Ketogenesis evaluation in perfused liver of diabetic rats submitted to short-term insulin-induced hypoglycemia

2009 ◽  
Vol 27 (6) ◽  
pp. 383-387 ◽  
Author(s):  
Helenton Cristhian Barrena ◽  
Vilma Aparecida Ferreira Godoi Gazola ◽  
Maria Montserrat Diaz Pedrosa Furlan ◽  
Rosângela Fernandes Garcia ◽  
Helenir Medri de Souza ◽  
...  
1976 ◽  
Vol 156 (3) ◽  
pp. 585-592 ◽  
Author(s):  
P D Whitton ◽  
D A Hems

1. A total loss of capacity for net glycogen synthesis was observed in experiments with the perfused liver of starved adrenalectomized rats. 2. This lesion was corrected by insulin or cortisol in vivo (over 2-5h), but not by any agent tested in perfusion. 3. The activity of glycogen synthetase a, and its increase during perfusion, in the presence of glucose plus glucogenic substrates, were proportional to the rate of net glycogen accumulation. 4. This complete inherent loss of capacity for glycogen synthesis after adrenalectomy is greater than any defect in hepatic metabolism yet reported in this situation, and is not explicable by a decrease in the rate of gluconegenesis (which supports glycogen synthesis in the liver of starved rats). The short-term (2-5h) stimulatory effect of glucocorticoids in the intact animal, on hepatic glycogen deposition, may be mediated partly through insulin action, although neither insulin or cortisol appear to act directly on the liver to stimulate glycogen synthesis.


2008 ◽  
Vol 26 (2) ◽  
pp. 228-232 ◽  
Author(s):  
G. G. Albuquerque ◽  
V. A. F. G. Gazola ◽  
R. F. Garcia ◽  
K. L. A. Souza ◽  
H. C. Barrena ◽  
...  
Keyword(s):  

2016 ◽  
Vol 311 (3) ◽  
pp. R466-R477 ◽  
Author(s):  
Trevor Hardigan ◽  
Abdul Yasir ◽  
Mohammed Abdelsaid ◽  
Maha Coucha ◽  
Sally El-Shaffey ◽  
...  

The antihyperglycemic agent linagliptin, a dipeptidyl peptidase-4 (DPP-IV) inhibitor, has been shown to reduce inflammation and improve endothelial cell function. In this study, we hypothesized that DPP-IV inhibition with linagliptin would improve impaired cerebral perfusion in diabetic rats, as well as improve insulin-induced cerebrovascular relaxation and reverse pathological cerebrovascular remodeling. We further postulated that these changes would lead to a subsequent improvement of cognitive function. Male Type-2 diabetic and nondiabetic Goto-Kakizaki rats were treated with linagliptin for 4 wk, and blood glucose and DPP-IV plasma levels were assessed. Cerebral perfusion was assessed after treatment using laser-Doppler imaging, and dose response to insulin (10−13 M–10−6 M) in middle cerebral arteries was tested on a pressurized arteriograph. The impact of DPP-IV inhibition on diabetic cerebrovascular remodeling was assessed over a physiologically relevant pressure range, and changes in short-term hippocampus-dependent learning were observed using a novel object recognition test. Linagliptin lowered DPP-IV activity but did not change blood glucose or insulin levels in diabetes. Insulin-mediated vascular relaxation and cerebral perfusion were improved in the diabetic rats with linagliptin treatment. Indices of diabetic vascular remodeling, such as increased cross-sectional area, media thickness, and wall-to-lumen ratio, were also ameliorated; however, improvements in short-term hippocampal-dependent learning were not observed. The present study provides evidence that linagliptin treatment improves cerebrovascular dysfunction and remodeling in a Type 2 model of diabetes independent of glycemic control. This has important implications in diabetic patients who are predisposed to the development of cerebrovascular complications, such as stroke and cognitive impairment.


2004 ◽  
Vol 997 (2) ◽  
pp. 185-193 ◽  
Author(s):  
Verónica Berta Dorfman ◽  
Juan José López-Costa ◽  
Cristina Vega ◽  
Julio César Bayona ◽  
Francisco Capani ◽  
...  

2002 ◽  
Vol 35 (7) ◽  
pp. 843-849 ◽  
Author(s):  
P. Dall'Ago ◽  
V.O.K. Silva ◽  
K.L.D. De Angelis ◽  
M.C. Irigoyen ◽  
R. Fazan Jr. ◽  
...  

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