2019
DOI: 10.1016/j.cmet.2019.04.001
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Amygdala NPY Circuits Promote the Development of Accelerated Obesity under Chronic Stress Conditions

Abstract: Highlights d Central amygdala NPY neurons control feeding d Stress combined with a high-caloric diet increases NPY expression in the central amygdala d Insulin controls NPY expression in central amygdala neurons d Stress combined with a high-caloric diet causes insulin resistance in central amygdala

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Cited by 90 publications
(118 citation statements)
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“…Nevertheless, caution should be taken when interpreting the normalized values, as changes in amygdala T2W SI values clearly caused a bias. Indeed, the amygdala itself has not only emerged as a brain feeding center with molecularly defined neuronal populations that increase (50)(51)(52) and decrease food intake (53), but it is also a site of high-fat diet-induced inflammation (54,55). Furthermore, amygdala inflammation is a cause of insulin resistance (55), which may explain the strong relationships we found between plasma insulin with T2W SI values in this brain region.…”
Section: Figure 4 Relationships Between Bmi Body Fat Mass Circulatmentioning
confidence: 79%
“…Nevertheless, caution should be taken when interpreting the normalized values, as changes in amygdala T2W SI values clearly caused a bias. Indeed, the amygdala itself has not only emerged as a brain feeding center with molecularly defined neuronal populations that increase (50)(51)(52) and decrease food intake (53), but it is also a site of high-fat diet-induced inflammation (54,55). Furthermore, amygdala inflammation is a cause of insulin resistance (55), which may explain the strong relationships we found between plasma insulin with T2W SI values in this brain region.…”
Section: Figure 4 Relationships Between Bmi Body Fat Mass Circulatmentioning
confidence: 79%
“…In contrast, Y1R antagonists only played a significant role in chow-fed rats ( 115 ). Thirdly, selective activation of CeA NPY neurons leads to increased food intake and reduced energy expenditure ( 116 ). Importantly, selective lack of NPY in CeA neurons attenuates the obesity phenotype, whereas excessive production of NPY in CeA further enhances that phenotype ( 116 ).…”
Section: Npy Indirectly Regulates the Immune Responsementioning
confidence: 99%
“…In the BLA, somatostatin interneurons express NPY2-receptors, some of which coexpress NPY; stimulating BLA NPY2-receptors reduces tonic GABA release onto local principal neurons [30]. A combination of stress and high-fat diet activates central amygdala NPY neurons, resulting in increased feeding and reduced energy expenditure [67].…”
Section: Cholecystokininmentioning
confidence: 99%
“…In patients with schizophrenia and bipolar disorder, somatostatin positive neurons decreased in the amygdala [42]. Selective activation of NPY neurons in the central amygdala (CeA) leads to increased food intake and decreased energy expenditure under stress [67]. GABAergic serotonin receptor 2a-expressing neurons in the CeA modulate food consumption [108].…”
Section: The Crosstalk Between the Gabaergic System And Thementioning
confidence: 99%
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