Glucose acts in the CNS to regulate gastric motility during hypoglycemia

2003 ◽  
Vol 285 (5) ◽  
pp. R1192-R1202 ◽  
Author(s):  
Min Shi ◽  
Allison R. Jones ◽  
Mark S. Niedringhaus ◽  
Rebecca J. Pearson ◽  
Ann M. Biehl ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Glucose ◽  
Motor Function ◽  
Gastric Motility ◽  
Motor Nucleus ◽  
Gastric Tone ◽  
Antral Motility ◽  
Gastric Motor Function ◽  
Gastric Contractions

Our purposes were to 1) develop an animal model where intravenously (iv) administered d-glucose consistently inhibited antral motility, and 2) use this model to assess whether iv glucose acts to inhibit motility from a peripheral or a central nervous system site and to elucidate the factor(s) that determine(s) whether stomach motor function is sensitive to changes in blood glucose. Rats were anesthetized with α-chloralose-urethane, and antral motility was measured by a strain-gauge force transducer sutured to the antrum. In some cases, antral motility and gastric tone were measured by monitoring intragastric balloon pressure. Increases in blood glucose were produced by continuous iv infusion of 25% d-glucose at 2 ml/h. Inhibition of antral motility and gastric tone was observed when gastric contractions were induced by hypoglycemia (subcutaneously administered insulin, 2.5 IU/animal). In contrast, no inhibition of gastric motor function was observed when glucose infusion was tested on gastric contractions that were 1) spontaneously occurring, 2) evoked by iv administered bethanechol in vagotomized animals, and 3) evoked by the TRH analog RX77368, microinjected into the dorsal motor nucleus of the vagus. Using the model of insulin-induced hypoglycemia to increase gastric motor activity, we found that neither sectioning the hepatic branch of the vagus ( n = 5), nor treating animals with capsaicin to destroy sensory vagal afferent nerves ( n = 5) affected the ability of iv d-glucose to inhibit gastric motor function. Our results indicate that an important factor determining whether stomach motor function will be sensitive to changes in blood glucose is the method used to stimulate gastric contractions, and that the primary site of the inhibitory action of iv glucose on gastric motility is the central nervous system rather than the periphery.

scholarly journals Leap Motion Controller Video Game-Based Therapy for Upper Extremity Motor Recovery in Patients with Central Nervous System Diseases. A Systematic Review with Meta-Analysis

Sensors ◽  
2021 ◽  
Vol 21 (6) ◽  
pp. 2065
Author(s):  
Irene Cortés-Pérez ◽  
Noelia Zagalaz-Anula ◽  
Desirée Montoro-Cárdenas ◽  
Rafael Lomas-Vega ◽  
Esteban Obrero-Gaitán ◽  
...  
Keyword(s):  
Systematic Review ◽  
Central Nervous System ◽  
Nervous System ◽  
Motor Function ◽  
Video Game ◽  
Meta Analysis ◽  
Leap Motion ◽  
Motion Controller ◽  
Motor Dexterity ◽  
Quality Evidence

Leap Motion Controller (LMC) is a virtual reality device that can be used in the rehabilitation of central nervous system disease (CNSD) motor impairments. This review aimed to evaluate the effect of video game-based therapy with LMC on the recovery of upper extremity (UE) motor function in patients with CNSD. A systematic review with meta-analysis was performed in PubMed Medline, Web of Science, Scopus, CINAHL, and PEDro. We included five randomized controlled trials (RCTs) of patients with CNSD in which LMC was used as experimental therapy compared to conventional therapy (CT) to restore UE motor function. Pooled effects were estimated with Cohen’s standardized mean difference (SMD) and its 95% confidence interval (95% CI). At first, in patients with stroke, LMC showed low-quality evidence of a large effect on UE mobility (SMD = 0.96; 95% CI = 0.47, 1.45). In combination with CT, LMC showed very low-quality evidence of a large effect on UE mobility (SMD = 1.34; 95% CI = 0.49, 2.19) and the UE mobility-oriented task (SMD = 1.26; 95% CI = 0.42, 2.10). Second, in patients with non-acute CNSD (cerebral palsy, multiple sclerosis, and Parkinson’s disease), LMC showed low-quality evidence of a medium effect on grip strength (GS) (SMD = 0.47; 95% CI = 0.03, 0.90) and on gross motor dexterity (GMD) (SMD = 0.73; 95% CI = 0.28, 1.17) in the most affected UE. In combination with CT, LMC showed very low-quality evidence of a high effect in the most affected UE on GMD (SMD = 0.80; 95% CI = 0.06, 1.15) and fine motor dexterity (FMD) (SMD = 0.82; 95% CI = 0.07, 1.57). In stroke, LMC improved UE mobility and UE mobility-oriented tasks, and in non-acute CNSD, LMC improved the GS and GMD of the most affected UE and FMD when it was used with CT.

