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Biomedical subjects

H Shamoon

Publications and source records attributed to H Shamoon.

At least 37 records · Page 2Linked to original sources
PubMed1992

Impaired glucose disposal following mild hypoglycemia in nondiabetic and type I diabetic humans.

Insulin-mediated glucose disposal was studied immediately prior to and following moderate hypoglycemia in nondiabetic subjects and subjects with insulin-dependent (type I) diabetes mellitus (IDDM), the latter having varying epinephrine secretory capacities. Plasma insulin concentration was fixed throughout the study at approximately 300 to 400 pmol/L to avoid effects of waning insulin action and plasma glucose was clamped at either 5 mmol/L (euglycemic control) or at 3.1 mmol/L (hypoglycemic) periods of 120 minutes. Baseline (clamp 1) and postexperiment (clamp 2) periods were assessed for net glucose disposal (as a function of the exogenous glucose infusion rate) and glucose kinetics using 3H-glucose. In normal subjects, glucose disposal increased progressively by 132% during control studies but only by 57% with intervening hypoglycemia (P less than .005). Similarly, 33% during hypoglycemia, P less than .025). These changes were mediated by reduction of whole-body glucose uptake (rate of glucose disappearance [Rd], [3H]-3-glucose) and metabolic clearance rates with comparable suppression of hepatic glucose production in both groups. The increase in plasma free-fatty acids (FFA) following hypoglycemia was modest but greater in subjects with IDDM (P less than .01), whereas IDDM had reduced concentrations of epinephrine (P less than .01) and glucagon (P less than .005) during hypoglycemia. In subjects with IDDM but not in normal subjects, the change in posthypoglycemia glucose disposal was inversely correlated with the increase in plasma norepinephrine (R2 = .54, P less than .004) and epinephrine (R2 = .32, P less than .04). Glucose disposal did not correlate with other counterregulatory hormones, plasma FFA, or antecedent glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effect of physiological hyperinsulinemia on counterregulatory hormone responses during hypoglycemia in humans.

UNLABELLED: We evaluated the effect of continuous physiological hyperinsulinemia on counterregulatory hormone responses in seven healthy subjects, each studied on two occasions. Hormone responses were measured during identical 2-h periods of hypoglycemia (plasma glucose target 3.5 mmol/L) at insulin levels of 350 pmol/L or 640 pmol/L. During hypoglycemia, there were significant (50-1400%) increases in glucagon, epinephrine, norepinephrine, GH, and cortisol which were comparable in the two groups. We further evaluated the influence of the duration of mild hyperinsulinemia on the responses in an additional group of normal subjects (n = 7). Brief (30 min) exposure to insulin was compared to a prolonged (3.5 h) insulin infusion, each followed by identical hypoglycemia. Plasma insulin (approximately 350 pmol/L) and plasma glucose (target 3.3 mmol/L) were similar in both groups. The increases in epinephrine, norepinephrine, GH, and cortisol during hypoglycemia were virtually identical in the two groups. However, the secretion of glucagon was blunted following prolonged hyperinsulinemia, increasing to levels of 249 +/- 17 ng/L in the brief studies and to only 185 +/- 20 ng/L in the prolonged studies (P < 0.005). The insulin-induced decrement in plasma amino acids were similar in the two studies and could not account for the impaired glucagon secretory response. CONCLUSIONS: 1) Brief exposure to even high physiological levels of insulin do not alter the magnitude of counterregulatory hormone secretion during hypoglycemia; 2) prolonged hyperinsulinemia results in a selective blunting of the plasma glucagon response to hypoglycemia, perhaps due to a direct suppressive effect of insulin on alpha-cell secretion.

Adult↗
PubMed1992

Pathophysiology of diabetes. A review of selected recent developments and their impact on treatment.

