Search PubMed⌕ Search

Biomedical subjects

J H Shah

Publications and source records attributed to J H Shah.

At least 37 records · Page 2Linked to original sources
PubMed1986

Symptomatic reactive hypoglycemia during glucose tolerance test in lithium-treated patients.

Glucose, insulin, glucagon, and cortisol responses during a five-hour oral glucose tolerance test (GTT) were evaluated in nine patients with bipolar affective disorders who were receiving lithium treatment and in seven control patients with bipolar affective disorders who were not receiving any treatment. Both the lithium-treated and the control patients were in stable mood at the time of GTT. During GTT mean nadir serum glucose of 48 +/- 2 mg/dL in the lithium-treated patients was significantly lower (P less than 0.001) than mean nadir serum glucose of 62 +/- 2 mg/dL observed in the control subjects. Seven of these nine lithium-treated patients, but none of the control patients, experienced hypoglycemic symptoms coinciding with low serum glucose concentration. In response to hypoglycemia, mean serum cortisol significantly rose (P less than 0.01) to 22 +/- 3 micrograms/dL in the lithium-treated patients, whereas mean serum cortisol levels gradually declined to 10 +/- 2 micrograms/dL in the control patients at 300 minutes. Despite symptomatic postglucose hypoglycemia, plasma glucagon levels in the lithium-treated patients were similar to those observed in the control patients. These findings suggest that chronic lithium treatment is associated with a symptomatic and biochemical hypoglycemia during GTT, which is characterized by a rise in serum cortisol but by lack of appropriate rise in plasma glucagon concentrations.

Adult↗
PubMed1980

The effect of lithium on glucose- and tolbutamide-induced insulin release and glucose tolerance in the intact rat.

The effects of lithium on stimulus-induced insulin release and glucose tolerance were examined in intact, unanesthetized, and unrestrained rats with indwelling intravascular catheters. In the first study, a 150-mg iv glucose pulse was administered at 30 min after rapid iv injection of lithium carbonate (1 meq/kg) or vehicle. After the glucose pulse, mean serum glucose levels throughout the observation period were significantly greater in the lithium-treated rats than in the vehicle-treated (control) rats. Similarly, a mean glucose disappearance rate of 2.8 +/- 0.2%/min in the lithium-treated rats was significantly less (P < 0.02) than the mean glucose disappearance rate of 3.4 +/- 0.2%/min observed in the control rats. In response to glucose pulse, acute insulin release was significantly inhibited in the lithium-treated rats compared with that observed in the control rats. In the second study, a 10-mg tolbutamide pulse was administered 30 min after a rapid iv injection of lithium carbonate or vehicle. Acute insulin release in response to tolbutamide pulse was markedly inhibited in the lithium-treated rats compared with that observed in the control rats. In lithium-treated rats, the decline in serum glucose between 10-45 min after the tolbutamide pulse was significantly less than that observed in the control rats. Therefore, in the intact rat, lithium inhibits glucose- and tolbutamide-induced insulin release, which, in turn, causes glucose intolerance and prevents tolbutamide-induced hypoglycemia.

Animals↗
PubMed1978

Impairment of glucose-induced insulin secretion and glucose tolerance during colchicine treatment.

The effect of acute and chronic colchicine treatment on glucose-induced immunoreactive insulin secretion and glucose tolerance was examined in fasting, unanesthetized, and unrestrained rats with indwelling jugular vein and aortic catheters. In the first study, intravenous glucose tolerance tests were performed by rapidly administering a glucose pulse (150 mg. intravenously) one hour after acute treatment with colchicine (0.5 mg. per kilogram of body weight, intravenously) or vehicle (control). Acute colchicine treatment caused significant suppression of glucose-induced insulin secretion and also markedly impaired glucose disappearance rates. In the second study, chronic colchicine treatment (in the lower dose of 0.2 mg. per kilogram of body weight, intraperitoneally, daily for 10 days) caused significant suppression of biphasic insulin secretion in response to a primed-constant glucose infusion (150 mg. of glucose pulse followed by 6 mg. per minute constant glucose infusion for 60 minutes) as compared with control rats (vehicle injection, intraperitoneally, daily for 10 days). Due to this marked decrease in biphasic insulin secretion, serum glucose concentrations were significantly higher between 10 and 45 minutes in the colchicine-treated rats than in the control rats. Therefore, acute and chronic colchicine treatment causes marked inhibition of glucose-induced insulin secretion and impairment of glucose tolerance in the intact rat. These observations suggest there is a need to evaluate carbohydrate metabolism in patients receiving colchicine treatment.

Animals↗
PubMed1977

A method for studying acute insulin secretion and glucose tolerance in unanesthetized and unrestrained rats. The effect of mild stress on carbohydrate metabolism.

