Disease relevance of 2-deoxy-D-glucose

• Since cervical cord transection has been shown to eliminate hyperglycemia induced by 2DG, we conclude that the caudal brainstem contains an essential part of the neural mechanism which both detects metabolic need and ameliorates that need through the release of stored fuels [1].
• None of the AS probes altered the magnitude of either 2DG-induced hyperphagia or ANG-II-induced hyperdipsia [2].
• Postweaning body weights did not differ from control values for rats given early insulin or 2DG [3].
• In Experiment 2, we assessed the effects of 2DG (1600 mg/kg/day) given on days 13 and 14 pp, on the duration of lactational infertility [4].
• The results indicate that the innervation of the liver via the vagus nerve or coeliac ganglion is not involved in the delayed eating response to insulin and 2DG injection [5].

Psychiatry related information on 2-deoxy-D-glucose

• Anorexia nervosa (AN) is associated with a paradoxical reduction in hunger ratings following 2-deoxy-D-glucose (2DG) induced glucose insufficiency [6].
• Golden hamsters failed to increase their food intake following food deprivation alone or in combination with insulin or 2-deoxy-D-glucose (2DG) treatment [7].

High impact information on 2-deoxy-D-glucose

• Maintenance of EA rosetting ability of monocytes cultured on surface-bound immune complexes was seen after a 3-h preincubation of the cells in 100 mM 2-deoxy-D-glucose (2dG) [8].
• It was found that the sun6 mutation makes plants unresponsive to these 2DG-induced effects [9].
• Passive immunization of 2DG-treated rats with a specific SRIF antiserum (AS) caused an initial surge of GH release and significant elevation of both trough and mean 6-h plasma GH levels, compared to 2DG-normal sheep serum controls [10].
• Administration of three iv boluses of human GRF (10 micrograms), at 90-min intervals, to 2DG-treated rats resulted in GH release which was variable and time dependent; the magnitude of the first response (1 h after 2DG injection) was significantly less than that of the other two [10].
• The rate-limiting step of 2DG uptake was transport rather than phosphorylation, in the control or valinomycin-treated cells [11].

Chemical compound and disease context of 2-deoxy-D-glucose

• This investigation determined if the weight-loss phenomenon is associated with a paradoxical suppression of food intake following 2DG and if the effect is related to reductions in prevailing glucose and insulin levels [6].
• In contrast, DPDPE failed to alter 2DG-induced hyperphagia, and kappa1 and kappa3 opioid agonists each produced small, but significant increases in 2DG-induced hyperphagia [12].

Biological context of 2-deoxy-D-glucose

• These results demonstrate that OM and S5B rats have a similar food intake response to 2DG but a dissimilar response to MA [13].
• These data suggest that 2DG does not suppress estrous cycles through a decrease in total calorie intake, but rather by inducing glucoprivation [14].
• Lesions of the AP/NTS prevent 2DG-induced anestrus [15].
• The glucose antimetabolite, 2-deoxy-D-glucose (2DG), elicits expression of the proto-oncogene product Fos, which is expressed in hypothalamic structures where DA is synthesized [16].
• In Experiment 3, the combined effects of 2DG (1600, 2000, or 2400 mg/kg/day) and MA (180 mg/kg/day) on the length of lactational diestrus were evaluated [4].

Anatomical context of 2-deoxy-D-glucose

• Furthermore, results indicate that hindbrain neurons involved in MA-induced feeding differ neurochemically from those important for 2DG-induced feeding [17].
• Catecholamine cell groups A1, A1/C1 and C2 (that provide the major NPY innervation of the hypothalamus) showed a basal level of NPY mRNA hybridization signal that was dramatically increased by 2DG [18].
• The area postrema (AP) is a caudal hindbrain structure shown previously to be involved in 2DG-induced glucoprivic feeding [19].
• TH-ir neurons in the zona incerta did not express Fos-ir following 2DG [16].
• Whereas Fos-ir was negligible after saline administration, 2DG induced expression of Fos-ir by TH-ir neurons in the paraventricular (PVN), periventricular (Pe) and arcuate nuclei (ARC), and in the anterior hypothalamic area (AHA) [16].

Associations of 2-deoxy-D-glucose with other chemical compounds

• In C1 and C3, where basal NPY mRNA expression was close to or below our detection threshold, the hybridization signal was also significantly increased by 2DG [18].
• Such treatment also suppresses food intake, which is reversed in male rats by reducing brain histamine levels prior to 2DG treatment [14].
• Both antagonists blocked the inhibitory effect of the beta2-adrenoceptor agonist clenbuterol (0.1 micromol/kg/h) on 2DG-induced acid secretion [20].
• However, the combination of IM with 2DG or His provoked severe lesions in the stomach or the duodenum, respectively, while fMLP did not modify or potentiate the mucosal ulcerogenic response to other treatments [21].
• In the present study, we examined changes in plasma levels of catecholamines (CA) and corticosterone (COR) of rats after a single (2-h) or long-term repeated immobilization (41 times, 2 h daily) and in rats adapted to long-term immobilization exposed once to the novel stress of cold exposure or insulin or 2-deoxy-D-glucose (2DG) administration [22].

Gene context of 2-deoxy-D-glucose

• One nanomolar IGF-1 restored 2DG uptake to levels seen after 2 hr or serum deprivation [23].
• Baseline level of GH was a reliable predictor of subsequent GH response to 2DG [24].
• Opiate antagonist inhibition of deprivation-induced intake and 2-deoxy-D-glucose (2DG) hyperphagia is significantly enhanced by the 5-hydroxytryptamine3 (5-HT3) antagonist, ICS-205,930 [25].
• The FDG LC calculated from our kinetic parameters for normal brain, possessing predominantly HK I, would be higher than the normal brain LC predicted from animal studies using 2DG or human PET studies using FDG or 2DG [26].
• In cell groups A2, A5, A6 and A7, neither basal nor 2DG-stimulated NPY mRNA expression was detected [18].

Analytical, diagnostic and therapeutic context of 2-deoxy-D-glucose

• Hypothalamic microinjection of the retrogradely transported catecholamine immunotoxin saporin conjugated to anti-dopamine-beta-hydroxylase destroyed hindbrain catecholamine/NPY neurons and abolished basal and 2DG-stimulated increases in NPY expression in hindbrain cell groups [18].
• Northern blot analysis revealed that DSAP lesions elevated basal but blocked 2DG-induced increases in AGRP mRNA levels [27].
• The present study assessed in rats the effects of muscarinic receptor antagonism upon analgesia induced by cold-water swims (CWS: 2 degrees C for 3.5 min) and 2-deoxy-D-glucose (2DG: 600 mg/kg) [28].
• In 42 male duodenal ulcer patients subjected to selective vagotomy and pyloroplasty (SV + PP), negative and positive tests according to different criteria were compared with respect to the acid response to insulin and 2-deoxy-D-glucose (2DG), and to the percentage reduction of the response to insulin by SV + PP [29].
• Male rats were pretreated with beta-funaltrexamine (mu antagonist), Mr-1452 MS (kappa antagonist), or vehicle prior to intraperitoneal injection of the glucose antimetabolite, 2-deoxy-D-glucose (2DG), then sacrificed by transcardial perfusion 2 h later [30].

References