Overexpression of MHC proteins in pancreatic islets: a link between cytokines, viruses, the breach of tolerance and insulindependent diabetes mellitus?

1995 ◽  
pp. 361-389 ◽  
Author(s):  
Marta Vives-Pi ◽  
Nuria Somoza ◽  
Francesca Vargas ◽  
Ricardo Pujol-Borrell
Keyword(s):  
Diabetes Mellitus ◽  
Pancreatic Islets ◽  
Insulindependent Diabetes

Nitric oxide donor SIN-1 inhibits insulin release

1996 ◽  
Vol 271 (4) ◽  
pp. C1098-C1102 ◽  
Author(s):  
A. Sjoholm
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Kinase C ◽  
Stimulus Secretion Coupling

Preceding the onset of insulin-dependent diabetes mellitus, pancreatic islets are infiltrated by macrophages secreting interleukin-1 beta, which exerts cytotoxic and inhibitory actions on islet beta-cell insulin secretion through induction of nitric oxide (NO) synthesis. The influence of the NO donor 3-morpholinosydnonimine (SIN-1) on insulin secretion from isolated pancreatic islets in response to various secretagogues was investigated. Stimulation of insulin release evoked by glucose, phospholipase C activation with carbachol, and protein kinase C activation with phorbol ester were obtained by SIN-1, whereas the response to adenylyl cyclase activation or K(+)-induced depolarization was not affected. It is concluded that enzymes involved in glucose catabolism, phospholipase C or protein kinase C, may be targeted by NO. Reversal of SIN-1 inhibition of glucose-stimulated insulin release by dithiothreitol suggests that NO may inhibit insulin secretion partly by S-nitrosylation of thiol residues in key proteins in the stimulus-secretion coupling. These adverse effects of NO on the beta-cell stimulus-secretion coupling may be of importance for the development of the impaired insulin secretion characterizing diabetes mellitus.

Autoimmunity and Genetics Contribute to the Risk of Insulindependent Diabetes Mellitus in Families: Islet Cell Antibodies and HLA DQ Heterodimers

1992 ◽  
Vol 136 (5) ◽  
pp. 503-512 ◽  
Author(s):  
Rebecca B.Lipton ◽  
Mirjana Kocova ◽  
Ronald E. LaPorte ◽  
Janice S. Dorman ◽  
Trevor J. Orchard ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Islet Cell ◽  
Islet Cell Antibodies ◽  
Hla Dq ◽  
Insulindependent Diabetes

Feline Insular Amyloid: Incidence in Adult Cats with No Clinicopathologic Evidence of Overt Diabetes Mellitus

1981 ◽  
Vol 18 (3) ◽  
pp. 310-315 ◽  
Author(s):  
B. L. Yano ◽  
D. W. Hayden ◽  
K. H. Johnson
Keyword(s):  
Diabetes Mellitus ◽  
Pancreatic Islets ◽  
Congo Red ◽  
Domestic Cats ◽  
Islet Amyloid ◽  
Overt Diabetes ◽  
Amyloid Deposits ◽  
Adult Cats

Pancreatic tissues from 93 adult domestic cats with no clinicopathologic evidence of overt diabetes mellitus were examined for islet amyloid. Amyloid deposits were found in the pancreatic islets of 44 cats. Approximately one-third of these deposits were not seen with HE, but subsequently were identified with Congo red stain. The proportion of islets with amyloid, the intra-islet location of amyloid, and the amount of amyloid in individual islets also were characterized. In this select population of adult cats, the presence or absence of islet amyloid was not linked significantly (p = > 0.05) to age, breed, sex or primary anatomic diagnosis. Results of this study indicate that: the incidence of islet amyloid in cats is higher than previously recognized; as in man, islet amyloid can occur in cats without concurrent overt diabetes mellitus; and islet amyloid should not be considered pathognomonic for diabetes mellitus.

High plasma prorenin in non diabetic siblings of non insulindependent diabetes mellitus patients

1999 ◽  
Vol 22 (10) ◽  
pp. 760-765 ◽  
Author(s):  
N. Glorioso ◽  
C. Troffa ◽  
G. Tonolo ◽  
F. Filigheddu ◽  
F. Dettori ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
High Plasma ◽  
Insulindependent Diabetes

scholarly journals Design and Estimation of Fast Dissolving Tablet by using Novel Techniques for Effective Treatment of Diabetes

2020 ◽  
Vol 9 (3) ◽  
pp. 2345-2349
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Pancreatic Islets ◽  
Protein Digestion ◽  
Lipid Digestion ◽  
Diabetes Mellitus Type Ii ◽  
Insulin Reaction ◽  
Patients With Diabetes ◽  
Treatment Of Diabetes ◽  
Postprandial Insulin

Diabetes mellitus is a metabolic issue it is brought about by a flat out or relative absence of insulin that, among different outcomes, increments in plasma glucose fixation related to change hyperglycemia and unsettling influence of lipid digestion, starch digestion, additionally protein digestion. Glipizide, a secondgen sulfonylurea, is utilized with diet to bring down blood glucose in patients with diabetes mellitus type II. The essential method of activity of glipizide in exploratory creatures seems, by all accounts, to be the incitement of insulin emission from the beta cells of pancreatic islet tissue and is in this way reliant on working -cells in the pancreatic islets. In human's glipizide seems to bring down the blood glucose intensely by invigorating the arrival of insulin from the pancreas, an impact subordinate after working -cells in the pancreatic islets. In man, incitement of insulin discharge by glipizide because of a feast is undoubtedly vital. Fasting insulin levels are not raised even on long haul glipizide organization, yet the postprandial insulin reaction keeps on being upgraded after at any rate a half year of treatment.

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