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Biomedical subjects

A Mengel

Publications and source records attributed to A Mengel.

16 recordsLinked to original sources
PubMed1994

Nerve conduction velocity in man: influence of glucose, somatostatin and electrolytes.

Insufficient metabolic control in diabetes mellitus is associated with a reversible reduction in nerve conduction velocity, but the mechanism behind this phenomenon is unknown. To examine the effect of acute hyperglycaemia on nerve conduction eight non-diabetic men (20-49 years of age) with no signs of peripheral neuropathy were studied before and after 3 h of hyperglycaemic clamping (plasma glucose approximately 15 mmol/l), while insulin secretion was suppressed by somatostatin [Study 1]. Nerve conduction velocity, as determined in the proximal part of the median nerve, fell by 2.8 +/- 3.0 m/s (2p-value: 0.033). However, during euglycaemic clamping (plasma glucose approximately 5 mmol/l) in five non-diabetic men (19-38 years of age) infused solely with somatostatin [Study 2], a comparable decrement in nerve conduction velocity was found (1.7 +/- 1.3 m/s, 2p-value: 0.043). In both studies relative hypoinsulinaemia was present. Serum-sodium decreased significantly (143 +/- 1 mmol/l vs 137 +/- 1 mmol/l [Study 1] and 143 +/- 1 mmol/l vs 142 +/- 2 mmol/l [Study 2]), while serum-potassium increased. In conclusion, the slight but significant reduction in nerve conduction velocity observed in both studies appears to be correlated to electrolyte changes. However, an effect of hypersomatostatinaemia or the hormonal changes associated with this cannot be excluded, while short-term hyperglycaemia per se seems to be without effect on nerve conduction velocity.

Adult↗
PubMed1994

Augmented effect of short-term pulsatile versus continuous insulin delivery on lipid metabolism but similar effect on whole-body glucose metabolism in obese subjects.

The present study was designed to examine the effect of pulsatile versus continuous insulin delivery on glucose and lipid metabolism in insulin-resistant subjects. Six obese women (body mass index, 40.0 +/- 2.8 kg/m2) underwent a euglycemic glucose clamp (plasma glucose, 90 mg/dL) twice. In random order, insulin was infused intravenously for 375 minutes either at a constant rate (0.4 mU/kg/min) or in a pulsatile manner (2.4 mU/kg/min for 2 minutes followed by an off interval of 10 minutes). Endogenous insulin release was suppressed by infusion of somatostatin (250 micrograms/h). Mean circulating insulin concentrations were similar during the two protocols (pulsatile v continuous infusion, 60 +/- 10 v 56 +/- 9 mU/L), but pulsatile infusion was accompanied by oscillations with an amplitude of 120 mU/L. After 6 hours of pulsatile versus continuous insulin, isotopically determined total glucose disposal (3-3H-glucose) and hepatic glucose production (HGP) were comparable (pulsatile v continuous, 2.80 +/- 0.56 v 2.82 +/- 0.51 and 0.37 +/- 0.14 v 0.32 +/- 0.17 mg/kg/min). However, the rate of glucose oxidation (indirect calorimetry) was augmented (P < .05), whereas lipid oxidation tended to be diminished (.10 > P > .05) following pulsatile infusion. In addition, blood glycerol was more suppressed with pulsatile (31 +/- 9 nmol/L) than with continuous infusion (36 +/- 10 nmol/L, P < .05), whereas blood lactate, alanine, and 3-hydroxybutyrate were similar in the two infusion protocols.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1994

Comparison of the effects of growth hormone and insulin-like growth factor I on substrate oxidation and on insulin sensitivity in growth hormone-deficient humans.

Insulin-like growth factor-I (IGF-I) is considered to be the mediator of the growth-promoting effects of growth hormone (GH). The metabolic effects of these two hormones, however, are different. Whereas GH treatment leads to elevated insulin and glucose levels, reduced insulin sensitivity, and impaired glucose tolerance, IGF-I treatment leads to reduced insulin and GH levels and enhanced insulin sensitivity. IGF-I may, therefore, not only be the mediator of the growth-promoting effects of GH but also a modulator of the effects of GH on insulin action and glucose metabolism. To study the influence of GH and IGF-I on substrate metabolism and insulin sensitivity (assessed by euglycemic, hyperinsulinemic clamping combined with indirect calorimetry and glucose tracer infusion), we have treated eight GH-deficient adults with GH (2 IU/m2 daily subcutaneously [s.c.]), IGF-I (10 micrograms/kg.h s.c.), or both hormones together for 7 d, respectively, and compared the effects of these treatment regimens with a control phase. Our findings suggest that (a) both GH and IGF-I promote lipolysis and lipid oxidation, albeit by different mechanisms; (b) treatment with either hormone is followed by enhanced energy expenditure and reduced protein oxidation; and (c) IGF-I reverses the insulin resistance induced by GH.

