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Biomedical subjects

D G Patel

Publications and source records attributed to D G Patel.

At least 37 records · Page 2Linked to original sources
PubMed1984

Lack of relationship between plasma insulin and glucagon levels and angiographically-documented coronary atherosclerosis.

In 120 consecutive patients undergoing diagnostic coronary arteriography, fasting blood glucose, plasma insulin, glucagon, serum cholesterol and triglyceride concentrations were measured. The insulin-glucose ratio and insulin-glucagon ratio were calculated. Forty-five patients had normal coronary arteries, 19 had single vessel coronary artery disease and 56 patients had multiple vessel disease. Fasting blood glucose was greater than 120 mg/100 ml in 37 patients (group A) and included 9 of the 10 known diabetics, 3 of whom were being treated with insulin. Seventy-seven patients included in group B had fasting blood glucose concentration less than 120 mg/100 ml. Patients with multiple vessel coronary disease in either group had higher blood glucose and cholesterol concentrations than those with normal coronary arteries or the ones with single vessel disease, but they did not have higher plasma insulin or glucagon levels nor increased insulin-glucose or insulin-glucagon ratios. With comparable extent of coronary artery disease patients in group A had higher plasma insulin levels and insulin-glucagon ratios than those in group B, but no correlation exists between the presence or extent of coronary atherosclerosis and these variables in either group. Thus, neither fasting plasma insulin level nor insulin-glucagon ratio predicts the status of underlying coronary atherosclerosis in either diabetics or nondiabetics.

Blood Glucose↗
PubMed1984

Role of parasympathetic nervous system in glucagon response to insulin-induced hypoglycemia in normal and diabetic rats.

Effects of cholinergic mechanisms on glucagon and epinephrine responses to insulin-induced hypoglycemia were examined in diabetic and age-matched control male rats. Atropine did not affect plasma glucose levels or plasma glucagon concentrations, in the basal state, in normal or short-term diabetic rats (10 to 15 days following streptozotocin injection). However, atropine blocked the glucagon response to insulin hypoglycemia in both normal and short-term diabetic rats. Subcutaneous injection of carbachol also failed to alter basal plasma glucose, glucagon, or epinephrine values in both normal and diabetic rats. The lack of glucagon and epinephrine responses to insulin hypoglycemia in long-term diabetic rats (80 to 100 days after streptozotocin injection) was reversed with a single dose of carbachol. Carbachol exaggerated the glucagon response to insulin hypoglycemia in normal and short-term diabetic rats. These results demonstrate that the parasympathetic nervus system plays an important role in the glucagon release in response to insulin hypoglycemia in rats. The lack of glucagon response to insulin hypoglycemia observed in long-term diabetic rats could be due to deteriorated parasympathetic nervous system and also could be corrected with carbachol.

Animals↗
PubMed1984

Role of sympathetic nervous system in glucagon response to insulin hypoglycemia in normal and diabetic rats.

The effects of adrenergic blockers on the glucagon response to insulin hypoglycemia were investigated in diabetic (10-15 days poststreptozocin [STZ] injection) and age-matched control rats. alpha-(Phentolamine nonspecific but predominantly alpha 1), alpha 2-(yohimbine), or beta-(propranolol) adrenergic blockers alone or in combination did not affect plasma glucose levels or plasma glucagon concentrations, in the basal state, in either control or diabetic rats. None of these adrenergic blockers, alone or in combination, inhibited the glucagon response to insulin hypoglycemia in control or diabetic rats. On the contrary, in control rats, the beta-adrenergic blocker alone or in combination with an alpha-adrenergic blocker and in diabetic rats, the alpha-adrenergic blocker alone significantly stimulated the glucagon response to insulin hypoglycemia. Second, the effects of yohimbine on the glucagon response to epinephrine infusion were studied in both young and old rats. Recently, Cherksey et al. (Proc. Soc. Exp. Biol. Med. 1982; 171:196-200) have reported that the adrenergic receptors on rat pancreatic islet cells are of the alpha 2-subtype. Yohimbine (alpha 2-adrenergic blocker) completely blocked the glucagon response to epinephrine infusion in both young and old rats, but had no inhibitory effect on the glucagon response to insulin hypoglycemia in control and short-term diabetic rats. From these observations, it could be inferred that the lack of glucagon response to insulin hypoglycemia in long-term diabetic rats is unlikely to be explained by an impairment of an adrenergic function.

Animals↗
PubMed1984

Immunochemical studies of the insulin-like material in the parotid gland of rats.

