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Biomedical subjects

A Nankervis

Publications and source records attributed to A Nankervis.

At least 19 recordsLinked to original sources
PubMed2001

Consumer issues in navigating health care services for type I diabetes.

Despite increasing interest in consumer awareness and participation in health care service delivery, there has been little exploration of consumer views in relation to services for people with type I diabetes. The purpose of this qualitative exploratory study was to identify strategies people with type I diabetes used to access health services and the barriers they perceived in accessing the services they needed. Data gathered in semi-structured interviews revealed that consumers experience significant barriers when navigating the health care system. Three dominant themes were identified. They relate to access to specialist medical skill, to the transition from teenager to young adult and to pre-pregnancy and obstetric care. Directions for change in service delivery and policy development are discussed.

Adaptation, Psychological↗
PubMed1998

Effects of perindopril on renal histomorphometry in diabetic subjects with microalbuminuria: a 3-year placebo-controlled biopsy study.

We conducted a 3-year randomized placebo-controlled double-blind study to determine the effects of the angiotensin-converting enzyme (ACE) inhibitor perindopril (PE) on the progress of renal function and histology in subjects with diabetes and microalbuminuria. Forty non-insulin-dependent (NIDDM) and insulin-dependent (IDDM) diabetic subjects, either normotensive or hypertensive, were randomly assigned to receive PE (n = 20) or placebo (n = 20). A percutaneous renal biopsy was performed initially in all patients and repeated in 29 patients after 3 years. The mean glomerular volume, glomerular basement membrane (GBM) thickness, interstitial fibrosis, sclerosed glomeruli, and volume fraction of capillary lumina were measured histomorphometrically. Before treatment, both groups had similar clinical characteristics, blood pressure, glycosylated hemoglobin (Hb), albumin excretion rate, glomerular filtration rate (GFR), serum creatinine, and renal structural damage. Blood pressure was well controlled in both groups. After 3 years' therapy, there was no significant change in renal function and albuminuria in the PE or placebo groups. The increase in GBM thickness in nine paired biopsies was significantly less in PE-treated subjects (P = .0275). Interstitial fibrosis tended to increase less in the PE group, although this did not reach statistical significance. This study indicates that long-term therapy with PE may decrease or delay the progression of structural glomerular damage in microalbuminuric diabetic subjects.

Adult↗
PubMed1993

Low-dose acarbose improves glycemic control in NIDDM patients without changes in insulin sensitivity.

OBJECTIVE: To examine the impact on metabolic control in NIDDM patients of the alpha-glucosidase inhibitor, acarbose, when administered at a low dose in powdered form. RESEARCH DESIGN AND METHODS: Six subjects were recruited for a double-blind cross-over trial using 25 mg powdered acarbose and a placebo 3 times a day with meals for 3 mo. In addition to parameters of diabetes control and body weight, glucose turnover and insulin sensitivity were measured with the hyperinsulinemic/euglycemic clamp technique combined with tracer kinetics. RESULTS: None of the subjects showed significant changes in FPG levels or body weight either on the 3-mo course of acarbose or placebo. HbA1c fell significantly from 10.6 +/- 1.0 to 9.4 +/- 1.3% (P = 0.05) during treatment with acarbose but failed to change on placebo (10.1 +/- 1.0 to 11.1 +/- 2.0%; P = 0.36). Basal HGP and glucose utilization were unchanged during either of the treatment periods, and hyperinsulinemia produced a similar degree of suppression of HGP before and after each treatment. At a physiological concentration, insulin failed to stimulate glucose clearance in these diabetic patients, and no improvement was seen with acarbose treatment. No changes in plasma lipids or lipoprotein profiles were demonstrated after 3 mo on acarbose. In acute studies, it was shown that administration of acarbose at a dose of 25 mg powder per meal significantly decreased the postprandial glycemic excursion. CONCLUSIONS: When administered in the powdered form at the low dose of 25 mg 3 times/day with meals over 3 mo, acarbose was well tolerated by the NIDDM patients and was without side effects. It improved glycemic control by reducing postprandial hyperglycemia, but had no effect on glucose turnover, insulin sensitivity, or lipid profile.