Adult↗
PubMed1993

Insulin resistance in microvascular angina (syndrome X)

Patients with microvascular angina (syndrome X) may be insulin resistant. We designed a study to establish whether this is the case. 11 patients with microvascular angina were compared with 9 matched subjects with noncardiac chest pain. Patients and controls were evaluated by coronary sinus catheterisation, and by isotopic measurement of glucose turnover, indirect calorimetry, and forearm technique during a 3 h baseline period after overnight fast and during a 2 h hyperinsulinaemic euglycaemic clamp. Pace-induced increase in coronary sinus blood flow was less in patients than in controls, whereas forearm blood flow did not differ between groups. Baseline measures of glucose metabolism were normal. During the clamp, glucose production and lipolysis were equally suppressed in both groups. Mean (SE) total insulin-induced glucose uptake was significantly impaired in patients compared with controls (3.9 [0.7] vs 6.4 [0.7] mg/kg per min; p < 0.01), and insulin-stimulated glucose uptake in the forearm was significantly reduced in patients (0.88 [0.10] vs 1.6 [0.30] mmol/L; p < 0.001). Reduced oxidative and nonoxidative metabolism accounted for the defect in overall glucose uptake in patients. No correlation between changes in coronary sinus blood flow and total body glucose uptake was seen. We found that microvascular angina was associated with substantial insulin resistance. Whether this relation is causal or coincidental is as yet unsettled.

Alanine↗
PubMed1993

Insulin-like growth factor I stimulates lipid oxidation, reduces protein oxidation, and enhances insulin sensitivity in humans.

To elucidate the effects of insulin-like growth factor I (IGF-I) on fuel oxidation and insulin sensitivity, eight healthy subjects were treated with saline and recombinant human (IGF-I (10 micrograms/kg.h) during 5 d in a crossover, randomized fashion, while receiving an isocaloric diet (30 kcal/kg.d) throughout the study period. On the third and fourth treatment days, respectively, an L-arginine stimulation test and an intravenous glucose tolerance test were performed. A euglycemic, hyperinsulinemic clamp combined with indirect calorimetry and a glucose tracer infusion were performed on the fifth treatment day. IGF-I treatment led to reduced fasting and stimulated (glucose and/or L-arginine) insulin and growth hormone secretion. Basal and stimulated glucagon secretion remained unchanged. Intravenous glucose tolerance was unaltered despite reduced insulin secretion. Resting energy expenditure and lipid oxidation were both elevated, while protein oxidation was reduced, and glucose turnover rates were unaltered on the fifth treatment day with IGF-I as compared to the control period. Enhanced lipolysis was reflected by elevated circulating free fatty acids. Moreover, insulin-stimulated oxidative and nonoxidative glucose disposal (i.e., insulin sensitivity) were enhanced during IGF-I treatment. Thus, IGF-I treatment leads to marked changes in lipid and protein oxidation, whereas, at the dose used, carbohydrate metabolism remains unaltered in the face of reduced insulin levels and enhanced insulin sensitivity.

Adult↗
PubMed1993

Normal basal and insulin-stimulated fuel metabolism in lean women with the polycystic ovary syndrome.