A technique is described for glucose infusions and for frequent sampling of small quantities of blood in unrestrained and unanesthetized small laboratory animals. Under pentobarbital anesthesia, polyethylene catheters were implanted into the jugular vein and the aorta, and distal ends were exteriorized on the back of the neck of 250-gm. rats. Five to seven days following surgery the rats regained weight and were in a normal anabolic state, despite indwelling catheters. On the day of the intravenous glucose tolerance test (ivGTT), the exterior ends of the indwelling jugular and aortic catheters were connected to specially prepared extension catheters, through which a glucose pulse was given and frequent blood samples in small quantities were collected, respectively. During the entire procedure, the animals were resting quietly, unrestrained and unanesthetized. In another group of similar rats with indwelling catheters, ivGTT was performed after they were restrained in plastic restrainers. During the ivGTT, serum glucose levels were significantly higher in the restrained rats than those observed in the control rats. The mean glucose disposal rate (K) of 2.2 +/- 0.2 was significantly slower in restrained rats than the K of 3.0 +/- 0.3 in unrestrained rats. Following the glucose pulse, insulin secretion was significantly lower in restrained rats than that observed in the unrestrained rats. These observations emphasize the importance of controlling the modifying effects of mild stress on glucose tolerance and insulin secretion.

Animals↗
PubMed1977

Effect of ethanol on stimulus-induced insulin secretion and glucose tolerance. A study of mechanisms.

The effect of ethanol on stimulus-induced insulin secretion was studied, and possible mechanisms were examined in fasting unanesthetized and unrestrained rats with indwelling jugular and aortic catheters. Glucose (150 mg.) or tolbutamide (10 mg.) was given rapidly, i.v., one hour after agavage of ethanol or saline (control). Acutely, ethanol treatment caused marked inhibition of glucose-induced insulin secretion and impaired glucose disappearance rate. Tolbutamide-induced insulin secretion was also significantly inhibited, and decline in glucose was significantly less in ethanol-treated rats. In response to ethanol, serum calcium concentration significantly declined for two hours. In another study, an ethanol metabolite, acetate (0.4 micronmole/min.) or vehicle (control) was infused for 60 minutes prior to 150 mg. glucose pulse. Acetate priming significantly potentiated glucose-induced insulin secretion and also improved glucose tolerance. It is proposed that (1) ethanol in vivo acutely induces hypocalcemia, which inhibits glucose- and tolbutamide-induced insulin secretion--which, in turn, causes glucose intolerance and prevents tolbutamide-induced hypoglycemia. (2)Acetate might be the actual petentiating influence on glucose-induced insulin secretion observed several hours after ethanol treatment.

Acetates↗
PubMed1975

Stimulation of the secretion of parathyroid hormone during hypoglycemic stress.

The effect and the mechanism of insulin-induced hypoglycemic stress on parathyroid hormone (PTH) secretion in man was evaluated. Porcine crystalline insulin (0.1 U/kg,iv) caused symtomatic hypoglycemia in all subjects. The maximum hypoglycemia occurred between 25 and 35 min following the insulin administration. A significant increase in the serum PTH concentration occurred promptly at 5 min following the time of maximum hypoglycemia, achieving peak levels between 5 and 15 min. Thereafter the serum PTH concentration gradually declined, reaching baseline values of 60 min. Serum cortisol levels were increased, but not until 30 min following the maximum hypoglycemia, and remained significantly elevated at 60 min. Therefore the stimulation of PTH secretion was not caused by elevated levels of serum cortisol. The serum calcium and magnesium levels remained unchanged throughout the procedure. A significant and sustained decline in the serum inorganic phosphate levels occurred following insulin administration. The results indicate that hypoglycemic stress stimulates PTH secretion, presumably via increased epinephrine levels, and further suggest that adrenergic stimuli play an important role in the physiology of PTH secretion.

Adult↗
PubMed1975

Insulin metabolism in hypothyroidism.

Insulin resistance has been invoked to explain the glucose intolerance observed in hypothyroid patients. This possibility was studied by determining fractional and metabolic clearances of intravenously administered porcine crystalline insulin (0.1 U./kg.) and its effect on plasma glucose concentration in ten hypothyroid patients, ten normal subjects, and six treated euthyroid patients. Following administration of porcine insulin, serum immunoreactive insulin concentrations during the period of observation were similar in hypothyroid patients, in normal control subjects, and in treated euthyroid patients. Similarly, no significant differences in the mean half-life, distribution space, or fractional and metabolic clearances of insulin were observed among any of the three groups. In response to insulin administration, plasma glucose concentrations declined to the nadir of 36 +/- 4, 43 +/- 3, and 38 +/- 4 mg. per 100 ml. in hypothyroid patients, normal control subjects, and treated euthyroid patients, respectively. Thereafter, plasma glucose steadily increased and approached the baseline value at ninety minutes in normal subjects and treated euthyroid patients. In contrast, the plasma glucose values remained significantly lower than the baseline for the rest of the procedure in hypothyroid patients. The present study demonstrates that there is no evidence of resistance to the action of insulin in hypothyroid patients. The observation of prolonged hypoglycemic action of exogenously administered insulin in hypothyroid patients might in fact suggest increased sensitivity to insulin action. These findings indicate that glucose intolerance of the hypothyroid state is not characterized by insulin resistance.

Antigens↗