Recent developments in epidemiology, physiology, anatomy and molecular biology have greatly increased our knowledge of the aetiology and immunological mechanisms involved in diabetes mellitus. This understanding has, in turn, facilitated progress in the diagnosis and treatment of the disease. It is generally accepted that both genetic and environmental factors have a role in the pathogenesis of insulin- and non-insulin-dependent diabetes mellitus. The contribution of insulin resistance or decreased insulin secretion to the pathogenesis of non-insulin-dependent diabetes remains controversial but it is likely that both have a role to play. Counterregulatory hormones, principally adrenaline (epinephrine) and glucagon, prevent blood glucose levels falling to extreme levels by antagonising the effect of insulin hypoglycaemia, and inducing hepatic glucose production. Patients with insulin-dependent diabetes frequently exhibit impaired glucose counterregulation and, although its aetiology is uncertain in some patients, intensification of insulin therapy per se has been implicated. Secondary failure of oral hypoglycaemic agents in patients with non-insulin-dependent diabetes is a major and often inevitable problem, necessitating combined use of sulphonylurea and insulin in most patients. Recently, new treatments for patients with diabetes have been developed, including insulin analogues administered by a variety of novel methods, pancreatic grafts and transplantation of islet cells. Although promising, the clinical viability of these techniques remains to be demonstrated.

Animals↗
PubMed1992

Further defects in counterregulatory responses induced by recurrent hypoglycemia in IDDM.

We evaluated the effect of previous experimental hypoglycemia on counterregulatory responses to hypoglycemia in 13 IDDM patients. These patients had defects in counterregulatory responses to hypoglycemia compared with 7 nondiabetic control subjects. Plasma EPI and glucagon responses to hypoglycemia in IDDM patients were approximately 60% of levels in nondiabetic subjects (P less than 0.02 and P less than 0.001, respectively). Hepatic glucose output ([3-3H]glucose) was reduced by approximately 60% of normal (P less than 0.005), and the glucose infusion rate required to maintain plasma glucose was correspondingly greater in people with IDDM (P less than 0.001). With a modified glucose clamp (plasma insulin approximately 330 pM), the diabetic subjects underwent two sequential 120-min periods of hypoglycemia (approximately 3.0 mM) with an intervening 60-min euglycemic recovery period. In the IDDM patients, there were 30-50% decreases in plasma GH (P less than 0.005) and cortisol (P less than 0.001) responses during the second hypoglycemic period compared with the first. In addition, glucose output, already defective compared with that in nondiabetic subjects, was further reduced by 33% (P = 0.03) during the second period of experimental hypoglycemia. There was no effect of repeated hypoglycemia on the responses of plasma glucagon, EPI, or NE, though plasma EPI was correlated directly with glucose output (P less than 0.001) and inversely with glucose uptake (P less than 0.05). There was no correlation between the rise in glucose output during hypoglycemia and antecedent glycemic control as measured by HbA1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effects of labetalol on perioperative stress markers and isoflurane requirements.

We have studied the effect of labetalol on anaesthetic requirements, cardiac and humoral responses in 16 healthy women during elective abdominal surgery. The experimental group (n = 8) received increments of i.v. labetalol 0.15-0.3 mg kg-1 to reduce mean arterial pressure (MAP) by 15% from values obtained before anaesthesia. All patients received thiopentone 6 mg kg-1 and anaesthesia was maintained with isoflurane and nitrous oxide. In the placebo group, tracheal intubation provoked a 33% increase in heart rate (HR) and a 52% increase in MAP (P less than 0.001 vs baseline for both). In contrast, pretreatment with labetalol resulted in a 7.3% increase in HR and a 21.3% increase in MAP (P less than 0.05 vs baseline for MAP). Two patients treated with labetalol had a reduction in MAP to 50-60 mm Hg during surgery. After tracheal extubation, the labetalol group had a significantly slower HR than the placebo group (P less than 0.05). The cardiovascular response to tracheal intubation was associated with an increase in plasma noradrenaline concentration in both groups. Labetalol did not affect isoflurane requirements, plasma concentrations of adrenaline, cortisol and aldosterone or arterial PO2, but prevented the decrease in plasma concentration of potassium which occurred in placebo treated patients (P less than 0.05) in early recovery. We conclude that preanaesthetic administration of labetalol attenuated the perioperative hypertensive and tachycardic responses, but was accompanied by intraoperative hypotension when given in doses greater than 0.5 mg kg-1, despite an increase in plasma noradrenaline concentrations.

Abdomen↗
PubMed1991

Deficient counterregulatory hormone responses during hypoglycemia in a patient with insulinoma.