Many reports have suggested that hyperandrogenaemic patients with the polycystic ovary syndrome (PCOS) may be insulin resistant. However, there have also been suggestions that their insulin resistance may relate to obesity and android fat distribution. To assess whether PCOS induces metabolic disturbances independently of obesity, we studied seven lean patients with PCOS (age, 27.1 +/- 2.0 yr; body mass index, 22.2 +/- 0.78 kg/m2; waist/hip ratio, 0.79 +/- 0.02; fat-free mass, 46.38 +/- 1.13 kg) and seven normal women (age, 25.7 +/- 1.4 yr; body mass index, 21.3 +/- 0.69 kg/m2; waist/hip ratio, 0.74 +/- 0.02; fat-free mass, 50.1 +/- 1.51 kg) for 3 h in the basal period and 2 h during a hyperinsulinemic (0.4 mU/kg.min) euglycemic clamp. In the basal state, comparable metabolic indices were recorded: serum insulin, 35.9 +/- 7.7 (PCOS) vs. 37.3 +/- 2.87 pmol/L (controls); plasma C-peptide, 364.1 +/- 66.2 vs. 397.2 +/- 66.2 pmol/L; plasma glucose, 4.95 +/- 0.09 vs. 4.77 +/- 0.09 mmol/L; forearm arterio-venous difference in glucose, 0.17 +/- 0.04 vs. 0.15 +/- 0.07 mmol/L; isotopically determined endogenous glucose production, 1.9 +/- 0.1 vs. 2.0 +/- 0.1 mg/kg.min; and serum nonesterified fatty acids, 545 +/- 40 vs. 617 +/- 54 mumol/L (all P > 0.05). During the clamp, all recordings were again similar: serum insulin, 282.7 +/- 21.5 vs. 270.5 +/- 13.6 pmol/L; plasma C-peptide, 331.0 +/- 33.1 vs. 364.1 +/- 66.2 pmol/L; plasma glucose, 4.99 +/- 0.07 vs. 4.99 +/- 0.05 mmol/L; glucose arterio-venous difference, 1.01 +/- 0.18 vs. 0.85 +/- 0.12 mmol/L; endogenous glucose production, -0.9 +/- 0.1 vs. -0.5 +/- 0.2 mg/kg.min; amount of exogenous glucose necessary to maintain euglycemia, 4.0 +/- 0.4 vs. 3.8 +/- 0.5 mg/kg.min; and nonesterified fatty acids, 205 +/- 7 vs. 246 +/- 18 mumol/L (all P > 0.05). By showing normal basal and insulin-stimulated substrate metabolism in lean hyperandrogenemic PCOS patients, these data suggest that insulin resistance may be an epiphenomenon, rather than a primary feature of PCOS.

Adult↗
PubMed1992

Assessment of glucose turnover rates in euglycaemic clamp studies using primed-constant [3-3H]-glucose infusion and labelled or unlabelled glucose infusates.

Underestimation of glucose turnover rates has been a problem in clamp studies using primed-constant [3-3H]-glucose infusion technique. Due to slow mixing in interstitial compartments concealed specific activity gradients may arise between plasma and interstitial compartments during intravenous unlabelled glucose infusion. Such specific activity gradients, however, can be prevented if plasma specific activity is maintained constant. Two euglycaemic clamp studies (insulin infusion 40 mU m-2 min-1) were performed in six lean normal subjects. Using conventional unlabelled glucose infusates plasma specific activity declined by 74%, tracer determined glucose appearance was smaller than actual glucose infusion rates (317 +/- 11 vs 366 +/- 15 mg m-2 min-1, p < 0.001), and erroneous negative values were calculated for glucose production (- 49 +/- 7 mg m-2 min-1). Average underestimation during the first 2 h correlated with glucose infusion rates (r = 0.88, p < 0.02). In contrast, when plasma specific activity was maintained constant, using appropriately labelled glucose infusates, tracer determined glucose appearance and glucose infusion rates were similar (385 +/- 16 vs 385 +/- 17 mg m-2 min-1), and negative errors for glucose production were avoided. In conclusion, using unlabelled glucose infusates, as in previous studies, suppression of glucose production is overestimated and stimulation of glucose utilization is underestimated. As errors were greater with larger glucose infusions, the mistakes may have been greatest in insulin sensitive control subjects, and smaller in insulin resistant subjects. Therefore, re-evaluation of hepatic insulin sensitivity seems appropriate in diabetes, obesity, and other insulin resistant states.

Adult↗
PubMed1991

Decreased hepatic glucagon responses in type 1 (insulin-dependent) diabetes mellitus.

The effect of glucagon infusion on hepatic glucose production during euglycaemia was evaluated in seven Type 1 (insulin-dependent) diabetic patients and in ten control subjects. In the diabetic subjects normoglycaemia was maintained during the night preceding the study by a variable intravenous insulin and glucose infusion. During the study endogenous insulin secretion was suppressed by somatostatin (450 micrograms/h) and replaced by insulin infusion (0.15 mU.kg-1.min-1). 3H-glucose was infused for isotopic determination of glucose turnover. Plasma glucose was clamped at 5 mmol/l for 2 h 30 min and glucagon (1.5 ng.kg-1.min-1) was then infused for the following 3 h. Hepatic glucose production and glucose utilisation were measured during the first, second and third hour of the glucagon infusion. Basal hepatic glucose production (just prior to glucagon infusion) was similar in diabetic (1.2 +/- 0.3 mg.kg-1.min-1) and control (1.6 +/- 0.1 mg.kg-1.min-1) subjects. In diabetic patients hepatic glucose production rose slowly to 2.1 +/- 0.5 mg.kg-1.min-1 during the first hours of glucagon infusion and stabilized at this level (2.4 +/- 0.5 mg.kg-1.min-1) in the third hour. In control subjects hepatic glucose production increased sharply to higher levels than in the diabetic subjects (3.4 +/- 0.3 mg.kg-1.min-1) during the first and second hour of glucagon infusion (p less than 0.05) and then gradually fell (2.9 +/- 0.4 mg.kg-1.min-1) during the third hour. In conclusion, when stimulated with glucagon at a physiologic plasma concentration diabetic patients had 1) an overall reduced hepatic glucose production response and 2) an abnormal sluggish response pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1991

