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Hyperproinsulinaemia and Islet Dysfuction in the NIDDM-Like Syndrome of Psammomys obesus

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Physiology and Pathophysiology of the Islets of Langerhans

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 426))

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Abstract

Patients with Type 2, non-insulin dependent diabetes (NIDDM) exhibit elevated plasma proinsulin to insulin ratios [1–9]. Recently, it has been shown that the plasma proinsulin-like fraction in these patients as well as in normal individuals is comprised of both proinsulin and partially cleaved proinsulin, primarily des 31, 32 proinsulin [7,8]. It is assumed that the elevated ratio between proinsulin-related peptides and insulin reflects a β-cell abnormality, since the metabolic clearance rate of these peptides does not differ appreciably between normal individuals and patients with diabetes [10]. Reduction of the plasma glucose concentration in patients with NIDDM, irrespective of the means, was shown to improve insulin production and reduce the degree of hyperproinsulinaemia [3, 11–15]. These observations in man, as well as studies in animal models of diabetes [16–23] have led to the notion that hyperglycaemia per se might be implicated in the generation of a defective β-cell secretory response [24]. Alternatively, hyperglycaemia may play an important contributory role by amplifying a genetically determined β-cell defect, which may not be apparent until unmasked by a chronic increase in secretory demand.

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Kaiser, N., Gadot, M., Leibowitz, G., Cerasi, E., Gross, D.J. (1997). Hyperproinsulinaemia and Islet Dysfuction in the NIDDM-Like Syndrome of Psammomys obesus . In: Soria, B. (eds) Physiology and Pathophysiology of the Islets of Langerhans. Advances in Experimental Medicine and Biology, vol 426. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1819-2_49

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  • DOI: https://doi.org/10.1007/978-1-4899-1819-2_49

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4899-1821-5

  • Online ISBN: 978-1-4899-1819-2

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