The Role of Interferon-α in the Development of Type I Diabetes

1996 ◽  
pp. 154-166
Author(s):  
Xiaojian Huang ◽  
Bruce Hultgren ◽  
Sharon Pitts-Meek ◽  
Jim Hully ◽  
Jim Maclachlan ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Interferon Α ◽  
Type I

scholarly journals Ingested interferon α suppresses Type I diabetes in non-obese diabetic mice

Diabetologia ◽  
1998 ◽  
Vol 41 (10) ◽  
pp. 1227-1232 ◽  
Author(s):  
S. A. Brod ◽  
M. Malone ◽  
S. Darcan ◽  
M. Papolla ◽  
L. Nelson
Keyword(s):  
Type I Diabetes ◽  
Interferon Α ◽  
Type I ◽  
Diabetic Mice

scholarly journals The Role of Type I Diabetes in Intervertebral Disc Degeneration

Spine ◽  
2019 ◽  
Vol 44 (17) ◽  
pp. 1177-1185 ◽  
Author(s):  
Fabrizio Russo ◽  
Luca Ambrosio ◽  
Kevin Ngo ◽  
Gianluca Vadalà ◽  
Vincenzo Denaro ◽  
...  
Keyword(s):  
Intervertebral Disc ◽  
Disc Degeneration ◽  
Intervertebral Disc Degeneration ◽  
Type I Diabetes ◽  
Type I

Glucagon enhances the direct suppressive effect of insulin on hepatic glucose production in humans

1997 ◽  
Vol 272 (3) ◽  
pp. E371-E378 ◽  
Author(s):  
G. F. Lewis ◽  
M. Vranic ◽  
A. Giacca
Keyword(s):  
Type I Diabetes ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Insulin Delivery ◽  
Suppressive Effect ◽  
Type I ◽  
Constant Rate ◽  
Hepatic Glucose ◽  
Infusion Method

The present study examines the role of glucagon in modulating the hepatic and extrahepatic effects of insulin on hepatic glucose production (HGP). We infused glucagon at a constant rate (0.65 ng x kg(-1) x min(-1)) during equimolar portal and peripheral insulin delivery in seven healthy males by our previously published tolbutamide infusion method. In contrast to our previous study, in which glucagon fell by approximately 30% during hyperinsulinemia and suppression of HGP was significantly greater with equimolar peripheral than with portal insulin delivery, HGP was actually suppressed to a lesser extent with peripheral insulin delivery (69 +/- 10%) than when insulin was delivered portally (76 +/- 5%, P < 0.05). To further examine whether glucagon was enhancing the effect of portal insulin, in four additional individuals HGP was suppressed to a greater extent during a tolbutamide infusion when glucagon was administered continuously throughout the basal and hyperinsulinemic periods than when glucagon was infused during the basal period only; HGP suppressed by 63 +/- 3 vs. 52 +/- 3%, respectively, P = 0.02). Tolbutamide had no effect on HGP when infused into three C-peptide-negative individuals with type I diabetes during a low-dose insulin and glucagon infusion. These data suggest that glucagon levels are an important determinant of the balance between insulin's direct and indirect effects on HGP, with glucagon likely potentiating the direct hepatic effect of insulin.

scholarly journals Cancer Biology and Prevention in Diabetes

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1380 ◽  
Author(s):  
Swayam Prakash Srivastava ◽  
Julie E. Goodwin
Keyword(s):  
Type Ii Diabetes ◽  
Cancer Biology ◽  
Cancer Metastasis ◽  
Type I Diabetes ◽  
Type I ◽  
Type Ii ◽  
Mesenchymal Transition ◽  
Wide Range ◽  
Risk Of Cancer