scholarly journals Disrupted Leptin Signaling in the Lateral Hypothalamus and Ventral Premammillary Nucleus Alters Insulin and Glucagon Secretion and Protects Against Diet-Induced Obesity

Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2671-2685 ◽  
Author(s):  
Heather C. Denroche ◽  
Maria M. Glavas ◽  
Eva Tudurí ◽  
Subashini Karunakaran ◽  
Whitney L. Quong ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Weight Gain ◽  
Blood Glucose ◽  
Glucagon Secretion ◽  
Hypothalamic Nucleus ◽  
Leptin Signaling ◽  
Glucose Levels ◽  
The Central Nervous System

Leptin signaling in the central nervous system, and particularly the arcuate hypothalamic nucleus, is important for regulating energy and glucose homeostasis. However, the roles of extra-arcuate leptin responsive neurons are less defined. In the current study, we generated mice with widespread inactivation of the long leptin receptor isoform in the central nervous system via Synapsin promoter-driven Cre (Leprflox/flox Syn-cre mice). Within the hypothalamus, leptin signaling was disrupted in the lateral hypothalamic area (LHA) and ventral premammillary nucleus (PMV) but remained intact in the arcuate hypothalamic nucleus and ventromedial hypothalamic nucleus, dorsomedial hypothalamic nucleus, and nucleus of the tractus solitarius. To investigate the role of LHA/PMV neuronal leptin signaling, we examined glucose and energy homeostasis in Leprflox/flox Syn-cre mice and Leprflox/flox littermates under basal and diet-induced obese conditions and tested the role of LHA/PMV neurons in leptin-mediated glucose lowering in streptozotocin-induced diabetes. Leprflox/flox Syn-cre mice did not have altered body weight or blood glucose levels but were hyperinsulinemic and had enhanced glucagon secretion in response to experimental hypoglycemia. Surprisingly, when placed on a high-fat diet, Leprflox/flox Syn-cre mice were protected from weight gain, glucose intolerance, and diet-induced hyperinsulinemia. Peripheral leptin administration lowered blood glucose in streptozotocin-induced diabetic Leprflox/flox Syn-cre mice as effectively as in Leprflox/flox littermate controls. Collectively these findings suggest that leptin signaling in LHA/PMV neurons is not critical for regulating glucose levels but has an indispensable role in the regulation of insulin and glucagon levels and, may promote the development of diet-induced hyperinsulinemia and weight gain.

scholarly journals Transglutaminase 6: a protein associated with central nervous system development and motor function

Amino Acids ◽  
2011 ◽  
Vol 44 (1) ◽  
pp. 161-177 ◽  
Author(s):  
Helen Thomas ◽  
Konrad Beck ◽  
Magdalena Adamczyk ◽  
Pascale Aeschlimann ◽  
Martin Langley ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Motor Function ◽  
System Development ◽  
Nervous System Development ◽  
Central Nervous System Development

scholarly journals A Systematic Literature Review of the Burden of Central Nervous System Complications for Patients with Sickle Cell Disease

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 10-10
Author(s):  
Soyon Lee ◽  
Dave Nellesen ◽  
Sedge Lucas ◽  
Jincy Paulose ◽  
Vivien A. Sheehan
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Function ◽  
Sickle Cell Disease ◽  
Motor Function ◽  
Future Research ◽  
Cell Disease ◽  
Wechsler Scales ◽  
Pro Instruments ◽  
Humanistic Burden

