scholarly journals Immaturity of insulin secretion by pancreatic islets isolated from one human neonate

2017 ◽  
Vol 9 (2) ◽  
pp. 270-273 ◽  
Author(s):  
Jean-Claude Henquin ◽  
Myriam Nenquin
Diabetes ◽  
1994 ◽  
Vol 43 (6) ◽  
pp. 827-830 ◽  
Author(s):  
P. Marchetti ◽  
D. W. Scharp ◽  
M. Mclear ◽  
R. Gingerich ◽  
E. Finke ◽  
...  

Diabetes ◽  
1994 ◽  
Vol 43 (11) ◽  
pp. 1345-1352 ◽  
Author(s):  
A. Gardemann ◽  
K. Jungermann ◽  
V. Grosse ◽  
L. Cossel ◽  
F. Wohlrab ◽  
...  

Diabetes ◽  
1988 ◽  
Vol 37 (7) ◽  
pp. 992-996 ◽  
Author(s):  
J. Turk ◽  
J. H. Hughes ◽  
R. A. Easom ◽  
B. A. Wolf ◽  
D. W. Scharp ◽  
...  

Endocrinology ◽  
2002 ◽  
Vol 143 (4) ◽  
pp. 1253-1259 ◽  
Author(s):  
Francoise Jamen ◽  
Raymond Puech ◽  
Joel Bockaert ◽  
Philippe Brabet ◽  
Gyslaine Bertrand

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ashley M. Fields ◽  
Kevin Welle ◽  
Elaine S. Ho ◽  
Clementina Mesaros ◽  
Martha Susiarjo

AbstractIn pancreatic islets, catabolism of tryptophan into serotonin and serotonin receptor 2B (HTR2B) activation is crucial for β-cell proliferation and maternal glucose regulation during pregnancy. Factors that reduce serotonin synthesis and perturb HTR2B signaling are associated with decreased β-cell number, impaired insulin secretion, and gestational glucose intolerance in mice. Albeit the tryptophan-serotonin pathway is dependent on vitamin B6 bioavailability, how vitamin B6 deficiency impacts β-cell proliferation during pregnancy has not been investigated. In this study, we created a vitamin B6 deficient mouse model and investigated how gestational deficiency influences maternal glucose tolerance. Our studies show that gestational vitamin B6 deficiency decreases serotonin levels in maternal pancreatic islets and reduces β-cell proliferation in an HTR2B-dependent manner. These changes were associated with glucose intolerance and insulin resistance, however insulin secretion remained intact. Our findings suggest that vitamin B6 deficiency-induced gestational glucose intolerance involves additional mechanisms that are complex and insulin independent.


Diabetes ◽  
1999 ◽  
Vol 48 (5) ◽  
pp. 1006-1012 ◽  
Author(s):  
H. Yajima ◽  
M. Komatsu ◽  
T. Schermerhorn ◽  
T. Aizawa ◽  
T. Kaneko ◽  
...  

1991 ◽  
Vol 177 (3) ◽  
pp. 932-938 ◽  
Author(s):  
Carol L. Broderick ◽  
Gerald S. Brooke ◽  
Richard D. DiMarchi ◽  
Gerald Gold

Diabetologia ◽  
1978 ◽  
Vol 15 (2) ◽  
pp. 129-132 ◽  
Author(s):  
B. A. Larson ◽  
T. L. Williams ◽  
U. J. Lewis ◽  
W. P. VanderLaan

2012 ◽  
Vol 90 (3) ◽  
pp. 371-378 ◽  
Author(s):  
Menakshi Bhat Dusane ◽  
Bimba N. Joshi

The present study investigates the antidiabetogenic effects of Murraya koenigii (L.) Spr. and Ocimum tenuflorum  L. on streptozotocin-induced diabetic Swiss mice. Treatment with extracts of M. koenigii (chloroform; MKC) and O. tenuflorum (aqueous; OTA) resulted in proper glucose utilization with an increase in liver glucose-6-phosphate dehydrogenase enzyme activity, and normal glycogenesis in hepatic and muscle tissues. Pancreatic and intestinal glucosidase inhibitory activity observed with MKC and OTA treatment indicated beneficial effects in reducing postprandial hyperglycemia with concomitant improvement in glucose metabolism. The glucosidase inhibition was prolonged, even after discontinuation of MKC and OTA treatment. Normalization of plasma insulin and C-peptide levels was observed in diabetic mice, indicating endogenous insulin secretion after treatment. The histochemical and immunohistochemical analysis of pancreatic islets suggests the role of MKC and OTA in pancreatic β-cell protection and the functional pancreatic islets that produce insulin. The study demonstrates the significance of MKC and OTA in glucosidase inhibition and islet protection in the murine diabetic model. These findings suggest the potential of the extracts in adjuvant therapy for the treatment of diabetes and the possible development of potential neutraceuticals.


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