scholarly journals Metabolic Sensing and the Brain: Who, What, Where, and How?

Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2552-2557 ◽  
Author(s):  
Barry E. Levin ◽  
Christophe Magnan ◽  
Ambrose Dunn-Meynell ◽  
Christelle Le Foll
Keyword(s):  
Energy Homeostasis ◽  
Distributed Network ◽  
Metabolic Substrates ◽  
Hepatic Portal Vein ◽  
Metabolic Sensing ◽  
Hepatic Portal ◽  
And Function ◽  
The Brain ◽  
Local Brain ◽  
Brain Barriers

Unique subpopulations of specialized metabolic sensing neurons reside in a distributed network throughout the brain and respond to alterations in ambient levels of various metabolic substrates by altering their activity. Variations in local brain substrate levels reflect their transport across the blood- and cerebrospinal-brain barriers as well as local production by astrocytes. There are a number of mechanisms by which such metabolic sensing neurons alter their activity in response to changes in substrate levels, but it is clear that these neurons cannot be considered in isolation. They are heavily dependent on astrocyte and probably tanycyte metabolism and function but also respond to hormones (e.g. leptin and insulin) and cytokines that cross the blood-brain barrier from the periphery as well as hard-wired neural inputs from metabolic sensors in peripheral sites such as the hepatic portal vein, gastrointestinal tract, and carotid body. Thus, these specialized neurons are capable of monitoring and integrating multiple signals from the periphery as a means of regulating peripheral energy homeostasis.

Hepatic modulation of insulin-induced gastric acid secretion and EMG activity in rats

1980 ◽  
Vol 238 (5) ◽  
pp. R346-R352 ◽  
Author(s):  
J. Granneman ◽  
M. I. Friedman
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Emg Activity ◽  
Glucose Levels ◽  
Hepatic Portal Vein ◽  
Inhibited Acid ◽  
Hepatic Portal ◽  
The Brain

Intravenous infusions of fructose, a hexose that does not cross the blood-brain barrier, suppressed insulin-induced gastric acid secretion and electromyographic (EMG) activity despite continuing hypoglycemia. Hepatic portal vein infusions of 0.15 M fructose inhibited acid output while the same concentration delivered via the jugular vein did not, suggesting a hepatic site of action of the hexose. Only infusions of fructose that began before onset of the insulin-induced gastric responses were effective, whereas glucose infusions, which elevated plasma glucose levels, readily reversed ongoing gastric activity. The suppressive effects of fructose on gastric activity were prevented by prior section of the hepatic branch of the vagus nerve. In contrast, hepatic vagotomy did not prevent suppression of gastric responses by infusions of glucose, a hexose utilized by both brain and liver. These results suggest that receptors in the brain may initiate and terminate insulin-induced gastric acid secretion and motor activity, whereas sensors in the liver may inhibit these responses.

Hepatic contribution to satiation of salt appetite in rats

1986 ◽  
Vol 251 (6) ◽  
pp. R1095-R1102 ◽  
Author(s):  
M. G. Tordoff ◽  
J. Schulkin ◽  
M. I. Friedman
Keyword(s):  
Portal Vein ◽  
Sodium Concentration ◽  
Reciprocal Relationship ◽  
Dietary Sodium ◽  
Salt Appetite ◽  
Nacl Solution ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Portal Vein Infusion ◽  
The Brain

We examined the influence of hepatic-portal vein infusion of NaCl and of hepatic vagotomy on 3% NaCl solution drinking by sodium-deficient rats. Combined dietary sodium restriction and administration of the natriuretic agent, furosemide (5 mg), produced a vigorous appetite for 3% NaCl solution that was attenuated by portal infusion of NaCl. Whereas infusions (1 ml/30 min) of NaCl into the hepatic-portal vein in concentrations as low as 0.15 M (isotonic) significantly reduced 3% NaCl consumption, a higher concentration (0.6 M) infused into the jugular vein, or portal infusions of KCl (0.6 M) or sucrose (1.2 M), were ineffective. Rats with selective hepatic vagotomy displayed an attenuated appetite for salt whether or not they received hepatic-portal NaCl. This was not due to altered excretion of sodium. Taken together, these results suggest that the liver or portal vein can provide a sodium-specific neural signal capable of attenuating the appetite for salt and this information is transferred to the brain by fibers in the hepatic vagus that fire in reciprocal relationship with portal sodium concentration.