Counterregulatory hormone responses were evaluated in a 37-yr-old woman before and after removal of a benign insulin-producing islet cell tumor. Counterregulatory hormone concentrations were measured during a glucose clamp with graded reductions of plasma glucose from 5.2 to 2.6 mmol/L. In the study before surgery, the increase in plasma epinephrine concentration was markedly blunted (by greater than 90%) compared to that in the study after surgery. The peak plasma norepinephrine concentration was similarly reduced by 71%, and plasma cortisol by 63%. In addition, the glycemic thresholds for secretion of the counterregulatory hormones were lower before removal of the tumor. Peak plasma GH responses were equivalent before and after surgery, but the threshold for GH secretion was 21% lower in the first hypoglycemia study. We conclude 1) that there is evidence for abnormal glucose counterregulatory hormone secretion in this patient, which may contribute to the pathogenesis of hypoglycemia seen in patients with insulinoma; 2) the reversal of reduced counterregulatory hormone secretion after tumor resection suggests that these defective hormonal responses may be related to recurrent hypoglycemia, persistent hyperinsulinemia, or both; and 3) that abnormal glucose counterregulation may exist in the absence of type 1 diabetes.

Adult↗
PubMed1991

Counterregulatory adaptation to recurrent hypoglycemia in normal humans.

We evaluated the effect of antecedent hypoglycemia on glucose counterregulation during hypoglycemia in non-diabetic human subjects. In single hypoglycemia studies, glucose production [( 3H]3-glucose) and counterregulatory hormone concentrations were measured (after a 3.5-h baseline period of euglycemia) during 120 min of hypoglycemia (glucose clamped at 3.0 mmol/L). During the final 60 min of hypoglycemia, counterregulation resulted in significant increments in glucose production (12.88 +/- 0.83 mumol/kg.min), and plasma glucagon (IRG; 185 +/- 22 ng/L), GH (29.3 +/- 7.0 micrograms/L), cortisol (630 +/- 100 nmol/L), epinephrine (3.44 +/- 0.76 nmol/L), and norepinephrine (2.02 +/- 0.21 nmol/L). In the recurrent hypoglycemia experiment, an antecedent period of identical hypoglycemia was induced. Glucose counterregulation during the second of two periods of hypoglycemia (HYPO 2) was then compared to that in single hypoglycemia studies. During HYPO 2, there were decreased responses in Ra (by 32%; P less than 0.03), GH (by 67%; P less than 0.05), F (by 41%; P less than 0.03), and norepinephrine (by 20%; P = 0.03) compared to those in the single hypoglycemia study. In contrast, plasma IRG values were similar in the single hypoglycemia studies and HYPO 2, but were reduced relative to those during the first hypoglycemic period of recurrent hypoglycemia (IRG, 263 +/- 18 ng/L; P less than 0.025 vs. HYPO 2 and P less than 0.05 vs. single hypoglycemia). Our results suggest that 1) antecedent hypoglycemia may alter glucose counterregulation during hypoglycemia; and 2) recurrent hypoglycemia may result in alterations in reduction of hepatic glucose production.

Acclimatization↗
PubMed1991

Quality assurance for blood glucose monitoring in health-care facilities.

OBJECTIVE: To describe the practice of quality assurance (QA) for capillary blood glucose monitoring (CBGM) in health-care facilities. RESEARCH DESIGN AND METHODS: Descriptive survey data were collected from a purposive sample of 378 health-care providers, who use CBGM and direct CBGM QA programs, from acute- and chronic-care facilities in 47 states. Subjects completed a 36-item multiple-choice survey about QA practices for CBGM by providers. RESULTS: Only 53.4% of respondents reported a multidisciplinary advisory group to assist in decision making for the CBGM program. Almost one-third reported no clinical laboratory involvement in their QA program. Over 70% of respondents reported inclusion of all clinical areas in the CBGM program. Comparison of results of the same patient sample by laboratory reference method and CBGM system was done routinely by only 43.6% of respondents. Scheduled proficiency testing was reported by 33.4%. Only 5.8% of respondents reported the coexistence of a CBGM advisory group, full participation of the laboratory, and quarterly proficiency testing. Over 50% of respondents reported a patient charge for CBGM. CONCLUSIONS: When survey results are compared with regulatory and accreditation standards, it is evident that a wide gap exists. Resources to bridge this gap may be scarce in many facilities. Further research is needed to determine minimal QA standards for CBGM that provide for optimal patient outcomes.

Blood Glucose↗
PubMed1990

Insulin response and glycemic effects of meals in non-insulin-dependent diabetes.