Acarbose↗
PubMed1992

Short-term effects of alterations in dietary fat on metabolic control in IDDM.

OBJECTIVE: Two experimental diets were evaluated to investigate the hypothesis that dietary fat has an independent influence on metabolic control in IDDM. RESEARCH DESIGN AND METHODS: The diets had similar CHO contents (26 and 22% of energy intake) but differed markedly in fat (53 vs. 16% energy) and protein (20 vs. 62% energy). We had 10 subjects follow the low-CHO, high-fat diet, and 8 subjects follow the low-CHO, low-fat, high-protein diet. In each case, markers of glycemic and lipid control obtained after adherence to the experimental diet for 2 wk were compared with corresponding data from a preceding control period during which subjects had followed their usual diet (protein 18-19%, CHO 41-46%, fat 33-37%). RESULTS: Despite the low CHO content of the high-fat diet, insulin requirements were unchanged relative to the control diet. Moreover, the glycemic response to a standard breakfast was elevated significantly (P < 0.001), suggesting that insulin resistance had either been induced or exacerbated. The small rise in total cholesterol concentration in response to the high-fat diet was accounted for by a rise in HDL cholesterol. Glycemic control and lipid metabolism were unchanged after the low-CHO, low-fat diet, although insulin requirements fell by an average of 6 U/day (P < 0.05) relative to those recorded during the 2-wk control period. CONCLUSIONS: Diets high in fat are deleterious to glycemic control in IDDM, but general applicability is limited by the small sample size and short duration of this study.

Adult↗
PubMed1987

Assessment of the Albuscreen microalbuminuria kit in diabetic outpatients.

Diabetic patients who have albumin excretion rates of greater than 30 micrograms/min (30 mg/L at normal urine volumes) are at increased risk of the development of diabetic nephropathy. The Albuscreen microalbuminuria kit detects albuminuria at concentrations of 30 mg/L and above by an agglutination-inhibition reaction. One hundred and ninety-five random urine samples from diabetic outpatients were assessed by Albuscreen and Albustix testing for albuminuria and the results were correlated with those of a sensitive radioimmunoassay technique. Albuscreen testing was simple, easy to use and had a sensitivity of 96%, with a specificity of 88%. Albustix testing at a detection level of 50 mg/L revealed a sensitivity of 100% and a specificity of 68% (43 samples, false-positive "trace" readings), while, at 30 mg/L, the sensitivity and specificity were 90% and 71%, respectively. Therefore, Albuscreen testing is well suited as a screening test for the presence of microalbuminuria in a diabetic outpatient setting. However, the role of Albustix in screening for microalbuminuria is less well defined, especially at the 30 mg/L level of detection, and requires further investigation.

Albuminuria↗
PubMed1985

Hyperinsulinaemia and insulin insensitivity: studies in subjects with insulinoma.

Hepatic glucose turnover, peripheral insulin sensitivity and insulin receptor binding were measured in four subjects with insulinoma before and 3 months after surgical resection of the insulinoma. Basal hepatic glucose production, quantitated employing a primed constant infusion of tritiated glucose, was low pre-operatively (5.2 +/- 1.7 mumol X kg-1 X min-1) but returned to normal post-operatively (14.9 +/- 2.8; normal subjects 13.9 +/- 0.8 mumol X kg-1 X min-1). Paired euglycaemic dose-response curves were developed for each subject. Insulin sensitivity, expressed as a right shift of the dose-response curve (ED50), was low pre- and post-operatively. However, insulin responsiveness (Vmax) remained normal (pre-operatively 13.9 +/- 2.2, post-operatively 13.8 +/- 0.8, normal subjects 16.7 +/- 0.8 ml X kg-1 X min-1). There was no consistent pattern in monocyte or erythrocyte receptor binding before or after surgery. These data suggest that the chronic hyperinsulinaemia causes suppression of hepatic glucose production, and a state of insulin insensitivity which appears to be due to a post-receptor defect.