scholarly journals Possible Mechanisms of Circulating PYY-Induced Satiation in Male Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 193-204 ◽  
Author(s):  
Ulrike Stadlbauer ◽  
Myrtha Arnold ◽  
Elisabeth Weber ◽  
Wolfgang Langhans
Keyword(s):  
Plasma Levels ◽  
Jugular Vein ◽  
Area Postrema ◽  
Central Area ◽  
Male Rats ◽  
Acute Effects ◽  
Paraventricular Nuclei ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
The Brain

Peptide tyrosine-tyrosine (PYY) is implicated in eating control, but the site(s) and mechanism(s) of its action remain uncertain. We tested acute effects of intrameal hepatic portal vein (HPV) PYY3-36 infusions on eating in adult, male rats and measured HPV and jugular vein (JV) plasma levels of PYY in response to a solid, mixed-nutrient meal. We also examined the effects of HPV PYY3-36 infusions on JV plasma levels, flavor acceptance, and neuronal activation. Intrameal HPV PYY3-36 infusions [1 and 3 nmol/kg body weight (BW)] selectively reduced (P < 0.05) ongoing meal size. HPV PYY levels increased (P < 0.05) during a chow (12.5 kcal) or an isocaloric high-fat meal. JV PYY levels were generally lower than HPV levels but also increased in response to the chow meal. HPV PYY3-36 infusion (1 nmol/kg BW) caused a greater increase in JV PYY than a meal, but neither 1 nor 3 nmol/kg BW PYY3-36 caused conditioned flavor avoidance. HPV PYY3-36 (1 nmol/kg BW) increased the number of c-Fos-expressing cells in the nucleus tractus solitarii, the hypothalamic arcuate and paraventricular nuclei, the central area of the amygdala, and the nucleus accumbens but not in the area postrema and parabrachial nucleus. These data show that HPV infusions of PYY3-36 inhibit eating in rats without causing avoidance, and they identify some brain areas that might be involved. Endogenous PYY may induce satiation by acting directly in the brain, but further studies should examine whether PYY3–36 administrations that mimic the meal-induced increase in plasma PYY are sufficient to inhibit eating.

scholarly journals Steroidogenic Factor 1 Regulates Expression of the Cannabinoid Receptor 1 in the Ventromedial Hypothalamic Nucleus

2008 ◽  
Vol 22 (8) ◽  
pp. 1950-1961 ◽  
Author(s):  
Ki Woo Kim ◽  
Young-Hwan Jo ◽  
Liping Zhao ◽  
Nancy R. Stallings ◽  
Streamson C. Chua ◽  
...  
Keyword(s):  
Energy Homeostasis ◽  
Cannabinoid Receptor ◽  
Hypothalamic Nucleus ◽  
Cannabinoid Receptor 1 ◽  
Steroidogenic Factor 1 ◽  
Ventromedial Hypothalamic Nucleus ◽  
Hypothalamic Slice ◽  
Responsive Element ◽  
And Function ◽  
The Brain

Abstract The nuclear receptor steroidogenic factor 1 (SF-1) plays essential roles in the development and function of the ventromedial hypothalamic nucleus (VMH). Considerable evidence links the VMH and SF-1 with the regulation of energy homeostasis. Here, we demonstrate that SF-1 colocalizes in VMH neurons with the cannabinoid receptor 1 (CB1R) and that a specific CB1R agonist modulates electrical activity of SF-1 neurons in hypothalamic slice preparations. We further show that SF-1 directly regulates CB1R gene expression via a SF-1-responsive element at −101 in its 5′-flanking region. Finally, we show that knockout mice with selective inactivation of SF-1 in the brain have decreased expression of CB1R in the region of the VMH and exhibit a blunted response to systemically administered CB1R agonists. These studies suggest that SF-1 directly regulates the expression of CB1R, which has been implicated in the regulation of energy homeostasis and anxiety-like behavior.

scholarly journals Measurement of pulsatile insulin secretion in the rat: direct sampling from the hepatic portal vein

