Neuroendocrine control of satiation

Asarian, Lori; Bächler, Thomas

doi:10.1515/hmbci-2014-0010

Cited by 13 publications

(8 citation statements)

References 319 publications

(361 reference statements)

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“…Noradrenaline has been known for its role in the pathogenesis of anxiety ( Kalk et al, 2011 ; Zheng et al, 2019 ) and depression ( Seki et al, 2018 ) for a long time. Interestingly, it appears NE also controls satiation ( Asarian and Bachler, 2014 ). In addition, it has been reported that the microbiota influenced NE level in the gut lumen of mice ( Asano et al, 2012 ), but whether the bacteria produce NE to alter behavior through an indirect path was not determined.…”

Section: Neurotransmitter Modulation and Behavioral Outcomes Identifimentioning

confidence: 99%

Brain Neurotransmitter Modulation by Gut Microbiota in Anxiety and Depression

Huang

2021

Front. Cell Dev. Biol.

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Anxiety and depression are highly prevalent mental illnesses worldwide and have long been thought to be closely associated to neurotransmitter modulation. There is growing evidence indicating that changes in the composition of the gut microbiota are related to mental health including anxiety and depression. In this review, we focus on combining the intestinal microbiota with serotonergic, dopaminergic, and noradrenergic neurotransmission in brain, with special emphasis on the anxiety- and depression-like behaviors in stress-related rodent models. Therefore, we reviewed studies conducted on germ-free rodents, or in animals subjected to microbiota absence using antibiotics, as well as via the usage of probiotics. All the results strongly support that the brain neurotransmitter modulation by gut microbiota is indispensable to the physiopathology of anxiety and depression. However, a lot of work is needed to determine how gut microbiota mediated neurotransmission in human brain has any physiological significance and, if any, how it can be used in therapy. Overall, the gut microbiota provides a novel way to alter neurotransmitter modulation in the brain and treat gut–brain axis diseases, such as anxiety and depression.

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Section: Neurotransmitter Modulation and Behavioral Outcomes Identifimentioning

confidence: 99%

Brain Neurotransmitter Modulation by Gut Microbiota in Anxiety and Depression

Huang

2021

Front. Cell Dev. Biol.

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“…Future studies with larger samples will be required to further explore the relationship between central nervous 5-HT and NPY in humans. Literature also suggests that the AA Leucine might also be involved in the regulation of appetite [ 44 ]; however, its relationship with NPY remains poorly understood. Given that Leucine was a compound of the ATD challenge, further investigation of how Leucine may impact on NPY levels may also benefit the current investigation of how central nervous 5-HT may be related to levels of NPY through the use of the ATD/BAL method.…”

Section: Discussionmentioning

confidence: 99%

Effects of Dietary Acute Tryptophan Depletion (ATD) on NPY Serum Levels in Healthy Adult Humans Whilst Controlling for Methionine Supply—A Pilot Study

et al. 2018

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Central nervous serotonin (5-HT) can influence behaviour and neuropsychiatric disorders. Evidence from animal models suggest that lowered levels of neuropeptide Y (NPY) may have similar effects, although it is currently unknown whether decreased central nervous 5-HT impact NPY concentrations. Given that the production of NPY is dependent on the essential amino acid methionine (MET), it is imperative to account for the presence of MET in such investigations. Hence, this study sought to examine the effects of acute tryptophan depletion (ATD; a dietary procedure that temporarily lowers central nervous 5-HT synthesis) on serum concentrations of NPY, whilst using the potential renal acid load indicator (PRAL) to control for levels of MET. In a double-blind repeated measures design, 24 adult humans randomly received an AA-load lacking in TRP (ATD) on one occasion, and a balanced control mixture with TRP (BAL) on a second occasion, both with a PRAL of nearly 47.3 mEq of MET. Blood samples were obtained at 90, 180, and 240 min after each of the AA challenges. ATD, and therefore, diminished substrate availability for brain 5-HT synthesis did not lead to significant changes in serum NPY concentrations over time, compared to BAL, under an acute acidotic stimulus.

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“…One particularly important area of research is in satiety hormones, which are secreted by the GI tract in response to nutrients to help terminate meals. Since impairments in satiety have been associated with overeating in [67]. CCK is released by L cells of the intestine in response to lipids and proteins, and CCK has numerous postprandial functions, including decreasing appetite, slowing gastric emptying, and increasing gall bladder stimulation [68].…”

Section: Binge Eating In Bn and Bed Neuroendocrinementioning

confidence: 99%

Emerging Treatments in Eating Disorders

Lutter

2017

Neurotherapeutics

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Eating disorders (EDs), including anorexia nervosa, bulimia nervosa, and binge-eating disorder, constitute a class of common and deadly psychiatric disorders. While numerous studies in humans highlight the important role of neurobiological alterations in the development of ED-related behaviors, the precise neural substrate that mediates this risk is unknown. Historically, pharmacological interventions have played a limited role in the treatment of eating disorders, typically providing symptomatic relief of comorbid psychiatric issues, like depression and anxiety, in support of the standard nutritional and psychological treatments. To date there are no Food and Drug Administration-approved medications or procedures for anorexia nervosa, and only one Food and Drug Administration-approved medication each for bulimia nervosa (fluoxetine) and binge-eating disorder (lisdexamfetamine). While there is little primary interest in drug development for eating disorders, postmarket monitoring of medications and procedures approved for other indications has identified several novel treatment options for patients with eating disorders. In this review, I utilize searches of the PubMed and ClinicalTrials.gov databases to highlight emerging treatments in eating disorders.

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Neuroendocrine control of satiation

Cited by 13 publications

References 319 publications

Brain Neurotransmitter Modulation by Gut Microbiota in Anxiety and Depression

Brain Neurotransmitter Modulation by Gut Microbiota in Anxiety and Depression

Effects of Dietary Acute Tryptophan Depletion (ATD) on NPY Serum Levels in Healthy Adult Humans Whilst Controlling for Methionine Supply—A Pilot Study

Emerging Treatments in Eating Disorders

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