Basal and insulin stimulated substrate metabolism in tumour induced hypoglycaemia; evidence for increased muscle glucose uptake.

While it has very recently been reported that tumour induced hypoglycaemia is characterised by elevated production of insulin-like growth factor 2, the tissues responsible for induction of hypoglycaemia are largely unknown. We have investigated a patient with a large retroperitoneal mass and spontaneous hypoglycaemia. When compared to a reference population the patient displayed: (1) An increased glucose disposal rate and a five-fold elevation of forearm glucose uptake. (2) A decreased endogenous glucose production rate. (3) Decreased circulating levels of lipid intermediates. (4) Increased glucose oxidation and decreased lipid oxidation. (5) Low circulating levels of insulin-like growth factor 2 and insulin-like growth factor-binding protein-3 and normal levels of insulin-like growth factor 1. (6) Normal insulin sensitivity (euglycaemic glucose clamp). Blood concentrations of insulin, C-peptide, proinsulin, glucagon, growth hormone and catecholamines were within normal range, but the growth hormone response to hypoglycaemia was blunted. The data suggest that the mechanisms behind tumour induced hypoglycaemia are of systemic nature and that the tissue most prominently affected is striated muscle.

Blood Glucose↗
PubMed1990

Essential factors in a community college-nursing home partnership.

The community college-nursing home partnership has two major objectives: to develop nursing potential in long-term care settings and to influence the redirection of associate degree nursing education to include active participation in long-term care settings. Successful partnerships are built on a commitment to high quality education for students and high quality service for patients. Other essential factors to a successful partnership include collaborative planning, pragmatic goal setting, clear communication, and mutual respect.

Community Health Nursing↗
PubMed1982

Coping: foreword.

Explore the source record for details and available documents.

Adaptation, Psychological↗
PubMedDate not supplied

Lack of effects of angiotensin-converting enzyme (ACE)-inhibitors on glucose metabolism in type 1 diabetes.

To evaluate the impact of ACE-inhibitors on insulin-mediated glucose uptake, glucose-induced glucose uptake, and hepatic glucose production, a sequential glucose clamp was performed in eight normotensive Type 1 diabetic patients after 3 weeks of enalapril therapy 20 mg day-1 and during control conditions. The experiments were carried out in random order. Mean arterial blood pressure was significantly reduced during ACE-inhibition (95 +/- 3 (+/- SE) vs 84 +/- 3 mmHg; p less than 0.02), while blood glucose control as assessed by HbA1c was unaltered (7.9 +/- 0.5 vs 7.6 +/- 0.5%). The night prior to the study normoglycaemia was maintained by a Biostator. A two-step hyperinsulinaemic euglycaemic clamp (insulin infusion rate 0.3 and 0.8 mU kg-1 min-1) was followed by a hyperinsulinaemic and hyperglycaemic clamp (insulin infusion rate 0.8 mU kg-1 min-1, plasma glucose 11 mmol l-1). Insulin concentrations were comparable with and without enalapril treatment. During the hyperinsulinaemic clamps isotopically determined glucose disposal was unchanged (low dose 2.5 +/- 0.3, high dose 4.3 +/- 0.7 vs 2.6 +/- 0.3 and 4.3 +/- 0.7 mg kg-1 min-1, enalapril vs control). Glucose-induced glucose disposal (9.2 +/- 1.2 vs 9.1 +/- 1.2 mg kg-1 min-1) was also similar, as were non-protein respiratory exchange ratios (indirect calorimetry). Glucose production was not changed by enalapril. In conclusion, treatment with enalapril has no significant effect on glucose metabolism in Type 1 diabetes.

3-Hydroxybutyric Acid↗