Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with idiopathic Fanconi syndrome and glucose intolerance were studied from a metabolic perspective. They had fasting hyperglycemia, massive glucosuria, insulinopenia, ketosis, and elevated serum free fatty acids. There was a markedly blunted insulin secretory response to glucagon, tolbutamide, glucose, and arginine. One patient had the findings of diabetic retinopathy and a sensory neuropathy. Neither patient could convert galactose to glucose, but they did not have galactosemia. As a result of these studies, and previous reports in which similar changes were noted, we conclude that diabetes mellitus may occur in patients who have had idiopathic Fanconi syndrome for many years.
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PMID:Metabolic abnormalities in the idiopathic Fanconi syndrome: studies of carbohydrate metabolism in two patients. 701 70

In the past few years, the development of pharmaceutical agents that enhance the physiological effects of glucagon-like peptide-1 (GLP-1), either through GLP-1 receptor agonism (GLP-1 agonists) or by inhibiting GLP-1 degradation (dipeptidylpeptidase-4 inhibitors) has broadened the range of treatment options for individuals with type 2 diabetes. It has been recognized for some time that GLP-1 also has extra-pancreatic effects, notably targeting the brain, where it regulates appetite and satiety, as well as peripheral functions highly controlled by the autonomic nervous system, such as gastric emptying. Furthermore, data are beginning to emerge that indicate a potential role for GLP-1 in neuroprotection. The increased risk of Alzheimer's disease, Parkinson's disease and stroke in people with type 2 diabetes suggests that shared mechanisms/pathways of cell death, possibly related to insulin dysregulation, may underlie all of these disorders. Although the disease anatomy varies with each disorder, a wide range of genetic and environmental triggers result in activation of similar biochemical pathways in all of them, suggesting a complex network of biochemical events that feed in to a final common path towards cellular dysfunction and death. This article summarizes the evidence for neuronal activity of GLP-1 and examines the limited data that currently exist on the therapeutic potential of GLP-1 in specific neurological and neurodegenerative conditions, namely Alzheimer's disease, Parkinson's disease, Huntingdon's disease, stroke and peripheral sensory neuropathy.
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PMID:Neuroprotective properties of GLP-1: theoretical and practical applications. 2122 67