Non-islet Cell Tumor-induced Hypoinsulinemic Hypoglycemia in the Setting of Metastatic Desmoplastic Round Cell Tumor

Bhuiyan, M. Nadir; Sharma, Purva

doi:10.7759/cureus.4669

Cited by 2 publications

(3 citation statements)

References 10 publications

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“… 81 , 203 In such patients, serum IGF2 levels are as much as fourfold higher than normal. 204 The hypoglycemia risk of exogenous IGF2 is primarily influenced by two factors: dose and route of administration. Whereas an intravenous dose of 1 mg/kg IGF2 induced hypoglycemia in mice, 87 a subcutaneous dose of 30 μg/kg (which was sufficient to cause acute cognitive enhancement) had no effect on blood glucose concentration in either mice 167 or rats.…”

Section: Igf2 Has Favorable Tolerability and Safetymentioning

confidence: 99%

“…Wilms's tumor, non‐islet cell tumor hypoglycemia) due to hyper‐secretion of IGF2 by the tumor itself 81,203 . In such patients, serum IGF2 levels are as much as fourfold higher than normal 204 . The hypoglycemia risk of exogenous IGF2 is primarily influenced by two factors: dose and route of administration.…”

Section: Igf2 Has Favorable Tolerability and Safetymentioning

confidence: 99%

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Insulin‐like growth factor‐2 is a promising candidate for the treatment and prevention of Alzheimer's disease

2023

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Alzheimer's disease (AD) is the most common form of dementia. Current AD treatments slow the rate of cognitive decline, but do not restore lost function. One reason for the low efficacy of current treatments is that they fail to target neurotrophic processes, which are thought to be essential for functional recovery. Bolstering neurotrophic processes may also be a viable strategy for preventative treatment, since structural losses are thought to underlie cognitive decline in AD. The challenge of identifying presymptomatic patients who might benefit from preventative treatment means that any such treatment must meet a high standard of safety and tolerability. The neurotrophic peptide insulin‐like growth factor‐2 (IGF2) is a promising candidate for both treating and preventing AD‐induced cognitive decline. Brain IGF2 expression declines in AD patients. In rodent models of AD, exogenous IGF2 modulates multiple aspects of AD pathology, resulting in (1) improved cognitive function; (2) stimulation of neurogenesis and synaptogenesis; and, (3) neuroprotection against cholinergic dysfunction and beta amyloid‐induced neurotoxicity. Preclinical evidence suggests that IGF2 is likely to be safe and tolerable at therapeutic doses. In the preventative treatment context, the intranasal route of administration is likely to be the preferred method for achieving the therapeutic effect without risking adverse side effects. For patients already experiencing AD dementia, routes of administration that deliver IGF2 directly access the CNS may be necessary. Finally, we discuss several strategies for improving the translational validity of animal models used to study the therapeutic potential of IGF2.

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Section: Igf2 Has Favorable Tolerability and Safetymentioning

confidence: 99%

Section: Igf2 Has Favorable Tolerability and Safetymentioning

confidence: 99%

Insulin‐like growth factor‐2 is a promising candidate for the treatment and prevention of Alzheimer's disease

2023

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“…Hypoglycemia can lead to several symptoms like weakness, sweating, followed by confusion/disorientation and shakiness (8). In hypoinsulinemic hypoglycemia, episodes of hypoglycemia are usually recurrent and refractory to conventional treatment, and they can cause lifethreatening consequences (9,10).…”

Section: Introductionmentioning

confidence: 99%

PTEN Deletion in Adult Mice Induces Hypoinsulinemia With Concomitant Low Glucose Levels

et al. 2022

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The PI3K/AKT pathway, negatively regulated by PTEN, plays a paramount role in glucose metabolism regulation due to its activation by the insulin receptor signaling pathway. We generated a PTEN-KO mouse to evaluate the systemic effect of the overactivation of the PI3K/AKT pathway in insulin signaling and glucose homeostasis. Our results demonstrate that PTEN-KO mice show very low glucose levels in the fasted state, which poorly respond to glucose and pyruvate administration. Insulinemia decreased without alterations in pancreatic islets. Among the possible reasons, we uncover the deregulation of the expression of proximal tubule glucose transporter and consequent glycosuria. Moreover, we evidence an altered activation of hepatic gluconeogenesis-related genes. In addition, the expression of several genes related to β-oxidation showed a delayed or even absent response to fasting, suggesting that the lack of PTEN not only impairs glucose metabolism but also slows down the use of lipids as a metabolic fuel. We conclude that the inducible full PTEN-KO mice could be a good model to study the metabolic interactions between glycidic and lipidic metabolism in hypoinsulinemic hypoglycemia and that PTEN could be an important mediator in the disease and/or a potential drug target.

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Non-islet Cell Tumor-induced Hypoinsulinemic Hypoglycemia in the Setting of Metastatic Desmoplastic Round Cell Tumor

Cited by 2 publications

References 10 publications

Insulin‐like growth factor‐2 is a promising candidate for the treatment and prevention of Alzheimer's disease

Insulin‐like growth factor‐2 is a promising candidate for the treatment and prevention of Alzheimer's disease

PTEN Deletion in Adult Mice Induces Hypoinsulinemia With Concomitant Low Glucose Levels

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