Role of Neuronal Glucosensing in the Regulation of Energy Homeostasis
Levin et al.
Diabetes 2006;55:S122-S130.
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The patient with a severe degree of metabolic acidosis: a deductive analysis.
Maccari et al.
QJM 2006;99:475-485.
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Acute and fatal hyponatraemia after resection of a craniopharyngioma: a preventable tragedy
Bohn et al.
QJM 2005;98:691-703.
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An approach to the patient with severe hypokalaemia: the potassium quiz
Groeneveld et al.
QJM 2005;98:305-316.
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Acidosis in a patient with cholera: a need to redefine concepts
Zalunardo et al.
QJM 2004;97:681-696.
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Osmotic demyelination syndrome: a potentially avoidable disaster
Lin et al.
QJM 2003;96:935-947.
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Hyponatraemia and hyperglycaemia during laproscopic surgery
Davids et al.
QJM 2002;95:321-330.
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Diabetic Ketoacidosis: New Concepts and Trends in Pathogenesis and Treatment
KREISBERG
ANN INTERN MED 1978;88:681-695.
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Hypoinsulinemia of Hypothyroidism
Shah and Cerchio
Arch Intern Med 1973;132:657-661.
ABSTRACT
-adrenergic receptor stimulation; β-adrenergic receptors are also described which stimulate insulin release, indicating a unique dual receptor system in the pancreatic islet. The possible physiologic importance of these findings is suggested in a discussion of the carbohydrate intolerance found in patients with pheochromocytoma and during severe hypothermia in children. A possible relation of the inhibition of insulin release and the increased fatty acid mobilization caused by catecholamines to exacerbations of the diabetic syndrome is examined. It is postulated that the catecholamine release which is stimulated by volume depletion, infection, or stress may be an important "reversible" factor in some patients with diabetic ketoacidosis.