Endocrine regulation of neurotransmitter transporters

Figlewicz, Dianne P.

doi:10.1016/s0920-1211(99)00072-8

Cited by 49 publications

(21 citation statements)

References 46 publications

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“…First, its most well described effect is a selective inhibition of presynaptic reuptake of the monoaminergic neurotransmitters serotonin (5-hydroxytryptamine; 5-HT), noradrenaline (NA) and, to a lesser extent, dopamine, at the CNS level, enhancing the appetite suppressing actions of these neurotransmitters [13]. Reuptake of these neurotransmitters from the synapse via high affinity and specific transporters present in the presynaptic membrane (which are inhibited by sibutramine), terminates its signaling [14]. Unlike the early amphetamine-like drugs such as dexamphetamine, phentermine and fenfluramines, sibutramine does not directly stimulate the release of 5-HT, NA nor dopamine, and so does not causes presynaptic neurotransmitters depletion nor the consequent neurotoxicity [15].…”

Section: Pharmacological Targets Of Sibutraminementioning

confidence: 99%

Sibutramine Effects on Central Mechanisms Regulating Energy Homeostasis

Araújo¹,

Martel²

2011

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During the last 50 years the global pandemic of obesity and associated life-threatening co-morbidities strongly promoted the development of anti-obesity pharmacotherapy. Sibutramine is an anti-obesity drug that in conjunction with lifestyle modifications reduces food intake and body weight. This may result from several effects: inhibition of presynaptic reuptake of monoaminergic neurotransmitters in the central nervous system, thereby suppressing appetite, induction of an increase in anorexigenic and a decrease in orexigenic neuropeptide secretion, induction of an increase in energy expenditure, and induction of peripheral sympathomimetic effects. The effects of sibutramine on anabolic and catabolic signals that regulate energy homeostasis in the hypothalamus are not completely understood. So, the aim of this review is to summarize the central mechanisms of action of sibutramine, responsible for its weight and food intake reducing potential. Despite being a useful drug in obesity treatment, awareness about the loss of long-term effectiveness and detrimental side effects of sibutramine has recently emerged. As a consequence, new drugs that produce safer and more persistent weight loss are currently undergoing clinical trials.

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Section: Pharmacological Targets Of Sibutraminementioning

confidence: 99%

Sibutramine Effects on Central Mechanisms Regulating Energy Homeostasis

Araújo¹,

Martel²

2011

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“…Related to the change in energy state is the potential role of insulin levels. Decreased levels of insulin, as seen in the fasted state, are known to reduce norepinephrine and increase dopamine activity, which can increase the seizure threshold [31]. However, insulin has also been reported to increase GABA receptors, decrease cell excitability in a seizure-protective fashion, and open ATP-sensitive potassium channels, ultimately causing membrane hyperpolarization [27•].…”

Section: Altered Energy Statementioning

confidence: 99%

State of the ketogenic diet(s) in epilepsy

Huffman¹,

Kossoff

2006

Curr Neurol Neurosci Rep

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Fasting has been recognized as a treatment for seizures since ancient times. The ketogenic diet is a low-carbohydrate, adequate-protein, high-fat diet that biochemically mimics the fasting state and has been used to successfully treat seizures for 85 years. The diet has enjoyed a resurgence in popularity over the past decade and is gaining acceptance and use worldwide. Many studies over the past several years have explored possible mechanisms of action for the ketogenic diet. This review addresses these studies, as well as recent research regarding possible indications for the diet, variations in its initiation, side effect profiles, and the recent use of modified formulations to improve tolerability.

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“…Indeed, available data show that insulin favors the recruitment of inhibitory GABA-A receptors (Wan et al, 1997), although insulin may increase the release of excitotoxic amino acids during reperfusion following ischemia (Guyot et al, 2000). An alternate possibility might be a hormonally induced change in neurotransmitter transporters (Figlewicz, 1999). A tempting speculation is that the ketogenic diet might augment or diminish the production of other hormones that affect synaptic transmission.…”

Section: The Ketogenic Diet Amino Acids and The Antiepileptic Effectmentioning

confidence: 99%

Ketogenic diet, amino acid metabolism, and seizure control

Yudkoff

Daikhin

Nissim

et al. 2001

J of Neuroscience Research

132

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The ketogenic diet has been utilized for many years as an adjunctive therapy in the management of epilepsy, especially in those children for whom antiepileptic drugs have not permitted complete relief. The biochemical basis of the dietary effect is unclear. One possibility is that the diet leads to alterations in the metabolism of brain amino acids, most importantly glutamic acid, the major excitatory neurotransmitter. In this review, we explore the theme. We present evidence that ketosis can lead to the following: 1) a diminution in the rate of glutamate transamination to aspartate that occurs because of reduced availability of oxaloacetate, the ketoacid precursor to aspartate; 2) enhanced conversion of glutamate to GABA; and 3) increased uptake of neutral amino acids into the brain. Transport of these compounds involves an uptake system that exchanges the neutral amino acid for glutamine. The result is increased release from the brain of glutamate, particularly glutamate that had been resident in the synaptic space, in the form of glutamine. These putative adaptations of amino acid metabolism occur as the system evolves from a glucose-based fuel economy to one that utilizes ketone bodies as metabolic substrates. We consider mechanisms by which such changes might lead to the antiepileptic effect.

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Endocrine regulation of neurotransmitter transporters

Cited by 49 publications

References 46 publications

Sibutramine Effects on Central Mechanisms Regulating Energy Homeostasis

Sibutramine Effects on Central Mechanisms Regulating Energy Homeostasis

State of the ketogenic diet(s) in epilepsy

Ketogenic diet, amino acid metabolism, and seizure control

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