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Biomedical subjects

R Dobbs

Publications and source records attributed to R Dobbs.

26 records · Page 2Linked to original sources

Effect of intravenously administered glucose on glucagon and insulin secretion during fat absorption.

The intravenous infusion of glucose was found to alter profoundly the response of insulin and glucagon to an intraduodenally administered fat meal in conscious dogs from that of dogs given only intravenous saline as a control. In the latter, insulin rose only 4 muu/ml and glucagon rose from 142 SEM plus or minus 8 to a peak of 221 pg/ml SEM plus or minus 50. When glucose was infused, raising plasma glucose above 173 mg/100 ml, the administration of fat was associated with a rise in mean insulin to 344 muu/ml, and glucagon remained suppressed by hyperglycemia to below baseline level, despite the fat meal. The peak insulin response to a fat meal plus glucose infusion was more than three times the peak level observed when glucose was infused alone without a meal or with a nonabsorbable intraduodenal volume load in the form of mineral oil. This suggests that the absorption of fat elicits an entero-insular signal that is greatly potentiated by exogenous glucose. These glucose-induced changes in the hormonal response to a fat meal may mediate certain of the metabolic effects of carbohydrates.

Animals↗

Heterogeneity of plasma glucagon immunoreactivity in normal, depancreatized, and alloxan-diabetic dogs.

Filtration of basal plasma from normal, alloxan-diabetic, and depancreatized dogs on Bio Gel P-10 yielded four glucagon-immunoreactive fractions. One of them appeared in the true glycagon area with the glucagon-125I (3500 mol vt). Of the other three, one appeared in the void volume (greater than 20000 mol wt), another just before the insulin-125I (congruent to 9000 mol wt), and the last one close to the salt peak (less than 2000 mol wt). The increase of total plasma glucagon immunoreactivity observed in depancreatized and alloxan diabetic dogs was mainly due to an increase in the 3500 and 9000 molecular-weight fractions. Arginine infusion in depancreatized dogs caused an increase in the 3500 molecular-weight fraction. Somatostatin or insulin infusion in depancreatized and alloxan-diabetic dogs resulted in disappearance of the 3500 molecular-weight fraction.

Animals↗

Cell contacts in human islets of Langerhans.

The freeze-fracturing technique was applied to fresh human islets of Langerhans. With this technique, the inside of cellular membranes was revealed, and specific membrane differentiations, hitherto unknown, were observed in the plasma membrane of the endocrine cells. The specific membrane differentiations represent two types of intercellular junctions, namely the tight junction, which determines a closure of the extracellular space and the gap junction which allows molecules and ions to diffuse from one cell to another (sharing the gap junction) without leaking in the extracellular space (intercellular coupling). The presence of such junctions may be important for the secretory behavior of the cells within the islet.

Adult↗

Somatostatin-induced changes in insulin and glucagon secretion in normal and diabetic dogs.

In conscious dogs intravenously infused somatostatin (3.3 mug per min for 1 h) caused prompt and sustained declines in mean plasma insulin and glucagon, even during alanine infusion and intraduodenal casein hydrolysate feeding; plasma glucose declined, but not significantly. 6.7 mug per min of somatostatin significantly lowered pancreatoduodenal vein glucagon and insulin within 2.5 min and profoundly suppressed their secretion throughout the infusion. Consistent bihormonal suppression occurred at rates as low as 24 ng per kg per min, but was variable at 12 and 2.4 ng per kg per min. When somatostatin-induced (3.3 mug per min) hypoglucagonemia was corrected by exogenous glucagon, hyperglycemia occurred. In dogs with long-standing insulin-requiring alloxan diabetes 3.3 mug per min of somatostatin suppressed glucagon to 55 pg per ml throughout the 30-min infusion and lowered glucose by 36.4+/-6.1 mg per dl, about 1 mg per dl per min. Glucagon suppression was maintained despite alanine infusion, and glucose, which rose 29 mg per dl during alanine infusion without somatostatin, declined 58 mg per dl in the somatostatin-treated diabetic dogs despite alanine. Continuous infusion of somatostatin for 24 h in five insulin-requiring alloxan-diabetic dogs suppressed glucagon and lowered glucose significantly, usually to below normal. It is concluded that in normal dogs pharmacologic doses of somatostatin virtually abolish insulin and glucagon secretion in the basal state and during hyperaminoacidemia. Hyperglycemia occurs during somatostatin-induced insulin lack only if hypoglucagonemia is corrected. Somatostatin suppresses glucagon in diabetic dogs and lowers their plasma glucose approximately 1 mg per dl per min, even when the gluconeogenic substrate alanine is abundant. Glucagon suppression can be maintained for several hours in such dogs and hyperglycemia is thereby reduced.

Alanine↗

The effects of triglyceride absorption upon glucagon, insulin, and gut glucagon-like immunoreactivity.

The effects of a fat meal upon plasma insulin, glucagon, and glucagon-like immunoreactivity (GLI) have been studied in conscious dogs and in human volunteers. In dogs the intraduodenal instillation of 10 g/kg of peanut oil was accompanied by increases in the mean plasma levels of all three polypeptides that averaged 5 muU/ml, 107 pg/ml, and 2.1 ng/ml, respectively. 3 g/kg of peanut oil, when emulsified with egg yolk, elicited a much greater response of the three hormones, and a physiologic dose of 1 g/kg in emulsified form also caused a significant rise in glucagon and GLI. The islet cell hormone response was not ascribable to chylomicronemia since intravenous infusion of canine chyle failed to stimulate glucagon secretion; moreover, in dogs with a thoracic duct fistula in which chyle was excluded from the circulation, the intraduodenal administration of a fat meal elicited the normal islet cell hormone response, as well as a rise in GLI. 10 g/kg of medium-chain triglycerides failed to elicit these same responses. In six human volunteers the oral administration of 3 g/kg peanut oil was accompanied by increments of 2 muU/ml, 26 pg/ml, and 1.5 ng/ml in the mean levels of insulin, glucagon, and GLI. The changes in insulin and glucagon in man were neither statistically significant nor biologically impressive. It is concluded that in dogs fat absorption is accompanied by prompt and substantial increases in plasma glucagon and GLI and a small transient rise in insulin. The evidence favors an enterogenic signal to the islets of Langerhans rather than their stimulation by chylomicrons. Pancreozymin is qualified to serve as such a signal. The physiologic implications of this study are considered.

Animals↗

National Burn Awareness Week: how are burn care facilities in the United States participating?

A survey was conducted from burn care facilities (BCF) regarding their participation in National Burn Awareness Week (NBAW). The second week in February has been proclaimed NBAW. This is the only national campaign of this scope and is supported by the American Burn Association. The NBAW Task Force meets annually to compose and review the burn awareness materials that are sent to all BCF. A telephone survey was conducted, and responses to questions were obtained from all 148 of the BCF listed in the American Burn Association's "Burn Care Resources in North America 1991-1992." The purpose of the study was to answer questions regarding BCF involvement with NBAW and burn prevention programs. Review of the literature reveals this to be the first national study to elicit this type of information. Information sharing of this magnitude can have a dynamic effect on the participation of BCF in NBAW and can result in increased burn awareness in the BCF's local communities. An added benefit is that the task force receives specific input direct from those using the campaign, which validates the continuation of NBAW and the support of the ABA.

Burn Units↗