2008 ◽  
Vol 295 (3) ◽  
pp. E569-E574 ◽  
Author(s):  
Aleksey V. Matveyenko ◽  
Johannes D. Veldhuis ◽  
Peter C. Butler
Keyword(s):  
Insulin Secretion ◽  
Portal Vein ◽  
Genetically Modified ◽  
Deconvolution Analysis ◽  
Direct Sampling ◽  
Hepatic Portal Vein ◽  
Underlying Mechanisms ◽  
Hepatic Portal ◽  
And Function ◽  
Pulsatile Insulin Secretion

It has previously been shown that insulin is secreted in discrete secretory bursts by sampling directly from the portal vein in the dog and humans. Deficient pulsatile insulin secretion is the basis for impaired insulin secretion in type 2 diabetes. However, while novel genetically modified disease models of diabetes are being developed in rodents, no validated method for quantifying pulsatile insulin secretion has been established for rodents. To address this we 1) developed a novel rat model with chronically implanted portal vein catheters, 2) established the parameters to permit deconvolution of portal vein insulin concentrations profiles to measure insulin secretion and resolve its pulsatile components, and 3) measured total and pulsatile insulin secretion compared with that in the dog, the species in which this sampling and deconvolution approach was validated for quantifying pulsatile insulin secretion. In rats, portal vein catheter patency and function were maintained for periods up to 2–3 wk with no postoperative complications such as catheter tract infection. Rat portal vein insulin concentration profiles in the fasting state revealed distinct insulin oscillations with a periodicity of ∼5 min and an amplitude of up to 600 pmol/l, which was remarkably similar to that in the dogs and in humans. Deconvolution analysis of portal vein insulin concentrations revealed that the majority of insulin (∼70%) in the rat is secreted in distinct insulin pulses occurring at ∼5-min intervals. This model therefore permits direct accurate measurments of pulsatile insulin secretion in a relatively inexpensive animal. With increased introduction of genetically modified rat models will be an important tool in elucidating the underlying mechanisms of impaired pulsatile insulin secretion in diabetes.

Food reward and gut-brain signalling

Neuroforum ◽  
2020 ◽  
Vol 26 (1) ◽  
pp. 1-9
Author(s):  
Sharmili Edwin Thanarajah ◽  
Marc Tittgemeyer
Keyword(s):  
Food Reward ◽  
Food Selection ◽  
Eating Behaviour ◽  
Processed Food ◽  
Hepatic Portal Vein ◽  
Reward Pathways ◽  
Hepatic Portal ◽  
The Brain ◽  
Possible Cause ◽  
Specific Food

AbstractThe increasing availability of ultra-processed, energy dense food is contributing to the spread of the obesity pandemic, which is a serious health threat in today’s world. One possible cause for this association arises from the fact that the brain is wired to derive pleasure from eating. Specifically, food intake activates reward pathways involving dopamine receptor signalling. The reinforcing value of specific food items results from the interplay between taste and nutritional properties. Increasing evidence suggests that nutritional value is sensed in the gut by chemoreceptors in the intestinal tract and the hepatic portal vein, and conveyed to the brain through neuronal and endocrine pathways to guide food selection behaviour. Ultra-processed food is designed to potentiate the reward response through a combination of high fat and high sugar, therebye seeming highly appetizing. There is increasing evidence that overconsumption of processed food distorts normal reward signalling, leading to compulsive eating behaviour and obesity. Hence, it is essential to understand food reward and gut-brain signalling to find an effective strategy to combat the obesity pandemic.

