scholarly journals Deletion of the Akt/mTORC1 Repressor REDD1 Prevents Visual Dysfunction in a Rodent Model of Type 1 Diabetes

Diabetes ◽  
2017 ◽  
Vol 67 (1) ◽  
pp. 110-119 ◽  
Author(s):  
William P. Miller ◽  
Chen Yang ◽  
Maria L. Mihailescu ◽  
Joshua A. Moore ◽  
Weiwei Dai ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Rodent Model ◽  
Visual Dysfunction

scholarly journals Dopamine Deficiency Contributes to Early Visual Dysfunction in a Rodent Model of Type 1 Diabetes

2014 ◽  
Vol 34 (3) ◽  
pp. 726-736 ◽  
Author(s):  
Moe H. Aung ◽  
Han na Park ◽  
Moon K. Han ◽  
Tracy S. Obertone ◽  
Jane Abey ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Rodent Model ◽  
Visual Dysfunction

1666-P: Increased Levels of Autophagy in a Rodent Model of Type 1 Diabetes

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1666-P
Author(s):  
CEREN KARACAY ◽  
PETRA KOTZBECK ◽  
BARBARA PRIETL ◽  
CLEMENS HARER ◽  
THOMAS PIEBER
Keyword(s):  
Type 1 Diabetes ◽  
Rodent Model

scholarly journals Erratum to: CX3CR1 deficiency accelerates the development of retinopathy in a rodent model of type 1 diabetes

2017 ◽  
Vol 95 (5) ◽  
pp. 565-566
Author(s):  
Eleni Beli ◽  
James M. Dominguez ◽  
Ping Hu ◽  
Jeffrey S. Thinschmidt ◽  
Sergio Caballero ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Rodent Model

scholarly journals Hypothalamic AMP-activated protein kinase activation with AICAR amplifies counterregulatory responses to hypoglycemia in a rodent model of type 1 diabetes

2009 ◽  
Vol 296 (6) ◽  
pp. R1702-R1708 ◽  
Author(s):  
X. Fan ◽  
Y. Ding ◽  
S. Brown ◽  
L. Zhou ◽  
M. Shaw ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Protein Kinase ◽  
Ventromedial Hypothalamus ◽  
Glucose Sensing ◽  
Rodent Model ◽  
Saline Control ◽  
Chronic Hyperglycemia ◽  
Bb Rats ◽  
Amp Activated Protein Kinase

In nondiabetic rodents, AMP-activated protein kinase (AMPK) plays a role in the glucose-sensing mechanism used by the ventromedial hypothalamus (VMH), a key brain region involved in the detection of hypoglycemia. However, AMPK is regulated by both hyper- and hypoglycemia, so whether AMPK plays a similar role in type 1 diabetes (T1DM) is unknown. To address this issue, we used four groups of chronically catheterized male diabetic BB rats, a rodent model of autoimmune T1DM with established insulin—requiring diabetes (40 ± 4 pmol/l basal c-peptide). Two groups were subjected to 3 days of recurrent hypoglycemia (RH), while the other two groups were kept hyperglycemic [chronic hyperglycemia (CH)]. All groups subsequently underwent hyperinsulinemic hypoglycemic clamp studies on day 4 in conjunction with VMH microinjection with either saline (control) or AICAR (5-aminoimidazole-4-carboxamide) to activate AMPK. Compared with controls, local VMH application of AICAR during hypoglycemia amplified both glucagon [means ± SE, area under the curve over time (AUC/ t) 144 ± 43 vs. 50 ± 11 ng·l−1·min−1; P < 0.05] and epinephrine [4.27 ± 0.96 vs. 1.06 ± 0.26 nmol·l−1·min−1; P < 0.05] responses in RH-BB rats, and amplified the glucagon [151 ± 22 vs. 85 ± 22 ng·l−1·min−1; P < 0.05] response in CH-BB rats. We conclude that VMH AMPK also plays a role in glucose-sensing during hypoglycemia in a rodent model of T1DM. Moreover, our data suggest that it may be possible to partially restore the hypoglycemia-specific glucagon secretory defect characteristic of T1DM through manipulation of VMH AMPK.

scholarly journals Nrf2-Mediated Neuroprotection Against Recurrent Hypoglycemia Is Insufficient to Prevent Cognitive Impairment in a Rodent Model of Type 1 Diabetes