Through the use of radioimmunoassay and immunocytochemical techniques, it was found that the parotid glands of male rats possess a population of cells that contain an insulin-like substance. These cells were situated mainly in groups along the intercalated ducts of the gland, or less frequently as isolated cells dispersed throughout the acini. No cells displaying insulin-like immunoreactivity were observed in the striated or main excretory ducts of the parotid. After intravenous (i.v.) injections of streptozotocin (STZ) there was a marked depletion of insulin from the pancreatic islets of rats having diabetes for a 3-27-day interval. Although this cytotoxin also reduced the amount of insulin extractable from the parotid, it did not destroy the insulin-like immunoreactive cells found in this gland. The results of this study suggest that the parotid may be an important source of extrapancreatic insulin. Moreover, these findings indicate that insulin-immunoreactive cells of this salivary gland are spared from the cytotoxic action of STZ.

Animals↗
PubMed1983

Effect of prolonged insulin treatment on blunted plasma catecholamine and glucagon increase during insulin hypoglycemia in streptozotocin diabetic rats.

The role of prolonged insulin treatment of diabetic rats on the lack of glucagon and catecholamine increases in response to insulin-hypoglycemia was investigated. Streptozotocin diabetic rats were maintained in a normoglycemic state for a long period by intraperitoneal constant infusion of insulin with the Alzet osmotic minipumps. Hyperglucagonemia observed in diabetic rats was normalized with insulin treatment. However, the blunted response of glucagon during insulin-hypoglycemia was not altered with insulin treatment. On the other hand, in diabetic rats the diminished catecholamine response to insulin-induced hypoglycemia was rendered normal after insulin treatment. The data indicate that the lack of glucagon and catecholamine responses in diabetic rats in response to insulin-hypoglycemia can vary independently. The persistent decreased glucagon response in normoglycemic diabetics could be the cause of their impaired recovery from hypoglycemia.

Animals↗
PubMed1983

Lack of glucagon response to hypoglycemia in long-term experimental diabetic rats.

Glucagon and catecholamine responses to insulin-induced hypoglycemia were investigated in streptozotocin-diabetic rats at various times after streptozotocin administration and in age-matched control male rats. Diabetic rats had basal glucagon levels higher than those in control rats, while basal epinephrine and norepinephrine levels were essentially identical. As the duration of diabetes increased, the glucagon and epinephrine responses to insulin hypoglycemia decreased. The response of control rats was not correlated with age. Increases in plasma norepinephrine values in response to hypoglycemia were similar in both diabetic and control rats. The data indicate a concurrent impaired response of glucagon and epinephrine release in response to insulin-induced hypoglycemia in streptozotocin-diabetic rats as the duration of diabetes prolongs.

Aging↗
PubMed1983

Rate of insulin infusion with a minipump required to maintain a normoglycemia in diabetic rats.

It is notoriously difficult to normalize plasma glucose profiles for a prolonged time by conventional methods of insulin administration in both human and animal diabetics. The present study was conducted to determine the dosage of insulin needed to maintain prolonged and around-the-clock normoglycemia as well as normoglucagonemia in streptozotocin diabetic rats with the Alzet osmotic minipump which releases insulin constantly for 14 days. A minipump was inserted into the peritoneal cavity of diabetic rats under chloral hydrate anesthesia. Diabetic rats were treated with several consecutive minipumps and body weights, plasma glucose, and plasma glucagon levels were monitored. Plasma glucose concentrations were determined every 8 hr for several days and were found essentially identical during the active life of the minipump. An average insulin dose of 8.0 to 9.0 U/kg/day was required to normalize body weights, plasma glucose, and plasma glucagon of streptozotocin diabetic rats treated with the Alzet osmotic minipump Model 2002.

Animals↗
PubMed1982

Does uncomplicated diverticular disease produce symptoms?

A questionnaire dealing with bowel symptoms was administered to 97 outpatients referred for air-contrast barium enema. Subsequently, the barium enema was interpreted by a radiologist who did not know the results of the questionnaire. Forty-nine had normal x-rays, and 27 had uncomplicated diverticular disease. Weight loss, rectal bleeding, abdominal pain, and pain at night were as common in those with a normal examination as in those with diverticula. Symptoms of colon dysfunction included abdominal pain relieved by defecation, altered stool frequency and consistency with pain onset, abdominal distension, feeling of incomplete evacuation after defecation, and mucus in the stool. These were equally prevalent in both groups. Therefore, no symptoms could be ascribed to the presence of diverticula.

Abdomen↗
PubMed1982

Hypolipidemic and glycogenolytic effect of clofibrate (CPIB) in hypothyroid mice: role of insulin and glucagon.