Adenoma, Islet Cell↗
PubMed1985

Gliclazide therapy is associated with potentiation of postbinding insulin action in obese, non-insulin-dependent diabetic subjects.

Six obese, non-insulin-dependent diabetic subjects were studied before and 3 mo after treatment with the sulfonylurea gliclazide, 40-80 mg b.i.d. Fasting plasma glucose fell significantly from 13.4 +/- 1.6 (SEM) to 8.6 +/- 1.2 mmol/L, accompanied by a significant reduction from 40.6 +/- 3.7 to 29.8 +/- 2.8 mM X h of the plasma glucose response to 75 g oral glucose. Fasting plasma insulin showed a nonsignificant increase from 24.8 +/- 2.0 to 31.3 +/- 2.3 mU/L. The percent specific binding of tracer 125I-insulin to erythrocytes and monocytes did not change significantly (from 9.8 +/- 1.7 to 8.5 +/- 0.7 for erythrocytes and 1.7 +/- 0.3 to 1.6 +/- 0.4 for monocytes). Glucose utilization was measured at three levels of insulin infusion (40, 100, and 300 mU/kg/h) by the euglycemic clamp technique. Overall there was a significant (P less than 0.05) increase in the disappearance rate (Rd) and metabolic clearance rate (MCRg) for glucose at the two higher insulin infusion rates (MCRg: 3.3 +/- 0.7 to 5.1 +/- 0.7 and 5.9 +/- 0.9 to 7.9 +/- 0.9 ml/kg/min), but not at the lowest infusion rate (MCRg: 3.6 +/- 0.8 to 3.3 +/- 0.6). Thus, the chronic hypoglycemic effect of gliclazide in obese diabetic subjects was associated with an improvement in insulin-mediated glucose utilization at high plasma insulin concentrations. This enhanced effect of insulin after gliclazide treatment was not accompanied by increased monocyte or erythrocyte insulin binding, which suggests that it was due to potentiation of postbinding insulin-sensitive pathways.

Aged↗
PubMed1984

Impaired insulin action in newly diagnosed type 1 (insulin-dependent) diabetes mellitus.

Hepatic and peripheral insulin sensitivity were investigated in five newly diagnosed Type 1 (insulin-dependent) diabetic subjects before and after 1 week of twice daily insulin therapy. Eight weight-matched control subjects were also studied. Hepatic glucose production and glucose utilization were measured basally and during two sequential 2-h insulin (25 and 40 mU X kg-1 X h-1)/ glucose infusion periods. In the untreated hyperglycaemic diabetic patients hepatic glucose production was 16.3 +/- 2.6, 8.1 +/- 1.1 and 3.6 +/- 2.8 mumol X kg-1 X min-1 respectively for each of the three periods (mean +/- SEM), and fell with treatment to 12.5 +/- 1.4, 0.5 +/- 0.5 and 0.5 +/- 0.5 mumol X kg-1 X min-1. Hepatic glucose production for normal subjects was 13.4 +/- 0.7, 2.3 +/- 0.8 and less than 0.1 mumol X kg-1 X min-1. Glucose utilization was 12.7 +/- 1.4, 18.2 +/- 0.7 and 22.1 +/- 3.4 mumol X kg-1 X min-1 before treatment in the diabetic subjects, and 11.8 +/- 1.7, 20.9 +/- 3.3 and 30.1 +/- 3.6 after treatment. These values compare with those in the euglycaemic control subjects (13.4 +/- 0.7, 18.7 +/- 1.6 and 36.3 +/- 2.7 mumol X kg-1 X min-1). The pre-treatment metabolic clearance rate of glucose in all diabetic studies with insulin levels greater than 30 mU/l was 2.6 +/- 0.4 and rose to 3.9 +/- 0.5 ml X kg-1 X min-1 following insulin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1984

Insulin resistance in cirrhosis: evidence for a post-receptor defect.

