Dual 24-hour feeding response to 2DG in rats: Daytime increase and nighttime decrease

Thompson, Carl I.; Fleming, Robert L.; Franken, Kenneth A.; Hornback, David A.; Boha, Steven P.

doi:10.1016/0031-9384(89)90179-0

Cited by 11 publications

(5 citation statements)

References 27 publications

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“…not reduce the duration or amplitude of the LH surge. The amplitude of the LH surge did decrease, however, when Glucose replacement (during insulin treatment at hours 12 and 16) ameliorated the hypoglycemic effects of insulin insulin was administered after the initiation of the estradiol be explained by altering the circadian rhythm underlying the surge mechanism; a reduction of energy interferes with a variety of circadian rhythm in rats (20,21). This hypothesis cannot account for the finding in this study of the sheep.…”

Section: Luteinizing Hormone Surge Systemcontrasting

confidence: 61%

Glucose Availability Modulates the Timing of the Luteinizing Hormone Surge in the Ewe

Medina

Nagatani

Darling

et al. 1998

J Neuroendocrinology

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To determine if glucose availability modulates the timing of the positive feedback action of oestrogen on gonadotropin secretion, we monitored the estradiol-induced luteinizing hormone (LH) surge in sheep (n = 5/group) made transiently hypoglycemic by insulin. Experiment 1 determined an effective insulin treatment, one which would depress tonic LH secretion. Two injections of insulin (5 IU/kg iv) 4 h apart were found to induce extended hypoglycemia (10-13 h) and to decrease the LH pulse frequency for 8 h (5.0 +/-0.32 pulses/4 h before versus 2.5+/-0.34 pulses/4 h after insulin; P<0.05; mean +/- SEM). Using this same paradigm, experiment 2 determined the influence of the transient hypoglycemia on the LH surge mechanism. In control sheep, estradiol (subcutaneous implants at hour 0) evoked an LH surge with a latency period of 12.4+/-0.5 h. When insulin was administered either before (hours -4 and 0) or after the estradiol stimulus (hours 4 and 8, or 12 and 16), the onset of the LH surge was delayed to 29.0+/-2.4 h (average of all three time groups, P <0.05). Infusion of glucose from hours 12-30, along with insulin, prevented hypoglycemia and restored the normal timing of the oestrogen-induced LH surge to that of controls (15.4+/-0.93 h, P>0.05). These findings suggest that not only is the tonic mode of LH secretion sensitive to metabolic fuel availability, but the surge mode of LH secretion is as well.

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Section: Luteinizing Hormone Surge Systemcontrasting

confidence: 61%

Glucose Availability Modulates the Timing of the Luteinizing Hormone Surge in the Ewe

Medina

Nagatani

Darling

et al. 1998

J Neuroendocrinology

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“…This strategy of impairing glucose utilization also found currency in other clinical domains, most notably in using 2-DG to assess physiological counterregulatory responses in humans [ 145 ] and other animals [ 146 , 147 , 148 ]. At the scale of the intact living organism, 2-DG has also been used as a means to experimentally induce food intake [ 74 , 148 , 149 , 150 , 151 , 152 , 153 ], a behavioral response that is influenced by time-of-day [ 151 ], diet [ 152 ], and nutritional status [ 153 ]. Notwithstanding that feeding and glucoregulatory control circuits are likely components of overlapping but nonredundant neural systems, the effects of 2-DG on both counterregulatory processes and food intake have been established well enough to provide justification of its continued utility for exploring these systems at this scale.…”

Section: Discussionmentioning

confidence: 99%

Glycemic Challenge Is Associated with the Rapid Cellular Activation of the Locus Ceruleus and Nucleus of Solitary Tract: Circumscribed Spatial Analysis of Phosphorylated MAP Kinase Immunoreactivity

Tapia

Agostinelli

Chenausky

et al. 2023

JCM

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Rodent studies indicate that impaired glucose utilization or hypoglycemia is associated with the cellular activation of neurons in the medulla (Winslow, 1733) (MY), believed to control feeding behavior and glucose counterregulation. However, such activation has been tracked primarily within hours of the challenge, rather than sooner, and has been poorly mapped within standardized brain atlases. Here, we report that, within 15 min of receiving 2-deoxy-D-glucose (2-DG; 250 mg/kg, i.v.), which can trigger glucoprivic feeding behavior, marked elevations were observed in the numbers of rhombic brain (His, 1893) (RB) neuronal cell profiles immunoreactive for the cellular activation marker(s), phosphorylated p44/42 MAP kinases (phospho-ERK1/2), and that some of these profiles were also catecholaminergic. We mapped their distributions within an open-access rat brain atlas and found that 2-DG-treated rats (compared to their saline-treated controls) displayed greater numbers of phospho-ERK1/2+ neurons in the locus ceruleus (Wenzel and Wenzel, 1812) (LC) and the nucleus of solitary tract (>1840) (NTS). Thus, the 2-DG-activation of certain RB neurons is more rapid than perhaps previously realized, engaging neurons that serve multiple functional systems and which are of varying cellular phenotypes. Mapping these populations within standardized brain atlas maps streamlines their targeting and/or comparable mapping in preclinical rodent models of disease.