Diabetes ◽  
2016 ◽  
Vol 65 (10) ◽  
pp. 3151-3160 ◽  
Author(s):  
Alison D. McNeilly ◽  
Jennifer R. Gallagher ◽  
Albena T. Dinkova-Kostova ◽  
John D. Hayes ◽  
John Sharkey ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Cognitive Impairment ◽  
Rodent Model ◽  
Recurrent Hypoglycemia

Effect of Combined Exercise Versus Aerobic-Only Training on Skeletal Muscle Lipid Metabolism in a Rodent Model of Type 1 Diabetes

2018 ◽  
Vol 42 (4) ◽  
pp. 404-411 ◽  
Author(s):  
Michelle S. Dotzert ◽  
Matthew W. McDonald ◽  
Michael R. Murray ◽  
J. Zachary Nickels ◽  
Earl G. Noble ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Type 1 Diabetes ◽  
Lipid Metabolism ◽  
Rodent Model ◽  
Muscle Lipid ◽  
Combined Exercise ◽  
Skeletal Muscle Lipid

Whole Egg Consumption Exerts a Nephroprotective Effect in an Acute Rodent Model of Type 1 Diabetes

2018 ◽  
Vol 66 (4) ◽  
pp. 866-870 ◽  
Author(s):  
Cassondra J. Saande ◽  
Samantha K. Jones ◽  
Matthew J. Rowling ◽  
Kevin L. Schalinske
Keyword(s):  
Type 1 Diabetes ◽  
Rodent Model ◽  
Egg Consumption ◽  
Nephroprotective Effect ◽  
Whole Egg

372-P: Activation of the Nrf2 Pathway Provides Protection against Hypoglycaemia-Induced Cognitive Impairment in a Rodent Model of Type 1 Diabetes

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 372-P
Author(s):  
ALISON D. MCNEILLY ◽  
JENNIFER GALLAGHER ◽  
ALBENA T. DINKOVA-KOSTOVA ◽  
RORY J. MCCRIMMON
Keyword(s):  
Type 1 Diabetes ◽  
Cognitive Impairment ◽  
Rodent Model ◽  
Nrf2 Pathway

scholarly journals Metabolic inflexibility and protein lysine acetylation in heart mitochondria of a chronic model of Type 1 diabetes

2012 ◽  
Vol 449 (1) ◽  
pp. 253-261 ◽  
Author(s):  
Shraddha S. Vadvalkar ◽  
C. Nathan Baily ◽  
Satoshi Matsuzaki ◽  
Melinda West ◽  
Yasvir A. Tesiram ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Fatty Acid ◽  
Diabetic Cardiomyopathy ◽  
Rodent Model ◽  
Heart Mitochondria ◽  
Lysine Residues ◽  
Progression Of Disease ◽  
Mitochondrial Defects ◽  
Metabolic Inflexibility

Diabetic cardiomyopathy refers to the changes in contractility that occur to the diabetic heart that can arise in the absence of vascular disease. Mitochondrial bioenergetic deficits and increased free radical production are pathological hallmarks of diabetic cardiomyopathy, but the mechanisms and causal relationships between mitochondrial deficits and the progression of disease are not understood. We evaluated cardiac mitochondrial function in a rodent model of chronic Type 1 diabetes (OVE26 mice) before the onset of contractility deficits. We found that the most pronounced change in OVE26 heart mitochondria is severe metabolic inflexibility. This inflexibility is characterized by large deficits in mitochondrial respiration measured in the presence of non-fatty acid substrates. Metabolic inflexibility occurred concomitantly with decreased activities of PDH (pyruvate dehydrogenase) and complex II. Hyper-acetylation of protein lysine was also observed. Treatment of control heart mitochondria with acetic anhydride (Ac2O), an acetylating agent, preferentially inhibited respiration by non-fatty acid substrates and increased superoxide production. We have concluded that metabolic inflexibility, induced by discrete enzymatic and molecular changes, including hyper-acetylation of protein lysine residues, precedes mitochondrial defects in a chronic rodent model of Type 1 diabetes.

scholarly journals CX3CR1 deficiency accelerates the development of retinopathy in a rodent model of type 1 diabetes

2016 ◽  
Vol 94 (11) ◽  
pp. 1255-1265 ◽  
Author(s):  
Eleni Beli ◽  
James M. Dominguez ◽  
Ping Hu ◽  
Jeffrey S. Thinschmidt ◽  
Sergio Caballero ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Rodent Model
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