Receptor and post-receptor abnormalities of insulin action and their possible role in the insulin resistance of cirrhosis were examined in eight biopsy-proven cirrhotic subjects and eight age-weight matched healthy volunteers. To this end, oral glucose tolerance tests (OGTT), insulin dose response curves and insulin binding to circulating monocytes were determined for each subject. The dose-response curves for the cirrhotic subjects were significantly shifted to the right compared to the control subjects, indicating the presence of insulin insensitivity (ED50 223 +/- 30 versus 64 +/- 8 mU/l respectively; P less than 0.001). The magnitude of the right shift of the insulin-dose response curves correlated significantly (P less than 0.001) with the OGTT 2 h insulin levels (r = 0.74) and the insulin areas under the OGTT curves (r = 0.86). In contrast, insulin responsiveness was marginally elevated in the cirrhotic group (maximal glucose disposal 680 +/- 47 versus 574 +/- 21 ml/m2/min; P less than 0.05). Insulin binding to circulating monocytes was normal in the cirrhotic subjects. It is concluded that the insulin resistance of cirrhosis is due to a post-receptor defect in insulin action which reduces insulin sensitivity but not insulin responsiveness.

Blood Glucose↗
PubMed1983

Glucose utilization in Type 1 (insulin-dependent) diabetes: Evidence for a defect not reversible by acute elevations of insulin.

It has long been assumed that replacement of insulin in insulin-deficient diabetic patients will normalise glucose utilization. In this study, glucose utilization was measured in nine long-standing, poorly controlled diabetic patients and five control subjects, matched for age (33 +/- 3 versus 33 +/- 2 years) and ponderal index (22.9 +/- 1.3 versus 21.7 +/- 1.0). Glucose uptake was measured during steady state insulinaemia in the diabetic patients and control subjects, at euglycaemia (5.5 +/- 0.5 versus 5.4 +/- 0.3 mmol/l, respectively) and moderate hyperglycaemia (11.8 +/- 0.9 versus 10.2 +/- 0.7 mmol/l, respectively). At euglycaemia with similar free insulin levels (50 +/- 19 versus 43 +/- 9 mU/l; p greater than 0.6), the diabetic patients utilized less glucose than the control subjects (27.8 +/- 4.2 versus 56.4 +/- 5.7 mumol.kg-1.min-1;.p less than 0.005). During hyperglycaemia, the diabetic patients utilized almost as much glucose as the control subjects did at euglycaemia (49.9 +/- 6.4 versus 56.4 +/- 5.7 mumol.kg-1.min-1, respectively). In the control subjects, a 1-mmol/l rise in glucose concentration (with insulin remaining constant) resulted in a 12.3 +/- 1.3 mumol.kg-1.min-1 rise in glucose utilization. In contrast, in the diabetic patients, a 1-mmol/l rise in blood glucose resulted in a rise in glucose utilization of only 3.8 +/- 0.8 mumol.kg-1.min-1 (p less than 0.001), in the presence of similar concentrations of plasma insulin. This defect of glucose utilization in Type1 diabetic patients could not be reversed by acutely raising insulin to 247 +/- 23 mU/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

The physiologic action of insulin on glucose uptake and its relevance to the interpretation of the metabolic clearance rate of glucose.

Glucose uptake (Ru) is dependent upon the concentrations of both glucose and insulin. The metabolic clearance rate of glucose (MCRG), has been used as an in vivo measure of insulin action, because it was said to be independent of the prevailing glucose concentration. The validity of this assumption has recently been challenged. In this study, the effect of insulin concentration on the rate of glucose uptake (Ru) and on the MCRG was studied during euglycemia (5.1 +/- 0.3 mmol/L) and moderate hyperglycemia (10.4 +/- 0.5 mmol/L) in 17 experiments on nine normal ambulant volunteers. Stable plasma insulin levels were maintained with fixed infusion rates of insulin (0-300 mU/kg/h) and somatostatin (7.5 micrograms/min). At low insulin concentrations (less than 5 microU/mL) the increase in glucose uptake in response to hyperglycemia was small (5.3 +/- 2.3 mumol/kg/min). In contrast, with insulin levels more than 25 microU/mL, there was a steep rise in glucose uptake with hyperglycemia (55 +/- 3 mumol/kg/min; range: 44-74 mumol/kg/min). The metabolic clearance rate of glucose fell by an average of 32% with hyperglycemia in the studies at the lowest insulin levels (2.2 +/- 0.6 v 1.5 +/- 0.1 mL/kg/min; 0.15 greater than P greater than 0.1). There was no change in the MCRG in the subjects studied at higher insulin levels. It is concluded that (1) low concentrations of insulin are essential for the increase in glucose disposal during hyperglycemia; and (2) provided insulin levels are more than 25 microU/mL and plasma glucose less than 11 mmol/L, MCRG is independent of the plasma glucose concentration and is therefore a valid measure of insulin-mediated glucose uptake.

