Cour, Charlotta Dornonville de la; Stegmark, Anna; Håkanson, R.; Erlanson–Albertsson, Charlotte

doi:10.1016/j.regpep.2005.05.002

Cited by 72 publications

(52 citation statements)

References 43 publications

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“…Likewise, other authors have reported a decrease in the ingestion of solid food in animals that received caloric soft drinks [9][10][11][12] and other sucrose-rich artificial beverages, and an increase in total fluid consumption due to the consumption of these beverages [16,17].…”

Section: Discussionmentioning

confidence: 84%

Consumo de refrigerante reduz a ingestão de alimentos em ratos Wistar

Cony

Goularte

Souza

et al. 2016

Sci Med

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Aims:To evaluate the effect of caloric and non-caloric soft drink intake on food consumption, body weight and composition, and metabolic parameters in rats. Methods: Controlled experimental study in which 30 male Wistar rats were divided into three groups and given food and beverage ad libitum during 17 weeks. The groups were as follows, according to the offered food: Control group -standard chow and water; Caloric soft drink group -standard chow, caloric soft drink, and water; and Non-caloric soft drink group -standard chow, non-caloric soft drink, and water. Results: There was no statistical difference in total energy intake, body weight, and fat deposition between groups. However, the chow energy intake was 45% lower in the caloric soft drink group compared to the control and non-caloric soft drink groups (198.7±0.7 kJ vs. 349.4±2.0 and 373.0±1.3 kJ, respectively), with 46% of the energy provided by the soft drink. The caloric soft drink group consumed 22% more carbohydrate, especially sucrose, compared to the control group (p<0.05). Macronutrient intake was not different between the control and non-caloric soft drink groups, but the caloric soft drink group consumed less protein and lipids when compared to the other groups (3.5±1.0 g of protein vs. 6.2±0.1 and 6.7±0.1 g, respectively; 0.7±0.01 g of lipids vs. 1.3±0.02 g and 1.4±0.02 g, respectively). Consumption of non-caloric soft drinks increased total sodium intake and consumption of both soft drinks decreased water intake. Although body weight varied during the experiment, there was no significant difference between groups at the end of the experiment, and no difference in fat deposition, fasting glucose, insulin and leptin, insulin resistance index, and lipid profile. Conclusions: The consumption of both types of soft drinks did not affect energy intake, body weight and composition, or metabolic parameters; however, it increased fluid intake and decreased water ingestion. Caloric soft drink intake influenced the amount and the quality of solid food consumed, compromising diet quality.KEY WORDS: soft drinks; food consumption; macronutrients. RESUMOObjetivos: Avaliar o efeito do consumo de refrigerante calórico e não calórico sobre a ingestão alimentar, composição corporal, massa corporal e parâmetros metabólicos em ratos. Métodos: Estudo experimental com grupo controle. Trinta ratos Wistar machos foram divididos em três grupos e receberam alimentos e bebidas ad libitum. Os grupos foram os seguintes, conforme o alimento oferecido: Grupo controle -ração padrão e água; Grupo refrigerante calórico -ração padrão, refrigerante calórico e água; e Grupo refrigerante não calórico -ração padrão, refrigerante não calórico e água. Resultados: Não houve diferença estatística na ingestão total de energia, peso corporal e depósito adiposo entre os grupos. Entretanto, a ingestão de energia da ração foi 45% menor no Grupo refrigerante calórico comparado ao Grupo controle e ao Grupo refrigerante não calórico (198,7±0,7 kJ vs. 349,4±2,0 kJ e 373,0±1,3 kJ, respecti...

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Section: Discussionmentioning

confidence: 84%

Consumo de refrigerante reduz a ingestão de alimentos em ratos Wistar

Cony

Goularte

Souza

et al. 2016

Sci Med

View full text Add to dashboard Cite

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“…With sucrose added, the ghrelin levels are suppressed in the fasting condition and not further suppressed by eating. 19 In a similar way fasting leptin levels are increased and not further increased by a sucrose meal, suggesting a blunted response. The driving force to eat is rather the reward system, as indicated by activated mureceptors in the hypothalamus.…”

Section: Type Of Carbohydrate Decides Feeding Behaviourmentioning

confidence: 86%

“…17,18 The reason for overeating is a blunted response in hunger and satiety signals. 19 The hunger signals ghrelin, which is raised after fasting and is normally suppressed 30 min after the intake of a meal. With sucrose added, the ghrelin levels are suppressed in the fasting condition and not further suppressed by eating.…”

Section: Type Of Carbohydrate Decides Feeding Behaviourmentioning

confidence: 99%

The effect of low carbohydrate on energy metabolism

Erlanson–Albertsson

Mei

2005

Int J Obes

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OBJECTIVE: To investigate whether low-carbohydrate diets are efficient for reduction of body weight and through which mechanism. DESIGN: A couple of studies using low-carbohydrate diets in the treatment of obesity are reviewed. Mechanisms for explaining the reduced appetite are described in relation to knowledge on regulation of appetite for fat and carbohydrate. RESULTS: Studies with low-carbohydrate diets demonstrate a rapid weight loss, being more pronounced after 3 and 6 months compared to low-fat diets. After 12 months there is no difference between the low-carbohydrate and the conventional low-fat diet on weight loss. Both diets lead to improvements in risk factors for coronary heart disease, the low-carbohydrate diet leading to a greater decrease in serum triglycerides and increase in HDL cholesterol compared to the low-fat diet. Blood pressure, insulin sensitivity and LDL cholesterol were improved to a similar degree by the two diets. The mechanism for the rapid weight loss with the low-carbohydrate diet is a suppressed appetite, first through the high-protein content of the diet, second through the ketogenic nature of the diet with satiety signals for fat being active and third through the absence of hunger-promoting carbohydrate components like sucrose and/or fructose. CONCLUSION: A rapid initial weight loss occurs with a low-carbohydrate diet due to a suppressed appetite. There is as yet no indication of an increased metabolic rate and an increased thermogenesis by the low-carbohydrate diet. The safety and efficacy of low-carbohydrate diets have to await further studies.

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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%

“…Moreover, weight gain and insulin resistance from habitual consump-tion of palatable foods decrease insulin and leptin blood-brain barrier (BBB) penetrability (Caro et al, 1996;Kaiyala et al, 2000;Banks, 2003;Banks and Farrell, 2003;Woods et al, 2003) and their CNS effects (Couce et al, 2001;Banks and Farrell, 2003;Lindqvist et al, 2005;Porte et al, 2005), albeit some homeostatic hypothalamic areas lack BBB (Peruzzo et al, 2000;Ganong, 2000). The resultant brain insulin and leptin 'resistance' renders normal satiety signals even more ineffective (Erlanson-Albertsson, 2005;Isganaitis and Lustig, 2005) leading to further impairments in physiologic mechanisms regulating food intake (eg, overeating) and shifting the set point for energy homeostasis towards the development of overweight and obesity (Levine et al, 2003;Erlanson-Albertsson, 2005;Isganaitis and Lustig, 2005).…”

Section: Repetitive Palatable Food Consumption May Dysregulate Homeosmentioning

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

133

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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Overeating of palatable food is associated with blunted leptin and ghrelin responses

Cited by 72 publications

References 43 publications

Consumo de refrigerante reduz a ingestão de alimentos em ratos Wistar

Consumo de refrigerante reduz a ingestão de alimentos em ratos Wistar

The effect of low carbohydrate on energy metabolism

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

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