INTRODUCTION: Sickle cell disease (SCD), a complex genetic blood disorder involving multicellular interactions between blood and endothelial cells, is often accompanied by central nervous system (CNS) complications. Effects range from silent cerebral infarct (SCI) to abnormal blood flow, and consequent overt stroke. This study assessed the humanistic and economic burden associated with CNS complications in patients with SCD and identified patient-reported outcome (PRO) instruments for future research. METHODS: MEDLINE, Embase, Cochrane CENTRAL/CDSR and 11 congresses were searched to identify English language studies published from January 2000 to May 2020 and screened with predefined criteria by two independent researchers. Clinical trials (CT) or observational studies assessing humanistic burden, economic burden, or instruments used to measure burden in patients with SCD and CNS complications (N≥15) were included. Humanistic burden was broadly defined to include quality of life (QoL), symptoms and function. RESULTS: Of the 3194 articles identified, 34 were included. Study designs were 29% retrospective observational (10/34), 29% cross-sectional (10), 26% prospective (9), 9% randomized CT (3), and 6% systematic reviews (2). Study size varied widely (16-4,485 patients with SCD and CNS complications). 77% (26) focused on pediatric patients. Separately, 77% (26) were in a US setting. Overt stroke (12), stroke and SCI (11), or SCI only (7) were the most frequently described CNS complications. Twenty-five studies reported on humanistic burden, 18 of which measured cognitive function using the Wechsler Intelligence Scales. A significant decrease was reported in full scale (FS) (stroke vs. no stroke: 73.5 vs. 84.7; P=.04), verbal (abnormal vs. normal MRI: 74.1 vs. 84.6; P=.02), and performance IQ (stroke vs. no stroke: 69.5 vs. 81.5; P=.02) for patients with overt strokes or SCI compared to non-stroke SCD controls. Greater impairment was reported for overt stroke compared with SCI (multivariate meta-analysis of mean IQ difference: -10.3; P=.0013). In addition to stroke/SCI, socio-environmental factors (i.e., family income level, lack of college education) were significantly associated with a decrease in IQ (P=.005 and P=.023, respectively). Five studies assessed motor function, reporting significantly impaired function for patients with stroke compared to non-stroke SCD controls (Purdue Pegboard both hands: 7.5 vs. 10.1; P=.0001). Among children with SCD who had experienced their first stroke, those receiving hydroxyurea (HU) for prevention of recurrent stroke had significantly less moderate to severe motor disability (physician assessed) than children not receiving HU (23.1 vs. 88.9%; P<.001). Nine studies reported economic outcomes related to healthcare resource use (HCRU) (8) and direct costs (5). HCRU and cost to manage CNS complications are high, with a median LOS of 5 days (IQR 3-9) and median hospitalization charges of $18,956 (2012 USD) for patients with SCD and stroke. Treatment costs were also substantial in patients with SCI, with annual transfusion plus chelation costs ranging between $18,149 and $67,361/year (2016 USD). No studies reported indirect costs. While many studies used clinician-administered performance outcome (PerfO) measures such as the Wechsler Scales, only 1 study employed a PRO instrument: the Children's Depression Index. In addition to the Wechsler Scales, PerfO measures of cognitive function included the Woodcock-Johnson Psychoeducational Battery (6 studies), Children's Memory Scale (4), and California Verbal Learning Test for Children (4). CONCLUSIONS: This systematic review found that SCD patients with CNS complications often experience diminished cognitive/motor function and incur substantial costs. In particular, the mean FSIQ for SCD patients with stroke and SCI was reported to be 'extremely low' to 'low' (65.9 to 83.6) and 'low' to 'average' (77.2 to 95.9), respectively across studies. The Wechsler Scales were the most commonly used PerfO measure of cognitive function, while use of disease-specific PRO instruments was extremely limited. Given that the majority of published data focuses on children, future research is needed to evaluate the burden of disease for SCD adults with CNS complications, and to assess patient perspectives and QoL to better quantify aspects of burden beyond cognitive performance. Disclosures Lee: Novartis Pharmaceuticals Corporation: Current Employment. Nellesen:Analysis Group, Inc.: Consultancy. Lucas:Analysis Group, Inc.: Consultancy. Paulose:Novartis Pharma AG: Current Employment.

scholarly journals Electroacupuncture at ST36 Improve the Gastric Motility by Affecting Neurotransmitters in the Enteric Nervous System in Type 2 Diabetic Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xu Han ◽  
Xiaoyan Chen ◽  
Xuan Wang ◽  
Meirong Gong ◽  
Mengjiang Lu ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Blood Glucose ◽  
Gastric Emptying ◽  
Food Intake ◽  
Enteric Nervous System ◽  
The Body ◽  
Antral Motility ◽  
Excitatory Neurotransmitters