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“…This strategy of impairing glucose utilization also found currency in other clinical domains, most notably in using 2-DG to assess physiological counterregulatory responses in humans [148] and other animals [149–151]. At the scale of the intact living organism, 2-DG has also been used as a means to experimentally induce food intake [73, 150–156], a behavioral response that is influenced by time of day [154], diet [155], and nutritional status [156]. Notwithstanding that feeding and glucoregulatory control circuits are likely components of overlapping but nonredundant neural systems, the effects of 2-DG on both counterregulatory processes and food intake have been established well enough to provide justification of its continued utility for exploring these systems at this scale.…”

Section: Discussionmentioning

confidence: 99%

Glycemic challenge is associated with the rapid cellular activation of the locus ceruleus and nucleus of solitary tract: Circumscribed spatial analysis of phosphorylated MAP kinase immunoreactivity

Tapia

Agostinelli

Chenausky

et al. 2022

Preprint

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Research using laboratory rats has shown that impaired glucose utilization or hypoglycemia is associated with cellular activation of neurons in the medulla (Winslow, 1733) (MY) that are implicated in the control of feeding behavior and hormonal counterregulatory responses. Changes in the activation of these neuronal populations are also associated with autonomic dysfunction that manifests itself in the form of blunted counterregulatory responses to repeated episodes of glucoprivation or hypoglycemia. An improved appreciation of the spatiotemporal dynamics of these medullary responses (and the phenotypes of the neurons responsible for them) could lead to the development of rational therapies or diagnostics to address patient complications associated with diabetes management, such as hypoglycemia-associated autonomic failure. At present, however, cellular-scale neural activation following glycemic challenge has been tracked in rodents primarily within hours of the challenge, rather than sooner, and these responses have been poorly mapped within standardized brain atlases in relation to the locations of cell types known to be present in the medulla and the larger Rhombic brain (His, 1893) (RB). Here, we report that within 15 min of receiving the glycemic challenge, 2-deoxy-D-glucose (2-DG; 250 mg/kg, i.v.), which is known to produce intracellular glucopenia and trigger glucoprivic feeding behavior, marked elevations were observed in the numbers of RB neuronal cell profiles immunoreactive for the cellular activation marker(s), phosphorylated p44/42 MAP kinases (phospho-ERK1/2). Dual immunostaining experiments showed that some, but not all, of these neurons were catecholaminergic, as identified by immunostaining for dopamine-beta-hydroxylase (DBH). To begin the process of mapping the locations of these rapidly-activated neurons in relation to known cytoarchitecture with standardized neuroanatomical nomenclature, we performed Nissl- and chemoarchitecture-based plane-of-section analysis to map their distributions at discrete rostrocaudal levels, along with associated basally-activated cholinergic and other catecholaminergic cell groups, within an open-access rat brain atlas. This analysis revealed that neurons of the locus ceruleus (Wenzel & Wenzel, 1812) (LC) and the nucleus of solitary tract (>1840) (NTS) displayed elevated numbers of phospho-ERK1/2+ neurons within 15 min following 2-DG administration. Notably, while catecholaminergic neurons co-labeled with phospho-ERK1/2 immunoreactivity, many non-catecholaminergic NTS neurons also displayed such activation. Both 2-DG and saline-treated groups also displayed phospho-ERK1/2+ neurons in the dorsal motor nucleus of vagus nerve (>1840), identified both by Nissl criteria and immunostaining for the cholinergic marker, choline acetyltransferase. Our results show that 2-DG-activation of certain RB catecholaminergic neurons is more rapid than perhaps previously realized, engaging neurons that serve multiple functional systems and are of varying cellular phenotypes. They also place these and other activated populations within standardized maps of cytoarchitectonically-defined RB regions, thereby streamlining their precise targeting and/or comparable mapping in preclinical rodent models of disease.

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Dual 24-hour feeding response to 2DG in rats: Daytime increase and nighttime decrease

Cited by 11 publications

References 27 publications

Glucose Availability Modulates the Timing of the Luteinizing Hormone Surge in the Ewe

Glucose Availability Modulates the Timing of the Luteinizing Hormone Surge in the Ewe

Glycemic Challenge Is Associated with the Rapid Cellular Activation of the Locus Ceruleus and Nucleus of Solitary Tract: Circumscribed Spatial Analysis of Phosphorylated MAP Kinase Immunoreactivity

Glycemic challenge is associated with the rapid cellular activation of the locus ceruleus and nucleus of solitary tract: Circumscribed spatial analysis of phosphorylated MAP kinase immunoreactivity

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