The Experts below are selected from a list of 57 Experts worldwide ranked by ideXlab platform
U. Nayar - One of the best experts on this subject based on the ideXlab platform.
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Ventromedial hypothalamic mediation of sucrose feeding induced pain modulation.
Pharmacology biochemistry and behavior, 2001Co-Authors: K. Mukherjee, Rashmi Mathur, U. NayarAbstract:Abstract Electrophysiological and behavioural studies suggest a modulatory role of ventromedial nucleus of the hypothalamus (VMH) in nociceptive behaviour. Lesion of the VMH produces hyperalgesia and a greater preference for sucrose solution. Hyperalgesia is also produced by sucrose feeding. To explore specifically the contribution of Glucoreceptor neurons of the VMH in the mediation of sucrose-fed hyperalgesia, 2-deoxy- d -glucose (2-DG, antimetabolite of glucose) was slowly albeit continuously infused (1 μl/h for 7 days by microinfusion pumps) into the VMH of adult male rats. Simultaneously, the rats underwent tests for their nociceptive responses in control and sucrose-fed states. The tests for nociception, namely, tail flick latency (TFL), thresholds of tail flick (TF), vocalization during stimulus (SV), vocalization after discharge (VA) were recorded at 0500 h. The tests were repeated after 6, 12, and 48 h in 1 M saline (control group) and 2-DG (experimental group) microinfused rats. Rats were presented with sucrose (20%) solution for 48 h at 0500 h ad libitum in addition to food pellets and tap water. Infusion of 2-DG per se in the VMH led to hypoalgesia (in threshold of TF, SV, VA) while feeding sucrose for 6–12 h per se led to hyperalgesia (in TFL, threshold of SV and VA). Sucrose feeding to 2-DG rats, however, attenuated the hypoalgesia of 2-DG as well as the hyperalgesia of sucrose feeding. The results suggest that the VMH Glucoreceptor neurons probably modulate sucrose mediated phasic pain responses.
K. Mukherjee - One of the best experts on this subject based on the ideXlab platform.
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Ventromedial hypothalamic mediation of sucrose feeding induced pain modulation.
Pharmacology biochemistry and behavior, 2001Co-Authors: K. Mukherjee, Rashmi Mathur, U. NayarAbstract:Abstract Electrophysiological and behavioural studies suggest a modulatory role of ventromedial nucleus of the hypothalamus (VMH) in nociceptive behaviour. Lesion of the VMH produces hyperalgesia and a greater preference for sucrose solution. Hyperalgesia is also produced by sucrose feeding. To explore specifically the contribution of Glucoreceptor neurons of the VMH in the mediation of sucrose-fed hyperalgesia, 2-deoxy- d -glucose (2-DG, antimetabolite of glucose) was slowly albeit continuously infused (1 μl/h for 7 days by microinfusion pumps) into the VMH of adult male rats. Simultaneously, the rats underwent tests for their nociceptive responses in control and sucrose-fed states. The tests for nociception, namely, tail flick latency (TFL), thresholds of tail flick (TF), vocalization during stimulus (SV), vocalization after discharge (VA) were recorded at 0500 h. The tests were repeated after 6, 12, and 48 h in 1 M saline (control group) and 2-DG (experimental group) microinfused rats. Rats were presented with sucrose (20%) solution for 48 h at 0500 h ad libitum in addition to food pellets and tap water. Infusion of 2-DG per se in the VMH led to hypoalgesia (in threshold of TF, SV, VA) while feeding sucrose for 6–12 h per se led to hyperalgesia (in TFL, threshold of SV and VA). Sucrose feeding to 2-DG rats, however, attenuated the hypoalgesia of 2-DG as well as the hyperalgesia of sucrose feeding. The results suggest that the VMH Glucoreceptor neurons probably modulate sucrose mediated phasic pain responses.
Rashmi Mathur - One of the best experts on this subject based on the ideXlab platform.
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Ventromedial hypothalamic mediation of sucrose feeding induced pain modulation.
