Biomedical subjects

D G Bruce

Publications and source records attributed to D G Bruce.

31 records · Page 2Linked to original sources

PubMed1991

Meal-time intranasal insulin delivery in type 2 diabetes.

Correction of the deficiency of early meal-time insulin secretion, using intravenous insulin in patients with Type 2 diabetes causes substantial improvement in post-prandial hyperglycaemia. The present study was designed to determine whether similar benefit would result from physiological supplementation using intranasal insulin delivery. Six patients with Type 2 diabetes were studied twice during a standard mixed meal. At the start of the meal they received a single intranasal spray containing either 15 units of insulin in 1% sodium glycocholate (adjuvant agent) or glycocholate alone (placebo) in a single-blind fashion. Intranasal insulin delivery resulted in rapid absorption of insulin with peak levels (92 +/- 8 (+/- SE) mU l-1) within 5-10 min. Peak insulin levels were at least equal to those in non-diabetic subjects, though occurring at an earlier time-point. However, no significant improvement in post-prandial hyperglycaemia was seen (peak blood glucose increment 4.9 +/- 0.6 vs 5.4 +/- 0.5 mmol l-1; total 3-h response 611 +/- 53 vs 668 +/- 41 mmol l-1 min). We conclude that an elevation of insulin levels, earlier and more transient than the normal physiological response, achieved by intranasal insulin delivery at the start of a meal, fails to significantly improve the blood glucose excursion in Type 2 diabetes.

Administration, Intranasal↗

PubMed1990

Acupressure and motion sickness.

The effectiveness of the "Sea Band" acupressure band compared with placebo and hyoscine (0.6 mg), also known as scopolamine, to increase tolerance to a laboratory nauseogenic cross-coupled motion challenge was assessed using 18 subjects. The results showed that the subjects had a significant increase in tolerance with hyoscine but had no increase in tolerance with the "Sea Band" or placebo. Possible reasons for the failure to show any significant protection from the use of these acupressure bands are insufficient movement of the wrist to provide continuous stimulation, and/or the likelihood that only a minority of the population would show non-negligible benefit as experience with medical acupressure would suggest. The application of transcutaneous electrical nerve stimulation may be worthy of study.

Acupuncture Therapy↗

PubMed1989

Mind over metabolism: the cephalic phase in relation to non-insulin-dependent diabetes and obesity.

The notion that a defect in hypothalamic function may be a critical factor in the aetiology of obesity and diabetes stems from observations of the important role that this brain region plays in both the behavioural and metabolic events related to feeding and energy balance. Sensory events associated with the beginning of a meal trigger a series of metabolic changes, the function of which is to prepare an organism to receive, and properly dispose of, the incoming nutrients. Insulin release and nervous control of hepatic glucose output are important components of these neural, or cephalic-phase, sensory-driven metabolic events. The present review firstly summarizes evidence for direct autonomic nervous system links between the hypothalamus and the pancreas and liver, that is, the physical basis for cephalic-phase reflexes. Secondly, an assessment is made of both the normal function of the cephalic phase and how derangements might be central to the aetiology of important disease states such as obesity and non-insulin-dependent diabetes mellitus. A central hypothesis in this article is that a primary failure of normal cephalic-phase responses, over time, leads to increased post-meal hyperglycaemia and decreased thermogenesis. The persistent hyperglycaemia (among other metabolic abnormalities) leads to insulin resistance (insulin not being effective in disposing of glucose). The reduced post-meal thermogenesis leads to weight gain through reduced energy expenditure rather than through increased intake. The obesity in turn leads to further insulin resistance and, in genetically predisposed individuals, on to frank diabetes.

Animals↗

PubMed1988

Regulation of hepatic glucose output during moderate exercise in non-insulin-dependent diabetes.

In normal subjects during moderate exercise there is a strong negative correlation between plasma glucose and hepatic glucose output (HGO) suggesting a negative feedback regulation of HGO by plasma glucose. Little information is available about HGO responses to exercise in non-insulin-dependent diabetes mellitus (NIDDM). To determine whether the same feedback relationship is operative, we have compared the glucose turnover responses to moderate exercise (50% Vo2max for 60 minutes) of nonobese non-insulin-dependent diabetic subjects (NIDDM, n = 7) with a group of age-matched controls (n = 5). Glucose turnover responses to exercise in NIDDM were heterogeneous. Plasma glucose showed sustained falls, no change, or sustained rises in different individuals. Similarly, HGO responses ranged from undetectable to responses comparable to those of normal subjects. The mean integrated HGO response in NIDDM was significantly reduced compared with controls (11 +/- 6 [SEM] v 33 +/- 7 mmol/h/70 kg, P less than .05); mean glucose utilization response was also reduced but not significantly different from controls (NIDDM 18 +/- 5 v control 35 +/- 6). In NIDDM there was no significant feedback-control relationship between plasma glucose and HGO (r = -0.20, P = NS) in contrast to controls (r = -0.87, P less than .01). We conclude that feedback control of HGO by plasma glucose during moderate exercise is impaired in NIDDM. This impairment may be due to defective nonpancreatic glucoregulatory mechanisms.

Aged↗

PubMed1988

Physiological importance of deficiency in early prandial insulin secretion in non-insulin-dependent diabetes.