Adult↗
PubMed1982

Differential effects of insulin therapy on hepatic and peripheral insulin sensitivity in Type 2 (non-insulin-dependent) diabetes.

Hepatic glucose production and metabolic clearance rate of glucose were measured using (3-3H) glucose at steady state, basally and during two sequential 2 h insulin (25 and 40 mU . kg -1 . h -1)/glucose (2 and 3 mg. kg -1 . min -1) infusion periods. Eight diabetic subjects were studied before and after 1 week of twice daily insulin therapy; six control subjects matched for age, weight and degree of obesity were also studied. In the diabetic patients, pre-treatment hepatic glucose production was 20.0 +/- 2.2, 9.9 +/- 2.9, and 1.4 +/- 0.8 mu mol . kg -1 . min -1 respectively (+/- SEM) for each of the three periods, and fell significantly with treatment to 12.8 +/- 1.7, 4.0 +/- 1.5 and 1.9 +/- 1.0 mu mol . kg -1 . min -1. Hepatic glucose production in normal subjects was 13.2 +/- 0.6, 2.2 +/- 0.8 and less than 1 mu mol . kg -1 . min -1. The pre-treatment metabolic clearance rate in all diabetic studies with insulin levels greater than or equal to 30 mU/l was 1.10 +/- 0.14 ml . kg -1 . min -1 and remained virtually unchanged following insulin therapy; this was significantly lower than in the control subjects (6.83 +/- 1.02, p less than 0.001). Basal non-esterified fatty acid levels were higher (p less than 0.02) in the pre-treated diabetic patients compared to post-treated diabetic patients and control subjects. Non-esterified fatty acids in each group fell to similar levels during the insulin infusions, but the rate of fall was slower in the pre-treated diabetic patients. Insulin receptor binding to erythrocytes was normal in the diabetic subjects and unchanged by treatment. Therefore, following insulin treatment of uncontrolled Type 2 (non-insulin-dependent) diabetes, the initially increased basal hepatic glucose production, and decreased hepatic sensitivity, return towards normal. However, the glucose clearance remains low, despite good diabetic control, and appears to be a major factor in the continuing glucose intolerance. As insulin receptor binding is normal, the defect of glucose clearance in Type 2 diabetes appears compatible with a post-receptor defect of glucose metabolism.

3-Hydroxybutyric Acid↗
PubMed1982

Validation of a practical in vivo insulin dose-response curve in man.

