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N Begum

Publications and source records attributed to N Begum.

65 records · Page 4Linked to original sources
PubMed1984

Mechanisms of the fasting-induced dissociation of insulin binding from its action in isolated rat hepatocytes.

Fasting leads to an increase in insulin binding to isolated rat hepatocytes from 12 to 17%. This increase was accounted for by changes in the affinity of insulin receptors without alteration in their number. In contrast, the responsiveness of hepatocytes to insulin was markedly diminished in fasted rats. Both basal and insulin-stimulated rates of 14C-glucose incorporation into glycogen were significantly decreased in fasted animals. When insulin-induced 14C-glucose incorporation into glycogen was expressed as a percent above the basal rate, hepatocytes isolated both from control and fasted animals showed the same magnitude of maximal response (66 +/- 13% in fed and 59 +/- 12% in fasted animals, respectively). However, more insulin must be bound to hepatocytes isolated from fasted animals in order to elicit the same percent of insulin's maximal effect. Incubation of 'fed' hepatocytes in the serum obtained from fasted rats significantly diminished their responsiveness to insulin. An addition of insulin (100 ng/ml), glucose (10 mM) and antibodies to glucagon (1:100) eliminated the inhibitory effect of 'fasted' serum on 'fed' hepatocytes. A 48-hour fast increased significantly the microviscosity (decreased fluidity) of hepatocyte plasma membranes and altered membrane phospholipid composition. These changes correlated with enhanced insulin binding to isolated membranes. Moreover, in response to insulin, plasma membranes isolated from 'fasted' hepatocytes generated only one half the amount of the second messenger (PDH activator) observed in membranes of fed animals. The amount of PDH activator generated by incubation of plasma membranes with insulin correlated inversely with both insulin binding and membrane microviscosity. We conclude that 1) fasting induces both coupling defect and post-receptor changes in insulin's action; 2) both extracellular and intracellular factors contribute to fasting-induced dissociation of insulin binding from insulin action; 3) insulin/glucagon ratio may influence hepatocyte responsiveness to insulin; 4) alterations in plasma membrane fluidity and phospholipid composition may alter insulin binding and contribute to its dissociation from the subsequent action; 5) membranes isolated from 'fasted' hepatocytes generate less mediator of insulin action than do membranes isolated from 'fed' hepatocytes.

Animals↗
PubMed1984

Effect of dexamethasone on adipose tissue and liver pyruvate dehydrogenase and its stimulation by insulin-generated chemical mediator.

Rats were treated with dexamethasone (50 micrograms/day, sc) for 4 days. Total pyruvate dehydrogenase (PDH) and insulin-stimulated PDHa activities were decreased in fat pads from dexamethasone-treated rats compared to control values. Coincubation experiments with adipocyte mitochondria, plasma membrane, and insulin demonstrated decreased stimulation of PDH in preparations from dexamethasone-treated rats. The responsiveness of the mitochondrial PDH system to insulin and control rat plasma membranes was not different in glucocorticoid-treated adipocyte preparations compared to controls. Liver mitochondria from dexamethasone-treated rats demonstrated decreased basal enzyme activity and a decreased percentage of stimulation of PDH when supernatants from insulin-exposed liver particulate fractions were tested. These experiments suggest that insulin resistance produced by glucocorticoid treatment, like that resulting from fat feeding, is accompanied by a decrease in the capacity of adipocyte and liver plasma membranes to generate PDH activator in response to insulin.

Adipose Tissue↗
PubMed1983

Decreased insulin-generation of pyruvate dehydrogenase inhibitor in insulin resistant states.

Insulin resistance produced in rats by feeding a high fat diet or by dexamethasone administration (50 micrograms/day, sc for 4 days) resulted in 50-70% decrease in the generation of pyruvate dehydrogenase inhibitor by insulin exposed liver particulate fractions. The inhibition was dose dependent. Treatment of insulin mediator preparations with neuraminidase and B-D-galactosidase resulted in inactivation of the pyruvate dehydrogenase inhibitor. Presence of exogenous enzyme substrates during enzyme digestion partially protected the inhibitor from inactivation. Protease treatment did not affect the inhibitor while the stimulatory activity of the insulin mediator was abolished by trypsin treatment. These results together with the previous report suggest that insulin resistance results in a decrease in the generation of both of the mediators of insulin action. This may result from a decrease in insulin binding, shown earlier, or from a decrease in precursor availability.

Animals↗
PubMed1983

Effects of high fat and high carbohydrate diets on liver pyruvate dehydrogenase and its activation by a chemical mediator released from insulin-treated liver particulate fraction: effect of neuraminidase treatment on the chemical mediator activity.

