scholarly journals In vivo and in vitro effect of p-chlorophenoxyisobutyrate on insulin binding and glucose transport in isolated rat adipocytes.

1985 ◽  
Vol 32 (6) ◽  
pp. 829-836
Author(s):  
NOBUAKI WATANABE ◽  
MASASHI KOBAYASHI ◽  
HIROSHI MAEGAWA ◽  
OSAMU ISHIBASHI ◽  
YASUMITSU TAKATA ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Insulin Binding ◽  
Rat Adipocytes ◽  
Vitro Effect ◽  
Isolated Rat

Effect of purified phospholipases on glucose transport, insulin binding, and insulin action in isolated rat adipocytes

1982 ◽  
Vol 4 (4) ◽  
pp. 261-271 ◽  
Author(s):  
Tj. Wieringa ◽  
G. Bruin ◽  
W. P. M. Meerwijk ◽  
H. M. J. Krans
Keyword(s):  
Glucose Transport ◽  
Insulin Action ◽  
Insulin Binding ◽  
Rat Adipocytes ◽  
Isolated Rat

The in vitro effect of corticosterone on insulin binding and glucose metabolism in mouse skeletal muscles

1985 ◽  
Vol 63 (9) ◽  
pp. 1133-1138 ◽  
Author(s):  
M. H. Tan ◽  
A. Bonen
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Extensor Digitorum Longus ◽  
Insulin Binding ◽  
In Vivo Model ◽  
In Vitro System ◽  
Vitro Effect ◽  
Contralateral Muscle

We studied the in vitro effect of corticosterone on insulin binding, uptake of 2-deoxy-D-glucose, glycolysis, and glycogenesis in the soleus and extensor digitorum longus (EDL) of Swiss–Webster mice. In each experiment, one muscle (soleus/EDL) was incubated with corticosterone (0.1, 1, 50, and 100 μg/mL) and the respective contralateral muscle was incubated without corticosterone, but at the same insulin and pH levels. Corticosterone did not affect insulin binding in both muscles. However, corticosterone decreased the uptake of 2-deoxy-D-glucose and the rate of glycolysis and glycogenesis in both muscles when the dose was pharmacologic (50 and 100 μg/mL), but not when it was physiologic (0.1 and 1 μg/mL). For glycolysis and glycogenesis, the suppression was greater in the EDL when compared with the soleus. This suppression was seen in both basal and insulin-stimulated conditions. In this in vitro system, where the experimental muscle is not exposed to prior hyperinsulinemia as in the in vivo model, corticosterone, at pharmacologic doses, affects postreceptor events without altering the insulin binding in the skeletal muscle.

Metformin ameliorates extreme insulin resistance in a patient with anti-insulin receptor antibodies: description of insulin receptor and postreceptor effects in vivo and in vitro

1992 ◽  
Vol 126 (2) ◽  
pp. 117-123 ◽  
Author(s):  
Salvatore Di Paolo
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Glucose Transport ◽  
Insulin Binding ◽  
Severe Insulin Resistance ◽  
Binding Data ◽  
Extreme Insulin Resistance ◽  
Receptor Antibodies

The effect of metformin on insulin binding and insulin action in the presence of anti-insulin receptor antibodies was investigated in a case of type B extreme insulin resistance. Oral administration of metformin (1 500 mg/d) for 10 days significantly decreased plasma blood glucose and insulin levels and enhanced the hypoglycemic response to exogenous insulin. In vitro preincubation of normal erythrocytes with insulin receptor antibody from the patient plus 4× 10−5 mol/l metformin markedly enhanced insulin binding to receptors, compared to cells incubated with antibody alone. This effect was apparent after 2 h, was maximal after 4 h and did not change up to 24 h. Closely similar results were found when human adipocytes were studied. Analysis of binding data confirmed the increase in both receptor number and affinity. One hour exposure of control adipocytes to metformin enhanced basal lipogenesis by more than 30%. Acute exposure of fat cells to the patient's receptor antibodies resulted in a stimulation of glucose transport and a state of severe insulin resistance. The addition of metformin to antibody in preincubation buffer strongly enhanced basal glucose incorporation into lipids, but did not prevent insulin unresponsiveness. It is suggested that metformin increases, possibly through a change in the spatial conformation of insulin receptor within the plasma membrane, the availability of preexisting receptors to insulin binding and/or decreases the availability of specific epitopes to antibody anchoring. Further, in the model of insulin resistance described here, metformin enhanced the basal rate of glucose transport through a direct insulin-mimicking activity and/or a potentiation of the sensitivity of glucose transport to the antibody.

