Evidence that decreased feeding induced by systemic injection of cholecystokinin is mediated by CCK-A receptors

Dourish, C T; Rückert, A; Tattersall, F.D.; Iversen, S.D.

doi:10.1016/0014-2999(89)90528-1

Cited by 112 publications

(40 citation statements)

References 4 publications

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“…Although exogenous CCK resulted in a dose related suppression of intake in LETO rats, CCK had no effect on glucose consumption in the OLETF rats (Moran, Katz, PlataSalaman, & Schwartz, 1998). These data were consistent with findings from studies using specific CCK receptor antagonists demonstrating that peripheral exogenous CCK inhibited food intake through interactions with CCK1 receptors (Dourish, Ruckert, Tattersall, & Iversen, 1989;Moran et al, 1993;Reidelberger et al, 1991).…”

Section: Disordered Patterns Of Food Intake In the Oletf Ratsupporting

confidence: 93%

Hyperphagia and obesity of OLETF rats lacking CCK1 receptors: Developmental aspects

Moran

2006

Dev. Psychobiol.

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Otsuka Long Evans Tokushima Fatty (OLETF) rats have a deletion in the gene encoding the cholecystokinin-1 (CCK1) receptor. This deletion prevents protein expression, making the OLETF rat a CCK1 receptor knockout model. Consistent with the absence of CCK1 receptors, OLETF rats do not reduce their food intake in response to exogenously administered CCK and consume larger than normal meals. This deficit in within-meal feedback signaling is evident in liquid as well as solid meals. Neonatal OLETF rats show similar differences in independent ingestion tests. Intake is higher and is reflected in greater licking behavior. Neonatal OLETF rats also have diminished latencies to consume and higher initial ingestion rats. Adult OLETF rats are hyperphagic and obese. Although arcuate nucleus peptide gene expression is apparently normal in OLETF rats, when obesity is prevented through pair-feeding to amounts consumed by control Long Evans Tokushima Otsuka (LETO) rats, dorsomedial hypothalamic NPY mRNA expression is significantly elevated in OLETF rats. NPY overexpression is also evident in preobese, juvenile OLETF rats suggesting a causal role for this overexpression in the hyperphagia and obesity. Running wheel exercise normalizes food intake and body weight in OLETF rats. When access to exercise is provided at a time when OLETF rats are obese, the effects are limited to the period of exercise. When running wheel access is available to younger, preobese OLETF rats, exercise results in long lasting reductions in food intake and body weight and improved glucose regulation. These lasting metabolic effects of exercise may be secondary to an exercise induced reduction in DMH NPY mRNA expression.

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Section: Disordered Patterns Of Food Intake In the Oletf Ratsupporting

confidence: 93%

Hyperphagia and obesity of OLETF rats lacking CCK1 receptors: Developmental aspects

Moran

2006

Dev. Psychobiol.

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“…Type A receptors are distributed in the CNS and the periphery whereas type B receptors are located exclusively in the CNS [39]. CCK is traditionally known as a short-term satiety factor involved in meal size reduction and termination [40,41,42] and also initiates a behavioral satiety sequence [43]. …”

Section: Potential Mediators Of Neatmentioning

confidence: 99%

Neuropeptidergic Mediators of Spontaneous Physical Activity and Non-Exercise Activity Thermogenesis

Teske¹,

Billington

Kotz³

2007

Neuroendocrinology

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Lean individuals have high levels of spontaneous physical activity (SPA) and the energy expenditure derived from that activity, termed non-exercise activity thermogenesis or NEAT, appears to protect them from obesity. Conversely, obesity in different human populations is characterized by low levels of SPA and NEAT. Like in humans, elevated SPA in rats appears to protect against obesity: obesity-resistant rats have significantly greater SPA and NEAT than obesity-prone rats. We review the literature on brain mechanisms important in mediating SPA and NEAT. The focus is on neuropeptides, including cholecystokinin, corticotropin-releasing hormone (also known as corticotropin-releasing factor), neuromedin U, neuropeptide Y, leptin, agouti-related protein, orexin-A (also known as hypocretin-1), and ghrelin. We also review information regarding interactions between these neuropeptides and dopamine, a neurotransmitter important in mediating motor function. Finally, we present evidence that elevated signaling of pathways mediating SPA and NEAT may protect against weight gain and obesity.

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“…CCK's satiating effects are mediated through interactions with CCK-1 receptors [96][97][98][99][100]. The Otsuka LongEvans Tokushima fatty rat (OLETF) rat bears a spontaneous null mutation of the CCK-1 receptor gene and is hyperphagic and obese [101,102].…”

Section: Gastrointestinal Peptides and Satiation: Introductionmentioning

confidence: 99%

Neuroendocrine control of satiation

Asarian¹,

Bächler

2014

Hormone Molecular Biology and Clinical Investigation

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Abstract:Eating is a simple behavior with complex functions. The unconscious neuroendocrine process that stops eating and brings a meal to its end is called satiation. Energy homeostasis is mediated accomplished through the control of meal size via satiation. It involves neural integrations of phasic negative-feedback signals related to ingested food and tonic signals, such as those related to adipose tissue mass. Energy homeostasis is accomplished through adjustments in meal size brought about by changes in these satiation signals. The best understood meal-derived satiation signals arise from gastrointestinal nutrient sensing. Gastrointestinal hormones secreted during the meal, including cholecystokinin, glucagon-like peptide 1, and PYY, mediate most of these. Other physiological signals arise from activation of metabolic-sensing neurons, mainly in the hypothalamus and caudal brainstem. We review both classes of satiation signal and their integration in the brain, including their processing by melanocortin, neuropeptide Y/agouti-related peptide, serotonin, noradrenaline, and oxytocin neurons. Our review is not comprehensive; rather, we discuss only what we consider the best-understood mechanisms of satiation, with a special focus on normally operating physiological mechanisms.

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Evidence that decreased feeding induced by systemic injection of cholecystokinin is mediated by CCK-A receptors

Cited by 112 publications

References 4 publications

Hyperphagia and obesity of OLETF rats lacking CCK1 receptors: Developmental aspects

Hyperphagia and obesity of OLETF rats lacking CCK1 receptors: Developmental aspects

Neuropeptidergic Mediators of Spontaneous Physical Activity and Non-Exercise Activity Thermogenesis

Neuroendocrine control of satiation

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