Glycemic and hormonal responses to two breakfast mixed meals were studied in six obese subjects with NIDDM. The study evaluated a high-glycemic-effect (HGE) and a low-glycemic-effect (LGE) meal, each with approximately 600 kcal and 12% protein, 15% fat, and 73% carbohydrate. Plasma insulin and counterregulatory hormones were measured at baseline and at 30-min intervals for 5 h after meals. Mean fasting plasma glucose and insulin concentrations were similar before both studies: for the LGE meal, 11.9 +/- 1.8 mmol/L and 261.9 +/- 50.1 pmol/L; for the HGE meal, 11.9 +/- 2.0 mmol/L and 262.6 +/- 43.1 pmol/L. Peak plasma glucose concentrations were approximately 25% lower with the LGE meal and the area under the glucose curve was 63% of that obtained for the HGE meal (p less than 0.05). Although the integrated insulin responses of the two meals did not differ, the peak occurred 60 min earlier in the LGE meal (p less than 0.05). The LGE meal may produce a lower glycemic response, in part because of earlier insulin secretion.

Aged↗
PubMed1990

Islet hormonal regulation of glucose turnover during exercise in type 1 diabetes.

A decline in plasma insulin and an increase in glucagon are known to occur during intense and/or prolonged exercise. However, it is not established whether changes in insulin and glucagon secretion are involved in the precise matching of hepatic glucose production to the enhanced glucose uptake by muscle during brief, low intensity exercise. We studied the effects of 30-min cycle exercise at 40% of maximal aerobic capacity in healthy subjects and C-peptide-deficient subjects with type 1 diabetes (IDDM) using [3-3H]glucose to estimate glucose turnover. Diabetic subjects were studied during continuous iv insulin infusion, which normalized glucose kinetics before experimental perturbations. In control (saline-infused) experiments, endogenous glucose appearance (Ra) increased by 80-90% above baseline to match the increase in glucose disappearance in both normal and IDDM subjects, even though the latter exercised at fixed levels of plasma free insulin, averaging 203 +/- 19 pmol/L. In other experiments, somatostatin was infused, and glucagon (1.0 ng/kg.min) and insulin (at two different rates) were maintained at constant levels. Infusion of insulin in normal subjects at doses sufficient to maintain constant peripheral plasma insulin was associated with no apparent effect on glucose turnover (plasma insulin, 80 +/- 21 pmol/L, compared to 52 +/- 5 pmol/L during saline; P = NS). However, insulin infusion at doses that normalized the portal insulin concentration (approximately 208 pmol/L) together with glucagon replacement inhibited the rise in glucose production in both normal and IDDM subjects. There were similar 45-55% reductions (P less than 0.03) of the increase in Ra seen with exercise in control experiments. When peripheral plasma free insulin (and presumably portal levels as well) were increased by about 20% in this experimental setting in IDDM (278 +/- 43 pmol/L), the suppression of Ra was even more profound, and Ra failed to increase at all with exercise. We conclude that the hormonal regulation of Ra in brief duration exercise in man does not necessitate the decrements in portal venous insulin observed under more intense exercise conditions as long as an exercise-induced glucagon secretory response can occur. Glucagon secretion alone cannot prevent hypoglycemia when portal venous insulin concentrations are increased by minimal amounts, such as in insulin-treated diabetics.

Adult↗
PubMed1990

Abnormal growth hormone responses to hypoglycemia and exercise in adults with type I diabetes.

Abnormal regulation of growth hormone (GH) secretion has been reported in some patients with insulin-dependent diabetes (IDD). We compared the GH responses in 32 healthy subjects (age 25 +/- 2 SE years) and in 23 IDD patients (28 +/- 1.9 years old, diabetes duration 10.4 +/- 2 years, and glycohemoglobin levels 9.3 +/- 2.0%). During acute, severe hypoglycemia (glucose less than 40 mg/dl), the mean GH levels were similar. When prolonged mild hypoglycemia was induced (58.0 +/- 2.0 mg/dl in the controls and 54.0 +/- 2.0 mg/dl in the IDD patients), the mean GH levels were similar, although the increase in GH was delayed in the latter group. During brief (30 min) exercise at 40-50% of VO2max, GH rose comparably in both groups (IDD patients maintained euglycemia with basal insulin infusion). However, with more prolonged and intense exercise using a glucose clamp to maintain euglycemia, GH rose to 5.4 +/- 2.2 ng/ml in controls and 26.4 +/- 12.6 ng/ml in the diabetics (P less than 0.05). When the combination of intense exercise and hypoglycemia (approximately 55 mg/dl) was used, GH rose to a peak of 21.7 +/- 2.7 ng/ml in the controls and to 33 +/- 3.0 ng/ml in the diabetics (P = NS). Our data show that in insulin-infused IDD patients made euglycemic for these experiments: a) The GH response to acute, severe hypoglycemia was identical to that in the controls and the response to mild, prolonged hypoglycemia was delayed, but of similar magnitude compared with controls; b) Exercise-induced GH responses were observed in both groups, but exaggerated in the diabetics at a higher exercise intensity; c) Hypoglycemia during exercise produced an additive effect on GH secretion in the controls but not in the IDD patients. We conclude that the wide range of abnormal GH secretory responses in type I diabetes reflects a central, possibly hypothalamic, defect in GH regulation.