1. The role of endogenous glucagon and insulin on the hypolipidemic and glycogenolytic effect of clofibrate was determined in the euthyroid and propylthiouracil (PTU)-induced hypothyroid mice. 2. PTU was fed in diet (0.15%) for 2 weeks and then clofibrate added to diet (0.25%) for 4 weeks. 3. Both PTU and clofibrate significantly increased liver weight but had no effect on kidney weight. PTU significantly decreased plasma triglycerides (TG) and increased cholesterol (Ch). 4. Clofibrate had a significant hypotriglyceridemic effect in both euthyroid and hypothyroid mice but did not affect plasma cholesterol. 5. Clofibrate decreased hepatic glycogen in euthyroid but not in hypothyroid mice. 6. Glucose-6-phosphatase activity was not affected by either PTU or clofibrate. 7. Neither PTU nor clofibrate affected hepatic TG or Ch. 8. Biliary lipid changes due to PTU treatment were reversed by clofibrate administration. 9. Since plasma insulin and glucagon levels were not affected by clofibrate in either euthyroid or hypothyroid mice, our results suggest that the hypotriglyceridemic and glycogenolytic effect of clofibrate is not mediated by changes in circulating insulin and glucagon ratio. 10. Moreover, while the glycogenolytic effect of clofibrate seems to be dependent, the hypotriglyceridemic effect seems to be independent of thyroid hormones.

Animals↗
PubMed1981

Hemostatic changes and postoperative deep-vein thrombosis associated with use of a pneumatic tourniquet.

In twenty patients who underwent a knee arthrotomy in which a pneumatic tourniquet was employed, there was a significant increase in fibrinolytic activity (measured by the amount of time for the lysis of euglobulin and by the fibrin-plate method) in the systemic circulation which peaked at fifteen minutes and lasted for thirty minutes after release of the tourniquet. No rebound occurred thereafter. The concentration of fibrinogen and the platelet count decreased and the concentration of the products of fibrin degradation increased after deflation of the tourniquet. Arterial PO2, PCO2, and pH were changed significantly. In contrast, fibrinolytic activity did not increase in patients undergoing operations on the lower extremity without a tourniquet. Deep-vein thrombosis developed in two patients who were treated with a tourniquet and in seven patients in whom a tourniquet was not used. We concluded that increased fibrinolytic activity, presumably mediated through enhanced release of plasminogen activator, might be partly responsible for the decreased incidence of venous thrombosis in the patients in this study for whom a tourniquet was used.

Adult↗
PubMed1980

Ethanol inhibition of insulin secretion by perifused rat islets.

In vivo and in vitro effects of ethanol on the kinetics of insulin secretion in response to glucose and tolbutamide were studied in perifused rat islets. Phases I and II insulin response to 16.7 mM glucose was decreased 46% and 48%, respectively, in islets of rats given ethanol intragastrically 1 g/kg 1 h prior to sacrifice. Mean blood ethanol levels at the time of animal sacrifice were 19.4 mmol/l. The magnitude of insulin suppression was not significantly enhanced with higher ethanol doses, 2 or 3 g/kg, although mean blood ethanol levels increased to 25.9 and 60.3 mmol/l, respectively. Similarly, significant inhibition of both phases of insulin response to glucose occurred when ethanol 1 or 3 g/kg was given intraperitoneally instead of orally. Ethanol had no effect on insulin secretion when given orally 4 h instead of 1 h prior to islet isolation. Ethanol, 65 mmol/l, added directly to rat islets perifusate simultaneously with 16.7 mM glucose decreased both phases I and II insulin response nearly half; whereas addition of 21.7 instead of 65 mmol/l ethanol had no effect. Pre-treatment of islets with 21.7 or 65 mmol/l ethanol during 30 min basal islets perifusion period had no effect on subsequent insulin response to 16.7 mM glucose. Insulin response to 10 mM tolbutamide was decreased nearly 81% by the simultaneous presence of 65 mmol/l ethanol in islets perifusate.

Administration, Oral↗
PubMed1979

Effect of ethanol and its metabolites on glucose mediated insulin release from isolated islets of rats.

Effects of ethanol and its metabolites, acetaldehyde and acetate, on insulin secretion were studied in isolated islets from normal rats. Addition of ethanol to the incubation media inhibited glucose mediated insulin release in a dose related manner. Prior exposure of islets to ethanol during the preincubation period had no influence on subsequent insulin response to either glucose or glucose plus ethanol. Acetaldehyde inhibited while sodium acetate potentiated insulin response to glucose. It is concluded that ethanol has a direct inhibitory effect on glucose mediated insulin release from rat islets.

Acetaldehyde↗
PubMed1976

Effects of ethanol on carbohydrate metabolism: I. Influence on oral glucose tolerance test.

To study the effect of ethanol on glucose tolerance test, a series of experiments were performed on Sprague-Dawley male rats weighing 250 g. After 18-hr fast, each rat was given, at random, the following test substances (one test substance at a time) intragastrically in a volume of 0.5 ml/100 g body weight: saline; glucose 0.75 g/kg (3 kcal); ethanol 0.4 g/kg (3 kcal); and ethanol with glucose. Saline or ethanol alone produced no significant changes in blood glucose or plasma insulin concentrations. Addition of ethanol to glucose load resulted in glucose intolerance as well as a lower and sluggish insulin response when compared to these with glucose load alone. The results suggest that ethanol per se has no effect on blood glucose or plasma insulin. However, when given together with glucose load, ethanol produces glucose intolerance as well as inhibition of glucose mediated insulin response.

Administration, Oral↗