Reduced pancreatic insulin release and reduced peripheral insulin sensitivity contribute to hyperglycaemia in cystic fibrosis

1995 ◽  
Vol 154 (5) ◽  
pp. 356-361 ◽  
Author(s):  
R. W. Holl ◽  
E. Heinze ◽  
A. Wolf ◽  
M. Rank ◽  
W. M. Teller



1986 ◽  
Vol 112 (3) ◽  
pp. 367-371 ◽  
Author(s):  
Annette Svenningsen ◽  
Thomas Dyrberg ◽  
Helle Markholst ◽  
Christian Binder ◽  
Åke Lernmark

Abstract. The pancreases of approximately 50 days old diabetes-prone BB/Hagedorn (BB/H) and of the genetically closely related, but non-diabetic BB w-subline (control BB) rats were perfused to determine the capacity of D-glucose to release insulin before the expected development of diabetes. The BB/H rats were from a colony with 82–84% incidence of insulin-dependent diabetes mellitus (IDDM) by 140 days of age. The total amount of insulin released from the BB/H rat pancreas during stimulation with 20 mmol/l D-glucose was reduced by nearly 50% (P <0.01). The initial peak of insulin release was similar between the two groups of animals, whereas the amount of insulin released during the second peak accounted for the diminished release (P < 0.01). The extractable pancreatic insulin was 30% (P < 0.05) less in the BB/H rats. Total insulin release expressed relative to the pancreatic insulin content, was therefore not different between the two groups. It is concluded that about 20–40 days before the mean age of clinical onset of IDDM in BB/H rats, the capacity to release insulin in response to D-glucose is reduced along with a diminished pancreatic insulin content. This abnormality seems to be preceded only by islet cell surface antibodies but not by insulitis.



2003 ◽  
Vol 149 (1) ◽  
pp. 53-59 ◽  
Author(s):  
F Lombardo ◽  
F De Luca ◽  
M Rosano ◽  
C Sferlazzas ◽  
C Lucanto ◽  
...  

OBJECTIVE: The loss of pancreatic beta-cells is thought to be one of the principal causes of diabetes mellitus (DM) in cystic fibrosis (CF), but the role of peripheral insulin resistance (IR) in the pathogenesis of DM in CF remains unclear. The aim of this study was to evaluate whether eventual changes of glucose tolerance (GT) over time were associated with modifications of insulin secretion or sensitivity. METHODS: Plasma glucose and insulin responses to an oral GT test (OGTT) were investigated and reinvestigated 13 Years later in 14 CF patients with initial and persistent fasting euglycemia and no history of insulin treatment. Insulin sensitivity (IS) at both tests was assessed on the basis of insulin and glucose levels both in the fasting state and during OGTTs. RESULTS: From the 1st to the 2nd OGTT: (a) the prevalence of DM responses significantly increased; (b) the areas beneath the respective glucose and insulin curves significantly increased and decreased respectively; (c) IR and IS indices decreased and increased respectively, even in the patients who developed DM; (d) pulmonary function significantly worsened in the entire series, especially in the patients who developed DM. CONCLUSIONS: (i) the natural history of glyco-metabolic status in CF is characterized by deteriorating GT over time; (ii) insulinopenia plays a prominent role in the pathogenesis of GT worsening; (iii) IR does not play any significant part in the pathogenesis of DM development; (iv) deterioration of lung function tests is more severe in the subjects who develop DM over time.



2014 ◽  
Vol 8 ◽  
pp. GRSB.S14116 ◽  
Author(s):  
M. Jawad Khan ◽  
Carolina B. Jacometo ◽  
Daniel E. Graugnard ◽  
Marcio N. Corrêa ◽  
Eduardo Schmitt ◽  
...  


Diabetes ◽  
2013 ◽  
Vol 63 (5) ◽  
pp. 1725-1737 ◽  
Author(s):  
Kirstine N. Bojsen-Møller ◽  
Carsten Dirksen ◽  
Nils B. Jørgensen ◽  
Siv H. Jacobsen ◽  
Annette K. Serup ◽  
...  


2004 ◽  
Vol 5 (3) ◽  
pp. 122-125 ◽  
Author(s):  
Robert P. Hoffman ◽  
Paolo Vicini ◽  
Claudio Cobelli


2017 ◽  
Vol 9 (3) ◽  
pp. 529-535 ◽  
Author(s):  
Yasuhiko Furukawa ◽  
Yoshifumi Tamura ◽  
Kageumi Takeno ◽  
Takashi Funayama ◽  
Hideyoshi Kaga ◽  
...  


Author(s):  
G. S. Moss ◽  
G. Cerchio ◽  
D. C. Siegel ◽  
P. C. Reed ◽  
A. Cochin ◽  
...  


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