scholarly journals The CREBRF diabetes-protective rs373863828-A allele is associated with enhanced early insulin release in men of Māori and Pacific ancestry

Diabetologia ◽  
2021 ◽  
Author(s):  
Hannah J. Burden ◽  
Shannon Adams ◽  
Braydon Kulatea ◽  
Morag Wright-McNaughton ◽  
Danielle Sword ◽  
...  
Keyword(s):  
1973 ◽  
Vol 72 (1) ◽  
pp. 46-53 ◽  
Author(s):  
D. S. Turner ◽  
D. A. B. Young

ABSTRACT The insulin secretory response in the rat to intravenous glucose was found to be greatly impaired by fasting for three days, whereas that to orally administered glucose was not significantly affected. Rats fasted for two days were given either protein or starch pellets for six hours, and then fasted for a further eighteen hours before the intravenous glucose test. The protein pre-feeding failed to affect significantly the subsequent insulin secretory response to intravenous glucose, whereas starch prefeeding greatly enhanced it. It is suggested that intestinal hormones released by glucose ingestion may exert not only an acute effect on insulin release, but also a 'priming' effect on the insulin release mechanism of the β cell, which enables it to respond to the subsequent stimulus of glucose alone.


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.


Diabetes ◽  
1980 ◽  
Vol 29 (6) ◽  
pp. 431-437 ◽  
Author(s):  
W. J. Malaisse ◽  
J. C. Hutton ◽  
A. R. Carpinelli ◽  
A. Herchuelz ◽  
A. Sener

Diabetes ◽  
1981 ◽  
Vol 30 (2) ◽  
pp. 168-171 ◽  
Author(s):  
M. S. Robbins ◽  
L. H. Grouse ◽  
R. L. Sorenson ◽  
R. P. Elde

Diabetes ◽  
1976 ◽  
Vol 25 (10) ◽  
pp. 949-954 ◽  
Author(s):  
S. Efendic ◽  
E. Cerasi ◽  
R. Luft ◽  
G. Gladnikoff

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