Adult↗
PubMed1990

Relationship of insulin secretion and glycemic response to dietary intervention in non-insulin-dependent diabetes.

Forty-two obese subjects with non-insulin-dependent diabetes mellitus had their plasma insulin, C peptide, and glucose levels measured after an overnight fast and in response to a 75-g oral glucose loading. Subjects were then prospectively followed up with dietary treatment, and the same measurements were repeated at 1 year. Although insulin values tended to be lower with greater fasting hyperglycemia at baseline, no correlation was observed among three parameters. However, near-normalization of glycemia (measured as the level of hemoglobin A1) was associated with significantly higher fasting and stimulated plasma insulin concentrations. Sixteen subjects were matched to each other for equivalent baseline hyperglycemia (by glycosylated hemoglobin) and divided into group 1 (normalization of the hemoglobin A1 value to 7.0% +/- 0.3% [mean +/- SE]) and group 2 (persistent hyperglycemia) (hemoglobin A1 value, 10.7% +/- 0.7% [mean +/- SE]). Before dietary therapy, the plasma insulin concentrations were twofold to threefold higher in group 1, and despite similar degrees of weight loss, group 2 failed to demonstrate improved glycemia. We concluded that the outcome of diet therapy for non-insulin-dependent diabetes mellitus is dependent on the duration of diabetes and endogenous insulin secretory reserve. There is a subgroup of patients with non-insulin-dependent diabetes mellitus in whom delayed dietary intervention may have a beneficial effect.

Blood Glucose↗
PubMed1989

Regulation of counterregulatory hormone secretion in man during exercise and hypoglycemia.

We examined the role of the plasma glucose concentration per se in the secretion of counterregulatory hormones during exercise. Ten men (average age, 24 yr; maximal aerobic capacity, 31.8 mL/kg.min) were studied during two 50-min bicycle exercise periods at either normal glucose [87 +/- 1 (+/- SE) mg/dL (4.8 +/- 0.1 mmol/L)] or low glucose [59 +/- 1 mg/dL (3.3 +/- 0.1 mmol/L)]. The plasma glucose targets were achieved by exogenous insulin and variable glucose infusions. These results were compared to studies in which saline was infused. Exercise at normal glucose was associated with significant increments in plasma epinephrine (maximum 3- to 5-fold above baseline) and norepinephrine (2-fold), comparable to those that occurred during saline administration. Plasma GH increased only at the most intense exercise level, while plasma cortisol and glucagon did not increase significantly. In low glucose-exercise studies, the increase in plasma epinephrine during exercise was significantly greater than that at normal glucose (P less than 0.01), although proportional to basal preexercise levels (r = 0.73; P less than 0.001). Plasma glucagon increased almost 100%, and plasma cortisol and GH increased by 150% and 400%, respectively. Compared to the effect of the same degree of hypoglycemia in the absence of exercise, only plasma epinephrine (P = 0.002) and norepinephrine (P less than 0.001) displayed effects independent of hypoglycemia during exercise. When low glucose was reversed to normal at the midpoint of exercise, plasma epinephrine and glucagon returned to the levels obtained for the same duration of exercise at normal glucose, while norepinephrine, GH, and cortisol were only partially responsive to the rise in plasma glucose. These data suggest that 1) moderate exercise is a stimulus for a sympathoadrenal and GH response, but not a peripheral glucagon response; 2) during exercise and hypoglycemia, plasma epinephrine and norepinephrine are enhanced, while the glucagon response is entirely glucose dependent; and 3) the epinephrine response to hypoglycemia can be dissociated from that to exercise, suggesting differing control mechanisms. We conclude that the activation of counterregulatory hormones during exercise is regulated by glucose-independent mechanisms, although these responses may be augmented by concurrent hypoglycemia.

