Influence of resting energy expenditure on weight gain in adolescents taking second-generation antipsychotics

Cuerda, C.; Merchán-Naranjo, Jessica; Velasco, Cristina; Gutiérrez, Alberto; Leiva, Marta; Castro, Elena; Parellada, Mara; Giráldez, Marisa; Bretón, Irene; Camblor, M.; García-Peris, Pilar; Dulín, Elena; Sanz, Inmaculada; Desco, Manuel; Arango, Celso

doi:10.1016/j.clnu.2011.03.007

Cited by 33 publications

(40 citation statements)

References 49 publications

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“…This is supported by in vitro studies in adipocytes, which have reliably shown AAP-associated increases in lipogenesis, anti-lipolysis (Albaugh et al 2011;Minet-Ringuet et al 2007;Vestri et al 2007), and pre-adipocyte differentiation (Hemmrich et al 2006;Yang et al 2007). This may be clinically relevant given that both psychotic illness and AAP treatment have been associated with visceral fat distribution (Cuerda et al 2011;xGilles et al 2010;Joseph et al 2011;Zhang et al 2004), which emerges as a strong and independent predictor of cardiovascular disease and related morbidities (Boyko et al 2000;Kramer et al 2009;Kuk et al 2006). If indeed AAP-induced changes in feeding are to some extent independent of AAP-induced increases in fat accumulation, this may imply different underlying mechanisms and, as a consequence, separate but complementary targets to attenuate AAP-induced weight gain.…”

Section: Discussion/conclusionmentioning

confidence: 93%

Atypical antipsychotics and effects on feeding: from mice to men

et al. 2016

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The findings from this review indicate that the varying levels of AAP-related weight gain reflect changes in both appetite and feeding behaviors, which differ by type of AAP. However, inconsistencies exist among the studies (both human and rodent) that may reflect considerable differences in study design and methodology. Future studies examining underlying mechanisms of antipsychotic-induced weight gain are recommended in order to develop strategies addressing the serious metabolic side effect of AAPs.

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Section: Discussion/conclusionmentioning

confidence: 93%

Atypical antipsychotics and effects on feeding: from mice to men

et al. 2016

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“…[32][33][34] On the other hand, there is less understanding of to what extent changes of resting metabolism rate and activity/sedation affect weight gain associated with APD medication, although current evidence suggests that they may play an important role in the development of APD-induced weight gain. 19,35,36 Altered eating behaviours have been reported in a number of clinical studies with treatment involving various APDs. Gothelf and colleagues first reported that increased food intake, but not resting energy expenditure and physical activity, was associated with olanzapine-induced weight gain in schizophrenia patients.…”

Section: The Effects Of Anti-psychotic Medication On Appetite/food Inmentioning

confidence: 99%

Effects of Antipsychotic Medications on Appetite, Weight, and Insulin Resistance

Deng¹

2013

Endocrinology and Metabolism Clinics of North America

139

100

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Although clozapine, olanzapine, and other atypical antipsychotic drugs (APDs) have fewer extrapyramidal side effects, they have serious metabolic side effects such as substantial weight gain, intra-abdominal obesity, and type 2 diabetes mellitus. Given that most patients with mental disorders face chronic, even life-long, treatment with APDs, the risks of weight gain/obesity and other metabolic symptoms are major considerations for APD maintenance treatment. This review focuses on the effects of APDs on weight gain, appetite, insulin resistance, and glucose dysregulation, and the relevant underlying mechanisms that may be help to prevent and treat metabolic side effects caused by APD therapy.

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“…[86] Patients treated with SGAs exert significantly decreased energy expenditure especially after chronic treatment (6-12 months). [95,[100][101][102] In the animal model, olanzapine, clozapine and quetiapine have been found to decrease energy expenditure. [99,[103][104] These findings support the hypothesis that during short-term SGA treatment, the rapid increase in body weight may be primarily caused by hyperphagia, while during long-term treatment, in which period food intake is no different from the control, decreases in energy expenditure may play the main role in SGA-induced obesity at least in animal models.…”

Section: Does Ampk-cpt1 Signaling Play a Different Role In The Threementioning

confidence: 99%

“…As has been reviewed, both clinical and preclinical studies found that treatment with obesogenic SGAs such as olanzapine, clozapine and quetiapine are associated with decreased energy expenditure. [95,[99][100][101][102][103][104] In the animal model, olanzapine, clozapine and quetiapine have been found to decrease energy expenditure by inhibiting sympathetic activity and BAT thermogenesis. [98,[102][103] A number of studies suggest that BAT thermoregulation is important in both humans and rodents in regulating body temperature and body weight, although some early studies found a wider distribution of BAT and less relevance to thermoregulation in humans than in rodents.…”

Section: The Role Of H1 Receptors In Sga-induced Decreased Energy Expmentioning

confidence: 99%

The Role of Hypothalamic H1 Receptor Antagonism in Antipsychotic-Induced Weight Gain

Deng

Huang

2013

CNS Drugs

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Treatment with second generation antipsychotics (SGAs), notably olanzapine and clozapine, causes severe obesity side effects. Antagonism of histamine H1 receptors has been identified as a main cause of SGAinduced obesity, but the molecular mechanisms associated with this antagonism in different stages of SGAinduced weight gain remain unclear. This review aims to explore the potential role of hypothalamic histamine H1 receptors in different stages of SGA-induced weight gain/obesity and the molecular pathways related to SGA-induced antagonism of these receptors. Initial data have demonstrated the importance of hypothalamic H1 receptors in both short-and long-term SGA-induced obesity. Blocking hypothalamic H1 receptors by SGAs activates AMP-activated protein kinase (AMPK), a well-known feeding regulator. During short-term treatment, hypothalamic H1 receptor antagonism by SGAs may activate the AMPK-carnitine palmitoyltransferase 1 signaling to rapidly increase caloric intake and result in weight gain. During long-term SGA treatment, hypothalamic H1 receptor antagonism can reduce thermogenesis, possibly by inhibiting the sympathetic outflows to the brainstem rostral raphe pallidus and rostral ventrolateral medulla, therefore decreasing brown adipose tissue thermogenesis. Additionally, blocking of hypothalamic H1 receptors by SGAs may also contribute to fat accumulation by decreasing lipolysis but increasing lipogenesis in white adipose tissue. In summary, antagonism of hypothalamic H1 receptors by SGAs may time-dependently affect the hypothalamus-brainstem circuits to cause weight gain by stimulating appetite and fat accumulation but reducing energy expenditure. The H1 receptor and its downstream signaling molecules could be valuable targets for the design of new compounds for treating SGA-induced weight gain/obesity.

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Influence of resting energy expenditure on weight gain in adolescents taking second-generation antipsychotics

Cited by 33 publications

References 49 publications

Atypical antipsychotics and effects on feeding: from mice to men

Atypical antipsychotics and effects on feeding: from mice to men

Effects of Antipsychotic Medications on Appetite, Weight, and Insulin Resistance

The Role of Hypothalamic H1 Receptor Antagonism in Antipsychotic-Induced Weight Gain

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