Mechanisms of insulin resistance in the amygdala: Influences on food intake

Areias, Maria Fernanda Condes; Prada, Patrícia O.

doi:10.1016/j.bbr.2015.01.003

Cited by 47 publications

(32 citation statements)

References 69 publications

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“…In addition, the regulation of food intake by insulin in non-hypothalamic NPY neurons may also be a key contributing factor to the overall phenotypes. This was supported by previous studies in which insulin administration reduced NPY expression in amygdala, leading to a significant reduction in food intake [36], [37]. While other contributions from NPY/AgRP co-expressing neurons to the overall control of energy homeostasis cannot be completely excluded, this neuronal population does not seem to be critical for mediating insulin actions in the regulation of feeding and energy expenditure.…”

Section: Discussionsupporting

confidence: 72%

Insulin controls food intake and energy balance via NPY neurons

Loh

Zhang

Brandon

et al. 2017

Molecular Metabolism

123

100

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ObjectivesInsulin signaling in the brain has been implicated in the control of satiety, glucose homeostasis and energy balance. However, insulin signaling is dispensable in energy homeostasis controlling AgRP or POMC neurons and it is unclear which other neurons regulate these effects. Here we describe an ancient insulin/NPY neuronal network that governs energy homeostasis across phyla.MethodsTo address the role of insulin action specifically in NPY neurons, we generated a variety of models by selectively removing insulin signaling in NPY neurons in flies and mice and testing the consequences on energy homeostasis.ResultsBy specifically targeting the insulin receptor in both fly and mouse NPY expressing neurons, we found NPY-specific insulin signaling controls food intake and energy expenditure, and lack of insulin signaling in NPY neurons leads to increased energy stores and an obese phenotype. Additionally, the lack of insulin signaling in NPY neurons leads to a dysregulation of GH/IGF-1 axis and to altered insulin sensitivity.ConclusionsTaken together, these results suggest that insulin actions in NPY neurons is critical for maintaining energy balance and an impairment of this pathway may be causally linked to the development of metabolic diseases.

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Section: Discussionsupporting

confidence: 72%

Insulin controls food intake and energy balance via NPY neurons

Loh

Zhang

Brandon

et al. 2017

Molecular Metabolism

123

100

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“…Moreover, the compensation of excessive caloric soft drink intake by a lower chow intake can be attributed to regulatory mechanisms of energy homeostasis by insulin, both in the hypothalamus and in the amygdala, which are two important brain sites that regulate food intake [20]. Recent data have shown that insulin receptors in the brain play an important role in weight maintenance, appetite, and energy balance, regulating the required and consumed energy [21].…”

Section: Discussionmentioning

confidence: 99%

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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“…It is worth noting that similar topics have been the object of several recent reviews (e.g., [5,56,78,98,109,117,139]). They include descriptions of studies linking food intake regulation to the amygdala [5] and the hippocampus Kanoski & Grill [78]; [117]) as well as studies showing the influence of memory on food reward processing [56] and obesity [98], and the impact of other factors such as environment and stress on obesity [109,139].…”

Section: The Anterior Medial Temporal Lobes -Classical Rolementioning

confidence: 99%

“…They include descriptions of studies linking food intake regulation to the amygdala [5] and the hippocampus Kanoski & Grill [78]; [117]) as well as studies showing the influence of memory on food reward processing [56] and obesity [98], and the impact of other factors such as environment and stress on obesity [109,139]. However, rather than reiterating the material covered by these scholarly works, the present review aims to integrate the literature on the functions of both the amygdala and the hippocampus in food intake and body weight regulation in two unique ways.…”

Section: The Anterior Medial Temporal Lobes -Classical Rolementioning

confidence: 99%

The anterior medial temporal lobes: Their role in food intake and body weight regulation

Coppin

2016

Physiology & Behavior

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• The amygdala and hippocampus play a major role in food intake and weight regulation.• These functions are far less known to cognitive and affective scientists.• This review uniquely expands on the interactions between these two brain structures. a b s t r a c t a r t i c l e i n f o The anterior medial temporal lobes are one of the most studied parts of the brain. Classically, their two main structures -the amygdalae and the hippocampi -have been linked to key cognitive and affective functions, related in particular to learning and memory. Based on abundant evidence, we will argue for an alternative but complementary point of view: they may also play a major role in food intake and body weight regulation. First, an overview is given of early clinical evidence in this line of thought. Subsequently, empirical evidence is presented on how food intake, including in the extreme case of obesity, may relate to amygdalian and hippocampal functioning. The focus is on the amygdala's role in processing the relevance of food stimuli, cue-induced feeding, and stress-induced eating and on the hippocampus' involvement in the use of interoceptive signals of hunger and satiety, as well as memory and inhibitory processes related to food intake. Additionally, an elaboration takes place on possible reciprocal links between food intake, body weight, and amygdala and hippocampus functioning. Finally, issues that seemed particularly critical for future research in the field are discussed.

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Mechanisms of insulin resistance in the amygdala: Influences on food intake

Cited by 47 publications

References 69 publications

Insulin controls food intake and energy balance via NPY neurons

Insulin controls food intake and energy balance via NPY neurons

Consumo de refrigerante reduz a ingestão de alimentos em ratos Wistar

The anterior medial temporal lobes: Their role in food intake and body weight regulation

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