Insulin binding and glucose transport activity in cardiomyocytes of a diabetic rat

1986 ◽  
Vol 250 (4) ◽  
pp. E402-E406 ◽  
Author(s):  
E. C. Almira ◽  
A. R. Garcia ◽  
B. R. Boshell
Keyword(s):  
Glucose Transport ◽  
Insulin Binding ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Heart Cells ◽  
Apparent Difference ◽  
Insulin Effect ◽  
Streptozotocin Induced Diabetes

We studied insulin binding and glucose transport in isolated adult cardiomyocytes from rats with 2-wk streptozotocin-induced diabetes. At 37 degrees C, cells from diabetic rats bound less 125I-insulin and exhibited lower rates of 3-O-methylglucose transport than cells from control rats. In contrast, the amount of 125I-insulin bound to myocytes at 4 degrees C was the same in both groups. Preincubation of cells from both groups with 10-10,000 ng/ml insulin significantly increased their basal rates of glucose transport by approximately 40%. However, the augmented rates in diabetics were still approximately 36% lower than the corresponding insulin-stimulated rates in the controls. When the glucose transport data were expressed as percent maximal insulin effect and plotted as a function of the amount of insulin bound, the curves obtained from both diabetic and nondiabetic controls were superimposable. These data demonstrate that 1) heart cells from diabetic rats bind less insulin than from control rats under conditions in which they exhibit impaired glucose transport rates, 2) there is no apparent difference in total receptor number between the two groups, but internalization of intact insulin appears to be diminished in diabetes, 3) coupling exists between insulin binding and glucose transport in both groups, and 4) these impaired processes are completely reversed by insulin treatment in vivo but not in vitro.

Effect of cicletanine on renal cGMP production

1998 ◽  
Vol 76 (12) ◽  
pp. 1151-1155
Author(s):  
J M Valdivielso ◽  
A I Morales ◽  
F Pérez-Barriocanal ◽  
J M López-Novoa
Keyword(s):  
Urinary Excretion ◽  
Wistar Rats ◽  
Urinary Flow ◽  
Oral Gavage ◽  
Cgmp Production ◽  
Vitro Effect ◽  
Isolated Rat ◽  
Do So

The aim of the present study was to assess the effect of cicletanine on renal cGMP production. To do so we measured mean arterial pressure (MAP), creatinine clearance (CC), and urinary excretion of electrolytes and cGMP under basal conditions and after 6 h of cicletanine administration (10 and 15 mg/kg body weight by oral gavage) in conscious Wistar rats. Also, the in vitro effect of cicletanine was assessed by incubating renal slices and isolated rat glomeruli with two concentrations of cicletanine (0.1 and 1 mM) for different times (1, 2, 5, and 30 min) in the presence of 3-isobutyl-1-methylxanthine. Oral administration of cicletanine induced an increase in urinary flow (V) and the urinary excretion of electrolytes and cGMP, with no changes in CC. In addition, a significant decrease in MAP was observed, but only with the lower dose. Incubation with cicletanine did not induce significant changes in cGMP production in glomeruli or renal slices. These results show that cicletanine, administered in vivo at diuretic and antihypertensive doses, induces an increase in urinary cGMP excretion.Key words: cicletanine, cGMP, renal glomeruli.

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