Rats were fed a high fat diet or a high glucose diet for 5-7 days. Basal pyruvate dehydrogenase activity (both the active form and the total enzyme activity) was decreased in liver homogenates from fat diet-adapted rats as compared to those fed the glucose diet. Supernatants from insulin-exposed liver particulate fractions from fat-fed rats showed decreased stimulation of pyruvate dehydrogenase activity as compared to those from glucose-fed rats. There was no difference in the response of the mitochondria from the two groups when they were stimulated by supernatants from insulin-treated liver particulate fractions from stock diet-fed rats. Liver particulate fractions from fat-fed rats showed decreased generation of the chemical activator in response to Concanavalin A and trypsin stimulation. This suggests that fat feeding results in a decrease in membrane protease substrate availability. Treatment of the insulin mediator with neuraminidase and beta-D-galactosidase resulted in inactivation of the mediator. Presence of exogenous enzyme substrates during enzyme digestion protected the mediator from inactivation, suggesting that carbohydrate residues are important in the action of the insulin mediator. This fat diet-induced decrease in the generation of a chemical mediator of insulin action may result from 1) a decrease in insulin binding, shown earlier; 2) a decrease in the amount of protease substrate; and 3) an alteration in its carbohydrate composition, which is important in its ability to activate pyruvate dehydrogenase.

Animals↗
PubMed1982

Effect of high fat and high carbohydrate diets on adipose tissue pyruvate dehydrogenase and its activation by a plasma membrane-enriched fraction and insulin.

Rats were fed a high lard diet or a high glucose diet for 5--7 days. Basal and insulin-stimulated epididymal fat pad pyruvate dehydrogenase (PDH) activities were decreased in fat diet-adapted rats compared to those fed the glucose diet. When adipocyte plasma membranes and mitochondria were incubated together with and without insulin, it was found that the insulin stimulation of PDH activity was lower in preparations from fat-fed rats on both an absolute and percentage basis. Supernatant fractions from insulin-stimulated glucose-fed rat plasma membranes activated mitochondrial PDH to a greater extent than those from lard-fed rat preparations. There was no difference in the response of mitochondria from the two groups when they were stimulated by insulin-treated plasma membranes from stock diet-fed rat adipose tissue. These experiments suggest that fat feeding results in adaptive changes in adipocyte plasma membranes which are involved in the generation of the insulin-stimulated chemical activator of PDH. This adaptive change is in addition to those described earlier.

Adipose Tissue↗
PubMed1982

Effects of high carbohydrate and high fat diets on rat adipose tissue pyruvate dehydrogenase responses to concanavalin A and spermine.

Rats were fed a high lard diet or a high glucose diet for 5-7 days. Basal and Concanavalin A (Con A)-stimulated epididymal fat pad pyruvate dehydrogenase (PDH) activities were decreased in fat diet-adapted rats compared to those fed the glucose diet. When adipocyte plasma membranes and mitochondria were coincubated with and without Con A, it was found that the lectin stimulation of PDH activity was lower in preparations from fat-fed rats. These results are comparable to our earlier observations with insulin on adipose tissue PDH. Spermine also stimulated PDH in whole adipose tissue pieces in both the absence and presence (0.5 mM) of medium glucose. The spermine stimulation of PDH in adipose tissue was decreased in fat-fed rats. In contrast to Con A, spermine failed to stimulate PDH in a cell-free system. This suggests that spermine activation of PDH in adipose tissue does not involve the generation of the second messenger responsible for the effects of insulin and Con A. The hypothesis was further substantiated by the findings that (1) the insulin and spermine effects were additive in whole adipose tissue and also in adipocytes, and (2) the spermine effect on fat cells was not significantly inhibited by protease inhibitors, which abolish the effects of insulin on fat cell PDH. The fat-induced decreases in response to Con A and spermine involve not only an adaptive change in the ability of the plasma membrane to generate the chemical modulator of PDH but are also related to postreceptor events.

Adipose Tissue↗
PubMedDate not supplied

Prevalence and management of ovarian tumours in Women and Children Hospital Abbottabad.

BACKGROUND: The purpose of study was to compare world incidence of ovarian tumours whether benign or malignant with that of our unit. We have also discussed management of all these patients at our center. RESULTS: In our unit out of total 1400 admissions in 24 months, 26 had ovarian tumours, out of these 6 were malignant. The over all malignancy in our unit was 23% as compared to 15% of over all world incidence, 24 of these patients, were admitted through the OPD with advanced size of tumours. None of them previously had any check up at proper Gynaecological Centers. All these 24 were admitted to the ward, investigated, operated and after receiving histopathology reports were further managed accordingly. Two patients had torsion of ovarian tumour and were admitted through emergency and operated as emergency cases. In our study group the majority, 77% had benign ovarian tumours in which simple salpingoophorectomies was performed.

Adolescent↗