The effect of different hyperglucagonemic states on monooxygenase activities and isozymic pattern of cytochrome P-450 in mouse

1985 ◽  
Vol 5 (4) ◽  
pp. 335-341 ◽  
Author(s):  
E. Rouer ◽  
P. Beaune ◽  
C. Augereau ◽  
J. P. Leroux
Keyword(s):  
Continuous Infusion ◽  
Experimental Model ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Low Dose ◽  
Liver Microsomes ◽  
Diabetic Mice ◽  
Isozymic Pattern ◽  
Cytochrome P 450

The continuous infusion of a low dose of glucagon (35 μg/kg/d, for 5 d) constitutes, in view of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities, a reliable experimental model of hyperglucagonemia. By conjunction of monooxygenase assays and immunoquantitation of specific isozymes of cytochrome P-450, the actual inducing ability of glucagon has been shown and it might explain some of the modifications of the drug metabolizing system in diabetic mice. The isozymic pattern of cytochrome P-430 of liver microsomes from diabetic mice appears very different from that produced by classical inducers.

Intestinal delivery of proinsulin and IL-10 via Lactococcus lactis combined with low-dose antiCD3 induces antigen-specific FoxP3+ Tregs in autoimmune diabetic mice

2020 ◽  
Author(s):  
Martens P-J ◽  
Sassi G ◽  
Viaene M ◽  
Laureys J ◽  
Teyton L ◽  
...  
Keyword(s):  
Lactococcus Lactis ◽  
Low Dose ◽  
Diabetic Mice ◽  
Intestinal Delivery

scholarly journals Specificity in the activation and inhibition by flavonoids of benzo[a]pyrene hydroxylation by cytochrome P-450 isozymes from rabbit liver microsomes.

1981 ◽  
Vol 256 (21) ◽  
pp. 10897-10901 ◽  
Author(s):  
M.T. Huang ◽  
E.F. Johnson ◽  
U. Muller-Eberhard ◽  
D.R. Koop ◽  
M.J. Coon ◽  
...  
Keyword(s):  
Liver Microsomes ◽  
Rabbit Liver ◽  
Cytochrome P 450

scholarly journals Rotation of cytochrome P-450. I. Investigations of protein-protein interactions of cytochrome P-450 in phospholipid vesicles and liver microsomes.

1982 ◽  
Vol 257 (12) ◽  
pp. 7023-7029 ◽  
Author(s):  
S Kawato ◽  
J Gut ◽  
R J Cherry ◽  
K H Winterhalter ◽  
C Richter
Keyword(s):  
Protein Interactions ◽  
Liver Microsomes ◽  
Phospholipid Vesicles ◽  
Protein Protein Interactions ◽  
Cytochrome P 450

scholarly journals Ethanol Oxidation by a Component of Liver Microsomes Rich in Cytochrome P-450

1973 ◽  
Vol 248 (4) ◽  
pp. 1183-1187
Author(s):  
Esteban Mezey ◽  
James J. Potter ◽  
W. Douglas Reed
Keyword(s):  
Ethanol Oxidation ◽  
Liver Microsomes ◽  
Cytochrome P 450

scholarly journals 25-hydroxylation of C27-steroids and vitamin D3 by a constitutive cytochrome P-450 from rat liver microsomes.

1983 ◽  
Vol 258 (11) ◽  
pp. 6777-6781 ◽  
Author(s):  
S Andersson ◽  
I Holmberg ◽  
K Wikvall
Keyword(s):  
Rat Liver ◽  
Vitamin D3 ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Cytochrome P 450

Renoprotective effects of a novel Nox1/4 inhibitor in a mouse model of Type 2 diabetes

2012 ◽  
Vol 124 (3) ◽  
pp. 191-202 ◽  
Author(s):  
Mona Sedeek ◽  
Alex Gutsol ◽  
Augusto C. Montezano ◽  
Dylan Burger ◽  
Aurelie Nguyen Dinh Cat ◽  
...  
Keyword(s):  
Body Weight ◽  
Low Dose ◽  
Transforming Growth Factor ◽  
Disease Process ◽  
Thiobarbituric Acid ◽  
Transforming Growth Factor Β ◽  
Mitogen Activated Protein Kinase ◽  
High Dose ◽  
Diabetic Mice ◽  
Mitogen Activated Protein

Nox (NADPH oxidase)-derived ROS (reactive oxygen species) have been implicated in the development of diabetic nephropathy. Of the Nox isoforms in the kidney, Nox4 is important because of its renal abundance. In the present study, we tested the hypothesis that GKT136901, a Nox1/4 inhibitor, prevents the development of nephropathy in db/db (diabetic) mice. Six groups of male mice (8-week-old) were studied: (i) untreated control db/m, (ii) low-dose GKT136901-treated db/m (30 mg/kg of body weight per day), (iii) high-dose GKT136901-treated db/m (90 mg/kg of body weight per day), (iv) untreated db/db; (v) low dose GKT136901-treated db/db; and (vi) high-dose GKT136901-treated db/db. GKT136901, in chow, was administered for 16 weeks. db/db mice developed diabetes and nephropathy as evidenced by hyperglycaemia, albuminuria and renal injury (mesangial expansion, tubular dystrophy and glomerulosclerosis). GKT136901 treatment had no effect on plasma glucose or BP (blood pressure) in any of the groups. Plasma and urine TBARSs (thiobarbituric acid-reacting substances) levels, markers of systemic and renal oxidative stress, respectively, were increased in diabetic mice. Renal mRNA expression of Nox4, but not of Nox2, increased, Nox1 was barely detectable in db/db. Expression of the antioxidant enzyme SOD-1 (superoxide dismutase 1) decreased in db/db mice. Renal content of fibronectin, pro-collagen, TGFβ (transforming growth factor β) and VCAM-1 (vascular cell adhesion molecule 1) and phosphorylation of ERK1/2 (extracellular-signal-regulated kinase 1/2) were augmented in db/db kidneys, with no change in p38 MAPK (mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase). Treatment reduced albuminuria, TBARS and renal ERK1/2 phosphorylation and preserved renal structure in diabetic mice. Our findings suggest a renoprotective effect of the Nox1/4 inhibitor, possibly through reduced oxidative damage and decreased ERK1/2 activation. These phenomena occur independently of improved glucose control, suggesting GKT136901-sensitive targets are involved in complications of diabetes rather than in the disease process.

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