Patients with non-insulin-dependent diabetes mellitus (NIDDM) have a deficiency in early prandial insulin secretion. To determine the contribution of this early deficiency to prandial hyperglycemia, exogenous intravenous insulin (1.8 U over 30 min) was delivered to eight NIDDM subjects in a profile designed to simulate the normal initial rise in insulin levels. The same dose of insulin was also administered 1) in the same profile but delayed by 30 min and 2) as a constant infusion over 180 min. Augmentation of the early insulin response caused a 33 +/- 4% reduction in the glycemic response to a mixed meal (P less than .005); the peak blood glucose increment above baseline was reduced by 1.4 mM (P less than .005) to an increment identical to nondiabetic subjects (3.3 +/- 0.3 vs. 3.2 +/- 0.2 mM), and blood glucose levels were still 0.9 mM lower after 180 min (P less than .05). In contrast, the delayed profile or constant infusion did not significantly alter the glycemic response to the meal. Early insulin augmentation resulted in elevated peripheral insulin levels initially (peak level 81 +/- 11 mU/L), but subsequent insulin and C-peptide levels were lower than in the control study (at 180 min after the meal, 22 +/- 5 vs. 33 +/- 8 mU/L, P less than .05, and 4.0 +/- 0.5 vs. 5.3 +/- 0.6 micrograms/L, P less than .02, respectively). Early insulin delivery caused free-fatty acid (FFA) levels to fall at a faster rate after the meal and also attenuated the initial rise in glucagon levels typical of NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1987

Fish oil prevents insulin resistance induced by high-fat feeding in rats.

Non-insulin-dependent diabetes mellitus is an increasingly prevalent disease in Western and developing societies. A major metabolic abnormality of non-insulin-dependent diabetes is impaired insulin action (insulin resistance). Diets high in fat from vegetable and nonaquatic animal sources (rich in linoleic acid, an omega-6 fatty acid, and saturated fats) lead to insulin resistance. In rats fed high-fat diets, replacement of only 6 percent of the linoleic omega-6 fatty acids from safflower oil with long-chain polyunsaturated omega-3 fatty acids from fish oil prevented the development of insulin resistance. The effect was most pronounced in the liver and skeletal muscle, which have important roles in glucose supply and demand. The results may be important for therapy or prevention of non-insulin-dependent diabetes mellitus.

Adipose Tissue↗

PubMed1987

Insulin therapy in patients with poorly controlled non-insulin dependent diabetes mellitus.

In spite of maximal doses of sulphonylurea agents, patients with poorly controlled non-insulin dependent diabetes (NIDDM) often do not have improved metabolic control after the introduction of insulin therapy. We have assessed 22 patients with NIDDM who commenced insulin therapy in order to identify those characteristics which were associated with an improvement in glycaemic control. Twelve months after the commencement of insulin therapy, 14 (64%) patients showed a decrease in glycosylated haemoglobin (HbA1) levels; 12 of the 14 (55%) patients had achieved HbA1 levels that were considered to reflect acceptable glycaemic control (HbA1 less than or equal to 11%; reference range, 6%-9%). The HbA1 levels in the other patients either remained unchanged or had increased (one subject). When the subjects who had achieved good glycaemic control with insulin therapy were compared with the remainder of the group, a failure to improve with insulin therapy was associated with a longer duration of diabetes, greater obesity and higher levels of cholesterol and triglycerides before the commencement of insulin therapy. Greater obesity and high levels of circulating lipids were found by means of multiple linear regression analysis to correlate independently with a poor response to insulin therapy. We conclude that standard insulin therapy can improve the majority of patients with poorly controlled NIDDM. However, there is a substantial number of patients, who tend to be obese and have high levels of circulating lipids, whose condition does not improve with insulin therapy, or who require more aggressive dosage increases than are used as a routine.

Adult↗

PubMed1987

Outpatient initiation of insulin therapy in patients with diabetes mellitus.

Before insulin therapy is begun, patients with diabetes are often admitted to hospital. In a retrospective study we have reviewed the initiation of insulin therapy in 54 unselected outpatients (12 of whom were insulin-dependent), when the initial stabilization of therapy was performed predominantly by nurse educators. Most patients found the procedure satisfactory; only one subject indicated dissatisfaction with the regimen and only two indicated that they would have preferred admission to hospital. No patient experienced an acute hypoglycaemic or hyperglycaemic problem that required admission to hospital nor was emergency intervention required during the 12 months that followed the initial stabilization period of insulin therapy. Metabolic control, as measured by glycosylated haemoglobin levels, improved in the majority of both insulin-dependent and non-insulin-dependent patients after 12 months of insulin therapy. A retrospective cost analysis that compared the cost of the outpatient procedure with the cost (hospital-bed costs only) of initiating insulin therapy in a similar group of patients who were admitted to hospital, indicated a saving of $1857 for each outpatient. We conclude that the outpatient initiation of insulin therapy is feasible where the facilities for education about diabetes exist, that it is safe, achieves satisfactory metabolic control, is acceptable to most patients, and offers a considerable saving in costs.

Australia↗

PubMed1987

Cephalic phase metabolic responses in normal weight adults.

The presence and physiologic importance of cephalic phase insulin release in humans remains controversial. The aim of these studies was to determine whether cephalic phase insulin release could be demonstrated in normal weight subjects and whether it would be associated with changes in blood glucose, free fatty acid, and pancreatic polypeptide levels. The studies were followed by a hyperglycemic clamp to determine whether cephalic responses would alter overall glucose disposal or glucose-stimulated insulin secretion. In all, 17 subjects were studied on two occasions with and without (control study) presentation of food stimuli. Tease-feeding alone (n = 6), or the administration of a sweet taste alone (aspartame, n = 5) failed to stimulate cephalic responses. However, the presentation of the combined stimuli (tease meals plus sweet taste, n = 7) resulted in a significant fall (P less than .005) in blood glucose levels and a variable rise in serum insulin (% insulin rise 38 +/- 15%, P less than .05) and C-peptide levels (7 +/- 6%, NS) within five minutes of the food presentation when compared with control studies, with no change seen in free fatty acid or pancreatic polypeptide levels. The blood glucose fall correlated strongly (r = .90, P less than .01) with a score of the subjective response to the food and taste.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1983