Ultrastructure of developing visual cortical synapses in the cat superior colliculus

1991 ◽  
Vol 49 ◽  
pp. 156-157
Author(s):  
Caroline A. Miller ◽  
Laura L. Bruce
Keyword(s):  
Superior Colliculus ◽  
Phosphate Buffer ◽  
Receptive Fields ◽  
Visual Cortical Area ◽  
Cortical Synapses ◽  
Visual Cortical ◽  
And Function ◽  
Phosphate Buffered Saline ◽  
The Brain ◽  
Cat Superior Colliculus

The first visual cortical axons arrive in the cat superior colliculus by the time of birth. Adultlike receptive fields develop slowly over several weeks following birth. The developing cortical axons go through a sequence of changes before acquiring their adultlike morphology and function. To determine how these axons interact with neurons in the colliculus, cortico-collicular axons were labeled with biocytin (an anterograde neuronal tracer) and studied with electron microscopy.Deeply anesthetized animals received 200-500 nl injections of biocytin (Sigma; 5% in phosphate buffer) in the lateral suprasylvian visual cortical area. After a 24 hr survival time, the animals were deeply anesthetized and perfused with 0.9% phosphate buffered saline followed by fixation with a solution of 1.25% glutaraldehyde and 1.0% paraformaldehyde in 0.1M phosphate buffer. The brain was sectioned transversely on a vibratome at 50 μm. The tissue was processed immediately to visualize the biocytin.

Revision Targeted Muscle Reinnervation Improves Secondary Pain Insult in an Upper Extremity Amputee: A Case Report

Hand ◽  
2021 ◽  
pp. 155894472199246
Author(s):  
David D. Rivedal ◽  
Meng Guo ◽  
James Sanger ◽  
Aaron Morgan
Keyword(s):  
Neuropathic Pain ◽  
Peripheral Nerves ◽  
Nerve Biopsy ◽  
Sensory Cortex ◽  
Denervated Muscle ◽  
Unique Case ◽  
Targeted Muscle Reinnervation ◽  
Muscle Reinnervation ◽  
And Function ◽  
The Brain

Targeted muscle reinnervation (TMR) has been shown to improve phantom and neuropathic pain in both the acute and chronic amputee population. Through rerouting of major peripheral nerves into a newly denervated muscle, TMR harnesses the plasticity of the brain, helping to revert the sensory cortex back toward the preinsult state, effectively reducing pain. We highlight a unique case of an above-elbow amputee for sarcoma who was initially treated with successful transhumeral TMR. Following inadvertent nerve biopsy of a TMR coaptation site, his pain returned, and he was unable to don his prosthetic. Revision of his TMR to a more proximal level was performed, providing improved pain and function of the amputated arm. This is the first report to highlight the concept of secondary neuroplasticity and successful proximal TMR revision in the setting of multiple insults to the same extremity.

scholarly journals The Ncoa7 locus regulates V-ATPase formation and function, neurodevelopment and behaviour

2020 ◽  
Author(s):  
Enrico Castroflorio ◽  
Joery den Hoed ◽  
Daria Svistunova ◽  
Mattéa J. Finelli ◽  
Alberto Cebrian-Serrano ◽  
...  
Keyword(s):  
Neurodevelopmental Disorders ◽  
Regulatory Protein ◽  
Molecular Function ◽  
Neuronal Connectivity ◽  
Nuclear Receptor Coactivator ◽  
Lysm Domain ◽  
Behavioural Assessment ◽  
And Function ◽  
The Brain

Abstract Members of the Tre2/Bub2/Cdc16 (TBC), lysin motif (LysM), domain catalytic (TLDc) protein family are associated with multiple neurodevelopmental disorders, although their exact roles in disease remain unclear. For example, nuclear receptor coactivator 7 (NCOA7) has been associated with autism, although almost nothing is known regarding the mode-of-action of this TLDc protein in the nervous system. Here we investigated the molecular function of NCOA7 in neurons and generated a novel mouse model to determine the consequences of deleting this locus in vivo. We show that NCOA7 interacts with the cytoplasmic domain of the vacuolar (V)-ATPase in the brain and demonstrate that this protein is required for normal assembly and activity of this critical proton pump. Neurons lacking Ncoa7 exhibit altered development alongside defective lysosomal formation and function; accordingly, Ncoa7 deletion animals exhibited abnormal neuronal patterning defects and a reduced expression of lysosomal markers. Furthermore, behavioural assessment revealed anxiety and social defects in mice lacking Ncoa7. In summary, we demonstrate that NCOA7 is an important V-ATPase regulatory protein in the brain, modulating lysosomal function, neuronal connectivity and behaviour; thus our study reveals a molecular mechanism controlling endolysosomal homeostasis that is essential for neurodevelopment. Graphic abstract

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