Hypoglycaemia secondary to the secretion of pro-insulin like growth factor ii by a metastatic neuroendocrine tumour with sarcomatous differentiation

Morgan, Mia; Nanzer, AM; Camacho‐Hübner, Cecilia; Kaltsas, Gregory; Monson, John P.

doi:10.14310/horm.2002.1192

Cited by 3 publications

(2 citation statements)

References 8 publications

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“…A large number of studies have shown that GABAergic neurons and glutamatergic neurons in the vlPAG play an important and complex role in nociceptive processes. Microinjection of glutamate receptor agonists or GABA antagonists into the vlPAG has a significant antinociceptive effect against noxious stimuli (Budai et al, 1998; Morgan et al, 2003). Since activation of GABAergic neurons alone in the vlPAG only partly attenuated the effect of EA, we speculated that glutamatergic and GABAergic neurons were both involved in these effects.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of GABAergic Neurons and Excitation of Glutamatergic Neurons in the Ventrolateral Periaqueductal Gray Participate in Electroacupuncture Analgesia Mediated by Cannabinoid Receptor

Zhang

Xiang

et al. 2019

Front. Neurosci.

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Although electroacupuncture (EA) has become a worldwide practice, little is understood about its precise target in the central nervous system (CNS) and the cell type-specific analgesia mechanism. In the present study, we found that EA has significant antinociceptive effects both in inflammatory and neuropathic pain models. Chemogenetic inhibition of GABAergic neurons in the ventrolateral periaqueductal gray (vlPAG) replicated the effects of EA, whereas the combination of chemogenetic activation of GABAergic neurons and chemogenetic inhibition of glutamatergic neurons in the vlPAG was needed to reverse the effects of EA. Specifically knocking out CB1 receptors on GABAergic neurons in the vlPAG abolished the EA effect on pain hypersensitivity, while specifically knocking out CB1 receptors on glutamatergic neurons attenuated only a small portion of the EA effect. EA synchronously inhibits GABAergic neurons and activates glutamatergic neurons in the vlPAG through CB1 receptors to produce EA-induced analgesia. The CB1 receptors on GABAergic neurons localized in the vlPAG was the basis of the EA effect on pain hypersensitivity. This study provides new experimental evidence that EA can bidirectionally regulate GABAergic neurons and glutamatergic neurons via the CB1 receptors of the vlPAG to produce analgesia effects.

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Section: Resultsmentioning

confidence: 99%

Inhibition of GABAergic Neurons and Excitation of Glutamatergic Neurons in the Ventrolateral Periaqueductal Gray Participate in Electroacupuncture Analgesia Mediated by Cannabinoid Receptor

Zhang

Xiang

et al. 2019

Front. Neurosci.

View full text Add to dashboard Cite

show abstract

“…A large number of studies have shown that GABAergic neurons and glutamatergic neurons in the vlPAG play an important and complex role in nociceptive processes. Microinjection of glutamate receptor agonists or GABA antagonists into the vlPAG has a significant antinociceptive effect against noxious stimuli (Budai et al, 1998;Morgan et al, 2003). Since activation of GABAergic neurons alone in the vlPAG only partly attenuated the effect of EA, we speculated that glutamatergic and GABAergic neurons were both involved in these effects.…”

Section: The Combination Of Chemogenetic Activation Of Gabaergic Neur...mentioning

confidence: 93%

Neuromodulatory Interventions for Pain

2022

Frontiers Research Topics

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Tumors, IGF-2, and Hypoglycemia: Insights From the Clinic, the Laboratory, and the Historical Archive

et al. 2013

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Tumors of mesenchymal and epithelial origin produce IGF-2, which activates pathways in the tumors. In a minority of patients, the tumors (hepatomas, fibromas, and fibrosarcomas are the most common among many) release into the circulation enough IGF-2-related peptides to mimic the fasting hypoglycemia characteristic of patients with insulin-producing islet-cell tumors. Rarely, markedly elevated IGF-2 levels produce somatic changes suggestive of acromegaly. Typically, the elevated IGF-2 levels are associated with suppressed plasma levels of insulin, IGF-1, and GH. Complicating the pathophysiology are the IGF binding proteins (IGFBPs) that can bind IGF-2 and IGF-1, modifying hormone metabolism and action. IGFBP concentrations are often altered in the presence of these tumors. At the cellular level, the 3 hormone-related ligands, IGF-2, IGF-1, and insulin, all bind to 4 (or more) types of IGF-1 receptor (IGF-1R) and insulin receptor (IR). Each receptor has its own characteristic affinity for each ligand, a tyrosine kinase, and overlapping profiles of action in the target cells. The IGF-2R, in addition to binding mannose-6-phosphate-containing proteins, provides an IGF-2 degradation pathway. Recent evidence suggests IGF-2R involvement also in signal transduction. Surgery, the treatment of choice, can produce a cure. For patients not cured by surgery, multiple therapies exist, for the tumor and for hypoglycemia. Potential future therapeutic approaches are sketched. From 1910 to 1930, hypoglycemia, insulin, insulinomas, and non-islet-cell tumors were recognized. The latter third of the century witnessed the emergence of the immunoassay for insulin; the IGFs, their binding proteins, and assays to measure them; and receptors for the insulin-related peptides as well as the intracellular pathways beyond the receptor. In closing, we replace non-islet-cell tumor hypoglycemia, an outdated and misleading label, with IGF-2-oma, self-explanatory and consistent with names of other hormone-secreting tumors.

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Hypoglycaemia secondary to the secretion of pro-insulin like growth factor ii by a metastatic neuroendocrine tumour with sarcomatous differentiation

Cited by 3 publications

References 8 publications

Inhibition of GABAergic Neurons and Excitation of Glutamatergic Neurons in the Ventrolateral Periaqueductal Gray Participate in Electroacupuncture Analgesia Mediated by Cannabinoid Receptor

Inhibition of GABAergic Neurons and Excitation of Glutamatergic Neurons in the Ventrolateral Periaqueductal Gray Participate in Electroacupuncture Analgesia Mediated by Cannabinoid Receptor

Neuromodulatory Interventions for Pain

Tumors, IGF-2, and Hypoglycemia: Insights From the Clinic, the Laboratory, and the Historical Archive

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