The available evidence suggests a complex relationship between diabetes and cancer. Epidemiological data suggest a positive correlation, however, in certain types of cancer, a more complex picture emerges, such as in some site-specific cancers being specific to type I diabetes but not to type II diabetes. Reports share common and differential mechanisms which affect the relationship between diabetes and cancer. We discuss the use of antidiabetic drugs in a wide range of cancer therapy and cancer therapeutics in the development of hyperglycemia, especially antineoplastic drugs which often induce hyperglycemia by targeting insulin/IGF-1 signaling. Similarly, dipeptidyl peptidase 4 (DPP-4), a well-known target in type II diabetes mellitus, has differential effects on cancer types. Past studies suggest a protective role of DPP-4 inhibitors, but recent studies show that DPP-4 inhibition induces cancer metastasis. Moreover, molecular pathological mechanisms of cancer in diabetes are currently largely unclear. The cancer-causing mechanisms in diabetes have been shown to be complex, including excessive ROS-formation, destruction of essential biomolecules, chronic inflammation, and impaired healing phenomena, collectively leading to carcinogenesis in diabetic conditions. Diabetes-associated epithelial-to-mesenchymal transition (EMT) and endothelial-to-mesenchymal transition (EndMT) contribute to cancer-associated fibroblast (CAF) formation in tumors, allowing the epithelium and endothelium to enable tumor cell extravasation. In this review, we discuss the risk of cancer associated with anti-diabetic therapies, including DPP-4 inhibitors and SGLT2 inhibitors, and the role of catechol-o-methyltransferase (COMT), AMPK, and cell-specific glucocorticoid receptors in cancer biology. We explore possible mechanistic links between diabetes and cancer biology and discuss new therapeutic approaches.

The possible role of Coxsackie A and echo viruses in the pathogenesis of type I diabetes mellitus studied by IgM analysis

1992 ◽  
Vol 24 (1) ◽  
pp. 13-22 ◽  
Author(s):  
G. Frisk ◽  
E. Nilsson ◽  
T. Tuvemo ◽  
G. Friman ◽  
H. Diderholm
Keyword(s):  
Diabetes Mellitus ◽  
Type I Diabetes ◽  
Type I Diabetes Mellitus ◽  
Type I

Interferon-α and induction of type I diabetes

1994 ◽  
Vol 48 (2) ◽  
pp. 112-113
Author(s):  
T. Stewart
Keyword(s):  
Type I Diabetes ◽  
Interferon Α ◽  
Type I

scholarly journals Influence of genetic background on albuminuria and kidney injury in Ins2+/C96Y (Akita) mice

2010 ◽  
Vol 298 (3) ◽  
pp. F788-F795 ◽  
Author(s):  
Susan B. Gurley ◽  
Carrie L. Mach ◽  
Johannes Stegbauer ◽  
Jihong Yang ◽  
Kamie P. Snow ◽  
...  
Keyword(s):  
Genetic Background ◽  
Type I Diabetes ◽  
Critical Role ◽  
Kidney Injury ◽  
Strain Differences ◽  
Type I ◽  
Naturally Occurring ◽  
Akita Mice ◽  
Renal Phenotype

Previous studies have shown that Akita mice bearing the Ins2 +/C96Y mutation have significant advantages as a type I diabetes platform for developing models of diabetic nephropathy (DN; Gurley SB, Clare SE, Snow KP, Hu A, Meyer TW, Coffman TM. Am J Physiol Renal Physiol 290: F214–F222, 2006). In view of the critical role for genetic factors in determining susceptibility to DN in humans, we investigated the role of genetic background on kidney injury in Akita mice. To generate a series of inbred Akita mouse lines, we back-crossed the Ins2 C96Y mutation more than six generations onto the 129/SvEv and DBA/2 backgrounds and compared the extent of hyperglycemia and renal disease with the standard C57BL/6- Ins2 +/C96Y line. Male mice from all three Akita strains developed marked and equivalent hyperglycemia. However, there were significant differences in the level of albuminuria among the lines with a hierarchy of DBA/2 > 129/SvEv > C57BL/6. Renal and glomerular hypertrophy was seen in all of the lines, but significant increases in mesangial matrix compared with baseline nondiabetic controls were observed only in the 129 and C57BL/6 backgrounds. In F1(DBA/2 x C57BL/6)- Ins2 +/C96Y mice, the extent of albuminuria was similar to the parental DBA/2- Ins2+/ C96Y line; they also developed marked hyperfiltration. These studies identify strong effects of genetic background to modify the renal phenotype associated with the Ins2 C96Y mutation. Identification of these naturally occurring strain differences should prove useful for nephropathy modeling and may be exploited to allow identification of novel susceptibility alleles for albuminuria in diabetes.

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