Vagal Nerve Function in Obesity: Therapeutic Implications

Kral, John G.; Paez, Wencesley; Wolfe, Bruce M.

doi:10.1007/s00268-009-0138-8

Cited by 48 publications

(28 citation statements)

References 123 publications

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“…thiazolidinediones) that also exert anti-inflammatory properties has been shown to improve neurocognitive function (McIntyre et al 2007). Vagal nerve stimulation (which is known to relay cytokine signals to the CNS) administered to depressed obese patients has also provided preliminary evidence of associated weight loss (Kral et al 2009). …”

Section: Resultsmentioning

confidence: 99%

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

et al. 2010

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The aim of this review is to evaluate the evidentiary base supporting the hypothesis that the increased hazard for obesity in mood disorder populations (and vice versa) is a consequence of shared pathophysiological pathways. We conducted a PubMed search of all English-language articles with the following search terms: obesity, inflammation, hypothalamic-pituitary-adrenal axis, insulin, cognition, CNS, and neurotransmitters, cross-referenced with major depressive disorder and bipolar disorder. The frequent co-occurrence of mood disorders and obesity may be characterized by interconnected pathophysiology. Both conditions are marked by structural and functional abnormalities in multiple cortical and subcortical brain regions that subserve cognitive and/or affective processing. Abnormalities in several interacting biological networks (e.g. immuno-inflammatory, insulin signaling, and counterregulatory hormones) contribute to the co-occurence of mood disorders and obesity. Unequivocal evidence now indicates that obesity and mood disorders are chronic low-grade pro-inflammatory states that result in a gradual accumulation of allostatic load. Abnormalities in key effector proteins of the pro-inflammatory cascade include, but are not limited to, cytokines/adipokines such as adiponectin, leptin, and resistin as well as tumor necrosis factor alpha and interleukin-6. Taken together, the bidirectional relationship between obesity and mood disorders may represent an exophenotypic manifestation of aberrant neural and inflammatory networks. The clinical implications of these observations are that, practitioners should screen individuals with obesity for the presence of clinically significant depressive symptoms (and vice versa). This clinical recommendation is amplified in individuals presenting with biochemical indicators of insulin resistance and other concurrent conditions associated with abnormal inflammatory signaling (e.g. cardiovascular disease).

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Section: Resultsmentioning

confidence: 99%

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

et al. 2010

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“…Bilateral truncal vagotomy has been used historically as a treatment for obesity refractory to other therapies, and has been associated with satiety and weight loss (Kral et al, 2009). Based upon this observation and although that it has been reported that the effects on body weight are lost over time (Camilleri et al, 2008) and that truncal vagotomy was virtually ineffective to reduce solid food intake (Gortz et al, 1990), vagal blockade therapy was tested in humans with the primary objective to reduce weight of morbid obese individuals.…”

Section: Invasive Neuromodulation Strategies: Recent Developments Andmentioning

confidence: 99%

Neuroimaging and neuromodulation approaches to study eating behavior and prevent and treat eating disorders and obesity

Val‐Laillet¹,

Aarts

Weber

et al. 2015

NeuroImage: Clinical

392

321

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Functional, molecular and genetic neuroimaging has highlighted the existence of brain anomalies and neural vulnerability factors related to obesity and eating disorders such as binge eating or anorexia nervosa. In particular, decreased basal metabolism in the prefrontal cortex and striatum as well as dopaminergic alterations have been described in obese subjects, in parallel with increased activation of reward brain areas in response to palatable food cues. Elevated reward region responsivity may trigger food craving and predict future weight gain. This opens the way to prevention studies using functional and molecular neuroimaging to perform early diagnostics and to phenotype subjects at risk by exploring different neurobehavioral dimensions of the food choices and motivation processes. In the first part of this review, advantages and limitations of neuroimaging techniques, such as functional magnetic resonance imaging (fMRI), positron emission tomography (PET), single photon emission computed tomography (SPECT), pharmacogenetic fMRI and functional near-infrared spectroscopy (fNIRS) will be discussed in the context of recent work dealing with eating behavior, with a particular focus on obesity. In the second part of the review, non-invasive strategies to modulate food-related brain processes and functions will be presented. At the leading edge of non-invasive brain-based technologies is real-time fMRI (rtfMRI) neurofeedback, which is a powerful tool to better understand the complexity of human brain–behavior relationships. rtfMRI, alone or when combined with other techniques and tools such as EEG and cognitive therapy, could be used to alter neural plasticity and learned behavior to optimize and/or restore healthy cognition and eating behavior. Other promising non-invasive neuromodulation approaches being explored are repetitive transcranial magnetic stimulation (rTMS) and transcranial direct-current stimulation (tDCS). Converging evidence points at the value of these non-invasive neuromodulation strategies to study basic mechanisms underlying eating behavior and to treat its disorders. Both of these approaches will be compared in light of recent work in this field, while addressing technical and practical questions. The third part of this review will be dedicated to invasive neuromodulation strategies, such as vagus nerve stimulation (VNS) and deep brain stimulation (DBS). In combination with neuroimaging approaches, these techniques are promising experimental tools to unravel the intricate relationships between homeostatic and hedonic brain circuits. Their potential as additional therapeutic tools to combat pharmacorefractory morbid obesity or acute eating disorders will be discussed, in terms of technical challenges, applicability and ethics. In a general discussion, we will put the brain at the core of fundamental research, prevention and therapy in the context of obesity and eating disorders. First, we will discuss the possibility to identify new biological markers of brain functions. Second, we will highli...

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“…This system consists of parasympathetic and sympathetic divisions [118]. The activity of this system influences heart rate, digestion, respiration rate, salivation, perspiration, pupil dilation, micturition, sexual arousal, and vascular tone [119, 120]. Sympathetic and parasympathetic divisions typically function in opposite but complementary fashion.…”

Section: Autonomic Functionsmentioning

confidence: 99%

Nonsocial Functions of Hypothalamic Oxytocin

et al. 2013

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Oxytocin (OXT) is a hypothalamic neuropeptide composed of nine amino acids. The functions of OXT cover a variety of social and nonsocial activity/behaviors. Therapeutic effects of OXT on aberrant social behaviors are attracting more attention, such as social memory, attachment, sexual behavior, maternal behavior, aggression, pair bonding, and trust. The nonsocial behaviors/functions of brain OXT have also received renewed attention, which covers brain development, reproduction, sex, endocrine, immune regulation, learning and memory, pain perception, energy balance, and almost all the functions of peripheral organ systems. Coordinating with brain OXT, locally produced OXT also involves the central and peripheral actions of OXT. Disorders in OXT secretion and functions can cause a series of aberrant social behaviors, such as depression, autism, and schizophrenia as well as disturbance of nonsocial behaviors/functions, such as anorexia, obesity, lactation failure, osteoporosis, diabetes, and carcinogenesis. As more and more OXT functions are identified, it is essential to provide a general view of OXT functions in order to explore the therapeutic potentials of OXT. In this review, we will focus on roles of hypothalamic OXT on central and peripheral nonsocial functions.

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Vagal Nerve Function in Obesity: Therapeutic Implications

Cited by 48 publications

References 123 publications

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus

Neuroimaging and neuromodulation approaches to study eating behavior and prevent and treat eating disorders and obesity

Nonsocial Functions of Hypothalamic Oxytocin

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