Pharmacology biochemistry and behavior, 2001Co-Authors: K. Mukherjee, Rashmi Mathur, U. NayarAbstract:Abstract Electrophysiological and behavioural studies suggest a modulatory role of ventromedial nucleus of the hypothalamus (VMH) in nociceptive behaviour. Lesion of the VMH produces hyperalgesia and a greater preference for sucrose solution. Hyperalgesia is also produced by sucrose feeding. To explore specifically the contribution of Glucoreceptor neurons of the VMH in the mediation of sucrose-fed hyperalgesia, 2-deoxy- d -glucose (2-DG, antimetabolite of glucose) was slowly albeit continuously infused (1 μl/h for 7 days by microinfusion pumps) into the VMH of adult male rats. Simultaneously, the rats underwent tests for their nociceptive responses in control and sucrose-fed states. The tests for nociception, namely, tail flick latency (TFL), thresholds of tail flick (TF), vocalization during stimulus (SV), vocalization after discharge (VA) were recorded at 0500 h. The tests were repeated after 6, 12, and 48 h in 1 M saline (control group) and 2-DG (experimental group) microinfused rats. Rats were presented with sucrose (20%) solution for 48 h at 0500 h ad libitum in addition to food pellets and tap water. Infusion of 2-DG per se in the VMH led to hypoalgesia (in threshold of TF, SV, VA) while feeding sucrose for 6–12 h per se led to hyperalgesia (in TFL, threshold of SV and VA). Sucrose feeding to 2-DG rats, however, attenuated the hypoalgesia of 2-DG as well as the hyperalgesia of sucrose feeding. The results suggest that the VMH Glucoreceptor neurons probably modulate sucrose mediated phasic pain responses.
Richard N. Bergman - One of the best experts on this subject based on the ideXlab platform.
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Importance of Hepatic Glucoreceptors in Sympathoadrenal Response to Hypoglycemia
Diabetes, 1991Co-Authors: Casey M. Donovan, Jeffrey B Halter, Richard N. BergmanAbstract:To ascertain whether hepatic Glucoreceptors are important to hypoglycemic counterregulation, a localized euglycemic clamp was employed across the liver during general hypoglycemia. Dogs were infused peripherally with insulin (18–21 pmol · kg−1 · min−1) for 150 min to induce systemic hypoglycemia. During the liver-clamp (LC) protocol, glucose was infused via the portal vein to maintain euglycemia at the liver. In control experiments, i.e., matched infusion (Ml), glucose was infused peripherally at a rate determined to yield similar arterial glycemia levels in the two protocols. Arterial glucose concentrations were not different between protocols during the final hour of insulin infusion (3.26 ± 0.21 and 3.25 ± 0.21 mM during LC and MI, respectively; P = 0.91). Calculated hepatic glucose concentrations during the same period were significantly higher for LC (5.22 ± 0.23 mM) than for MI (3.25 ± 0.21 mM). During MI, both epinephrine and norepinephrine rose significantly from basal values of 562 ± 87 pM and 1.21 ± 0.19 nM to plateaus of 3691 ± 1097 pM ( P = 0.0001) and 2.38 ± 0.35 nM ( P = 0.0002), respectively. However, during LC, the elevation in epinephrine was suppressed by 42 ± 8% ( P = 0.015) relative to MI. Six of seven animals demonstrated a suppression in the norepinephrine response, averaging 32 ± 13% (NS, P = 0.068). The glucagon response to hypoglycemia was unaffected by the level of hepatic glycemia. Hepatic hypoglycemia is essential to produce the full sympathoadrenal response to insulin-induced hypoglycemia.
Willy Malaisse - One of the best experts on this subject based on the ideXlab platform.
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History of the Research on the Glucose Receptor
Glucose-sensing Receptor in Pancreatic Beta-cells, 2018Co-Authors: Willy MalaisseAbstract:The history of the research on the glucose receptor represents the main matter of the present chapter. A short introduction mentions two reviews published in 1972 and introduces the concept of a pancreatic islet B-cell Glucoreceptor. Attention is then drawn to the anomeric specificity of glucose-stimulated insulin secretion and its possible metabolic determinants. The verbal care required for the use of the Glucoreceptor word is duly underlined. Examples of the modulation of key enzyme activity in insulin-producing pancreatic islet cells by D-glucose itself or one of its metabolites are then provided in the framework of the interaction of phosphorylase a with D-glucose anomers, the activation of glucokinase by a fructose-1-phosphate-sensitive regulatory protein, and the activation of phosphofructokinase by fructose-2,6-bisphosphate. The riddle of L-glucose pentaacetate insulinotropic action, the effects of artificial sweeteners on insulin release, and last but not least, the presence of the sweet taste TIR3 receptor in pancreatic insulin-producing islet cells are eventually and duly also considered.
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EFFECT OF FRUCTOSE AND OTHER SUGARS ON ISLET FUNCTION IN VITRO
Acta Medica Scandinavica, 2009Co-Authors: Diana L Hager, André Herchuelz, Daniel Pipeleers, Willy MalaisseAbstract:. Glucose and mannose stimulate insulin release, insulin biosynthesis and calcium uptake in rat isolated islets. Their insulinotropic action is enhanced by caffeine or theophylline. Ribose and xylitol might also exert a minor insulinotropic action. Fructose and galactose do not stimulate insulin release whether in the presence or absence of methylxanthine (10.0 mM), and do not affect insulin biosynthesis or calcium uptake by the islets. These converging findings on several parameters of islet function support the concept that the insulinotropic effect of sugars is dependent on their intracellular metabolism, or possibly on the activation of a highly-selective Glucoreceptor.