Electroacupuncture (EA) can effectively relieve hyperglycemia and gastric emptying disorders in diabetic gastroparesis (DGP). However, the effect of EA on type 2 diabetes mellitus (T2DM) gastroparesis and its mechanism in the enteric nervous system (ENS) are rarely studied. We investigated the therapeutic effect of EA at ST36 and its effect on the main inhibitory and excitatory neurotransmitters in the ENS in DGP rats. Male Sprague-Dawley (SD) rats were fed a high-fat diet for 2 weeks and injected with streptozotocin (STZ) at 35 mg/kg to induce T2DM. T2DM rats were divided into the diabetic mellitus (DM) group and the EA group. The control (CON) group comprised normal rats without any intervention. EA treatment was started 6 weeks after the induction of DM and continued for 5 weeks. The body weight and food intake of the rats were recorded every week. Blood glucose, insulin, glucose tolerance, gastric emptying, and antral motility were measured after treatment. The expression of protein gene product 9.5 (PGP9.5), neuronal nitric oxide synthase (nNOS), and choline acetyltransferase (ChAT) in gastric antrum were quantified by western blotting and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The T2DM gastroparesis model was successfully established. EA treatment reduced the body weight, food intake, and blood glucose; improved glucose intolerance and insulin resistance; increased the gastric emptying rate, the mean antral pressure, and the amplitude of antral motility; and decreased the frequency of antral motility compared with those in the DM group. EA treatment increased the expression level of nNOS, ChAT, and PGP9.5 proteins, and nNOS and ChAT mRNA. The results suggested that EA at ST36 could ameliorate DGP, partly restore the damage to general neurons, and increase nNOS and ChAT in the gastric antrum. EA improved DGP partly via reducing the loss of inhibitory and excitatory neurotransmitters in the ENS.

Rehabilitation promotes functional movement in atypical populations

1996 ◽  
Vol 19 (1) ◽  
pp. 82-83
Author(s):  
Meg Morris ◽  
Thomas Matyas ◽  
Robert Iansek ◽  
Ross Cunnington
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Motor Function ◽  
Skill Learning ◽  
Motor Skill Learning ◽  
Term Outcome ◽  
Functional Movement ◽  
Long Term Outcome ◽  
Cns Dysfunction

AbstractThe suggestion that movement disorders exhibited by people with central nervous system (CNS) dysfunction should be considered normal and therefore not rehabilitated is rejected from three standpoints: (1) the CNS does not always select the best movement patterns for optimal long term outcome, (2) there is literature demonstrating that rehabilitation enhances motor function and independence, and (3) there exists a capacity for motor recovery and motor skill learning following brain damage.

scholarly journals Brain-derived Neurotrophic Factor Regulates Energy Expenditure Through the Central Nervous System in Obese Diabetic Mice

2001 ◽  
Vol 2 (3) ◽  
pp. 201-209 ◽  
Author(s):  
Takeshi Nonomura ◽  
Atsushi Tsuchida ◽  
Michiko Ono-Kishino ◽  
Tsutomu Nakagawa ◽  
Mutsuo Taiji ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Glucose ◽  
Energy Expenditure ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Central Administration ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
The Central Nervous System

It has been previously demonstrated that brain-derived neurotrophic factor (BDNF) regulates glucose metabolism and energy expenditure in rodent diabetic models such as C57BL/KsJ-leprdb/leprdb(db/db) mice. Central administration of BDNF has been found to reduce blood glucose indb/dbmice, suggesting that BDNF acts through the central nervous system. In the present study we have expanded these investigations to explore the effect of central administration of BDNF on energy metabolism. Intracerebroventricular administration of BDNF lowered blood glucose and increased pancreatic insulin content ofdb/dbmice compared with vehicle-treated pellet pair-feddb/dbmice. While body temperatures of the pellet pair-feddb/dbmice given vehicle were reduced because of restricted food supply in this pair-feeding condition, BDNF treatment remarkably alleviated the reduction of body temperature suggesting the enhancement of thermogenesis. BDNF enhanced norepinephrine turnover and increased uncoupling protein-1 mRNA expression in the interscapular brown adipose tissue. Our evidence indicates that BDNF activates the sympathetic nervous systemviathe central nervous system and regulates energy expenditure in obese diabetic animals.

Insulin secretion: mechanism of the stimulation by glucose

1975 ◽  
Vol 8 (1) ◽  
pp. 1-41 ◽  
Author(s):  
Erol Cerasi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Food Intake ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Glucose Concentration ◽  
The Central Nervous System ◽  
The Stability

Glucose is one of the substrates that is controlled with the most efficient hormonal mechanisms in higher organisms. The presence of tissues such as the central nervous system which, under normal conditions, depend solely on glucose as substrate, and the sporadic type of food intake with periods of fasting of various lengths in the mammalians necessitate that the distribution of energy-rich substrates among various tissues be continuously adjusted by changes in the secretion of a number of hormones. The efficiency of this system is evidenced by the stability of the blood glucose level in man, in whom after a carbohydrate-rich meal more than 70% of the glucose that has been ingested will be retained in the liver during a single passage of portal blood, resulting in only small changes of the glucose concentration in peripheral blood. Likewise, periods of fasting up to24–36 h are followed by modest to minimal reductions of the blood glucose level, the liver now supplying the circulation with the hexose.

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