Hypoglycemic Detection at the Portal Vein

Donovan, C. M.; Bohland, MaryAnn

doi:10.2337/db08-1437

Cited by 9 publications

(5 citation statements)

References 20 publications

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“…This is associated with a reduced sensitivity of jejunal afferents (primarily vagal) to low-level distension and reduced excitability of identified jejunal vagal afferents within the nodose ganglion to CCK and 5-HT exposure ( Daly et al, 2011 ). Corresponding reductions in vagal afferent expression of receptors for CCK, 5-HT and other anorexic GI peptides have been reported in the nodose ganglion ( Donovan and Bohland, 2009 ). Additionally, HFD reduced the responses of gastric vagal tension receptors to distension and augmented the inhibitory effect of ghrelin on vagal afferents.…”

Section: Invasive Neuromodulation Strategies: Recent Developments Andsupporting

confidence: 52%

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

383

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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Section: Invasive Neuromodulation Strategies: Recent Developments Andsupporting

confidence: 52%

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

383

321

View full text Add to dashboard Cite

show abstract

“…The peripheral gluco-sensors appear to be critical for the activation of the sympathetic and sympatho-adrenal response because infusion of glucose into the portal vein suppresses hypoglycaemia-induced increase in plasma epinephrine levels in rats and dogs (9,(146)(147)(148)(149) and the sympatho-adrenal response is suppressed by denervation of the portal vein also in rats and dogs (146,150,151). However, it should be noted that human studies investigating this have reported inconsistent results and conflicting conclusions regarding the importance of portal gluco-sensing (152)(153)(154)(155)(156). Activation of catecholamine neurones within the ventromedial hypothalamus is also important for modulation of the sympatho-adrenal and glucagon response to hypoglycaemia (157).…”

Section: Cns Activation Of Counter-regulatory Hormone Response To Hypmentioning

confidence: 99%

Effect of Insulin‐Induced Hypoglycaemia on theCentral Nervous System: Evidence from Experimental Studies

Jensen

Bøgh

Lykkesfeldt

2014

J Neuroendocrinology

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Insulin-induced hypoglycaemia (IIH) is a major acute complication in type 1 as well as in type 2 diabetes, particularly during intensive insulin therapy. The brain plays a central role in the counter-regulatory response by eliciting parasympathetic and sympathetic hormone responses to restore normoglycaemia. Brain glucose concentrations, being approximately 15-20% of the blood glucose concentration in humans, are rigorously maintained during hypoglycaemia through adaptions such as increased cerebral glucose transport, decreased cerebral glucose utilisation and, possibly, by using central nervous system glycogen as a glucose reserve. However, during sustained hypoglycaemia, the brain cannot maintain a sufficient glucose influx and, as the cerebral hypoglycaemia becomes severe, electroencephalogram changes, oxidative stress and regional neuronal death ensues. With particular focus on evidence from experimental studies on nondiabetic IIH, this review outlines the central mechanisms behind the counter-regulatory response to IIH, as well as cerebral adaption to avoid sequelae of cerebral neuroglycopaenia, including seizures and coma.

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“…While some studies have shown that oral glucose loading (to elevate portal glucose concentration only) during a hyperinsulinemic‐hypoglycemic clamp can suppress 54 or augment 55 the counterregulatory response, others have shown that increasing portal vein glucose concentrations during hypoglycemia has no effect on counterregulatory or symptomatic responses to hypoglycemia 56 . Some of these inconsistencies may be related to subtle methodologic differences in protocols 57 . Beyond their function in glucose sensing in the postprandial state, the role of peripheral glucose sensors in the initiation of the counterregulatory response during hypoglycemia is yet to be clarified.…”

Section: Neuroendocrine Responses To Hypoglycemiamentioning

confidence: 99%

Neuroendocrine responses to hypoglycemia

Tesfaye¹,

Seaquist²

2010

Annals of the New York Academy of Sciences

116

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The counterregulatory response to hypoglycemia is a complex and well-coordinated process. As blood glucose concentration declines, peripheral and central glucose sensors relay this information to central integrative centers to coordinate neuroendocrine, autonomic, and behavioral responses and avert the progression of hypoglycemia. Diabetes, both type 1 and type 2, can perturb these counterregulatory responses. Moreover, defective counterregulation in the setting of diabetes can progress to hypoglycemia unawareness. While the mechanisms that underlie the development of hypoglycemia unawareness are not completely known, possible causes include altered sensing of hypoglycemia by the brain and/or impaired coordination of responses to hypoglycemia. Further study is needed to better understand the intricacies of the counterregulatory response and the mechanisms contributing to the development of hypoglycemia unawareness.

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Hypoglycemic Detection at the Portal Vein

Cited by 9 publications

References 20 publications

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

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

Effect of Insulin‐Induced Hypoglycaemia on theCentral Nervous System: Evidence from Experimental Studies

Neuroendocrine responses to hypoglycemia

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