To adequately investigate the state of insulin resistance, an insulin dose-response curve should be constructed so that insulin sensitivity (right shift of dose-response curve) and insulin responsiveness (maximal response) can be determined. This paper describes and validates in man a practical in vivo insulin dose-response curve technique, using a modification of the euglycaemic clamp described by De Fronzo et al. Insulin action at steady state was expressed as metabolic clearance rate of glucose (MCRG) rather than overall rate of glucose disappearance (M or Rd). MCRG was chosen because at plasma insulin concentrations greater than 25 microunits/ml it was shown (n = 5) not to be altered by changes in blood glucose concentration (MCRG 379 +/- 23 and 408 +/- 19 ml/m2/min; at plasma glucose concentrations 5.4 +/- 0.3 and 10.2 +/- 0.7 respectively), whereas Rd was critically dependent on the prevailing blood glucose concentration (Rd 2007 +/- 128 and 4124 +/- 219 mumol m2/min respectively). MCRG was demonstrated to be stable over a 6 hr period (n = 8) and to be reproducible (n = 4). Insulin dose-response curves (MCRG Versus insulin concentration) were performed on two obese and seven normal weight individuals. The insulin dose-response curves were linearized, allowing accurate prediction of the maximal MCRG, as compared to the experimentally determined maximal response (r = 0.953 p less than 0.01). The use of this transformation obviates the need to employ very high insulin infusion rates to determine the maximal insulin response. In conclusion, the technique permits, in a single 6 hr study, a precise insulin dose-response curve to be constructed for accurately determining insulin sensitivity and responsiveness.

Adult↗
PubMed1981

The metabolic effects of chronic hyperglucagonaemia.

A subject with a benign glucagonoma was studied before and after complete resection of his pancreatic tumour. Studies were undertaken pre- and post-operatively to determine the effects of chronic hyperglucagonaemia on glucose tolerance and glucose kinetics both in the fasting state and during physiological insulin infusions, employing the [3H]-3-glucose technique. In addition the plasma cyclic AMP response to an acute infusion of glucagon was studied pre- and post-operatively. The basal immunoreactive glucagon levels pre- and post-operatively were 10492 +/- 1296 and 149 +/- 15 pg/ml respectively. Pre- and post-operative oral glucose tolerance tests did not differ but were abnormal. Pre-operatively basal hepatic glucose production was normal and it was suppressed rapidly by the low dose insulin infusion, despite continuing hyperglucagonaemia. The metabolic clearance rate of glucose was slightly reduced. There was no plasma cyclic AMP response to a glucagon infusion, suggesting down-regulation of the glucagon receptor by the chronic hyperglucagonaemia. Post-operatively the hepatic glucose production and clearance rate of glucose fell, whereas the plasma cyclic AMP responses to the glucagon infusion reverted to a normal pattern. It is concluded that chronic hyperglucagonaemia is not a major factor in the development of the glucose intolerance, but it may lead to down-regulation of the biological action of glucagon.

Adenoma, Islet Cell↗
PubMed1980

Appraisal of a new rapid enzyme strip.

The accuracy and reliability of new blood glucose measurement strips, BM Test-Glycemie 20-800, were assessed in 99 consecutive patients attending the diabetic clinic and seven subjects at home. The BM Test-Glycemie 20-800 strip technique was compared with the automated hexokinase method and the Reflotest-Glucose test strip technique employing the Boehringer Reflomat. The mean of the blood glucose values was 12.6 +/- 0.6 mmol/L for the hexokinase method and 12.9 +/- 0.6 mmol/L for the 20-800 strip technique, with a mean difference between the hexokinase and the 20-800 strip methods of 1.9 +/- 0.2 mmol/L. In the range 4 mmol/L to 12 mmol/L, the 20-800 strips were found to be extremely accurate, but for blood glucose levels less than 3.5 mmol/L and greater than 12 mmol/L, they were less reliable. Importantly, the strips were often misleading in indicating hypoglycaemia. It is concluded that the BM Test-Glycemie 20-800 strips have a practical and valuable role when used by suitably instructed staff members, or by patients in the management of diabetes, and represent a major advance over urine testing on previously available direct reading enzyme strip methods.

Blood Glucose↗
PubMed1980

Drug trials: treatment of urinary tract infection with multiple-dose intramuscular administration of cephamandole.

Therapy with cephamandole (1.0 g, every eight hours) for five days was effective in eliminating cephamandole-sensitive microorganisms from the urinary tract. A 75% cure rate was achieved in a group of 20 patients, 45% of whom had abnormalities of the urinary tract. Local pain (despite addition of lignocaine) was sufficiently prolonged and severe to make multiple-dose intramuscular administration unacceptable. No other toxic effects were encountered.

Anti-Infective Agents, Urinary↗