Adult↗
PubMed1988

Hormonal and metabolic effects of calcium channel antagonists in man.

Calcium is a component of many metabolic reactions. By blocking calcium transport across cell membranes, calcium channel antagonists can therefore theoretically affect numerous metabolic and hormonal processes. In vitro studies have often documented just such an effect. Because of the expanding use and prevalence of calcium antagonists in clinical practice, a review of their in vivo effects on hormones and metabolism is warranted. The effect on glucoregulatory hormones, calcium regulatory hormones, anterior and posterior pituitary secretion, the renin-angiotensin axis, plasma catecholamines, and plasma lipids and lipoproteins is herein reviewed. The various calcium antagonists, by virtue of their distinct chemical structures, influence metabolism in their own unique manner. Despite the widespread involvement of calcium in hormone action, however, calcium channel antagonists have little dramatic impact on hormone regulation. This is, in part, due to the drug dosage used in clinical practice and to the inherent compensatory mechanisms built into normal endocrine function. The development of agents with greater and more potent metabolic specificity, however, coupled with the ability to target drug action, holds promise for expanded therapeutic application in the future.

Adrenal Cortex Hormones↗
PubMed1987

Defective epinephrine and growth hormone responses in type I diabetes are stimulus specific.

The counterregulatory hormone responses to hypoglycemia and a non-glucose stimulus, exercise, were evaluated in 18 subjects with type I diabetes and in 9 normal controls. Subjects with diabetes had no overt neuropathy, with R-R variations and postural plasma norepinephrine increments that were similar to those of controls. The diabetic subjects exhibited normal increments in plasma growth hormone (GH), norepinephrine, and cortisol but blunted or absent responses in plasma epinephrine and glucagon when hypoglycemia was severe (less than 40 mg/dl). During a 60-min clamped reduction in plasma glucose at approximately 65 mg/dl, plasma GH and epinephrine increased 6- to 15-fold in controls but 2- to 4-fold in diabetics (P less than .05). However, when subjects were exercised at this plasma glucose level (50 W for 10 min), plasma epinephrine and GH in diabetics rose markedly by 150-400% to attain the peaks reached by the controls. Plasma norepinephrine and cortisol increased to similar levels in both groups, and plasma glucagon was not significantly changed. We conclude that epinephrine and GH secretion in response to hypoglycemia are reduced in type I diabetes but that these defects are stimulus specific because the responses to exercise are not reduced.

Adult↗
PubMed1986

Assessment of long-term glycemia in type I diabetes using multiple blood glucose values stored in a memory-containing reflectometer.

The relationship between repetitive hemoglobin A1 values and daily blood glucose tests performed by 20 insulin-dependent diabetic outpatients was assessed over a six-week period using a modified reflectance meter capable of storing blood glucose determinations automatically. An average of four and a half determinations per subject per day was recorded with a range of average blood glucose values between 82 +/- 2 mg/dl and 316 +/- 5 mg/dl (mean +/- SE). The relationship between average blood glucose and hemoglobin A1 values was significant when hemoglobin A1 values at the end of the six-week period were correlated with the mean blood glucose level over that period (r = 0.55, p less than 0.02), but improved when a more remote hemoglobin A1 value obtained at 10 weeks was used (r = 0.64, p less than 0.005). Hemoglobin A1 values covering two-week intervals were extremely poor in reflecting average glycemia. The average fasting blood glucose level in these subjects was highly correlated with the overall daily blood glucose values (r = 0.89, p less than 0.0001), although the coefficients of variation of these parameters averaged 43 +/- 3 percent and 47 +/- 2 percent, respectively, and were greater than that of the hemoglobin A1 values over six weeks (10 +/- 2 percent). It is concluded that labile blood glucose control in patients with insulin-dependent diabetes is accurately reflected by the average fasting blood glucose level, although multiple determinations must be employed. Satisfactory assessment may be made by use of hemoglobin A1 value provided that the hemoglobin A1 determination follows a sufficiently long period of time, presumably related to the turnover of glycosylated hemoglobin.

Blood Glucose↗
PubMed1986

Beta-adrenergic contribution to glucagon-induced glucose production and insulin secretion in uremia.

Spontaneous or propranolol-induced hypoglycemia can occur in uremic humans. We studied glucose kinetics (using [3-3H]glucose) in five uremic humans 24 h after hemodialysis and in seven normal controls. The effect of glucagon infusion at rates of 3, 6, 12, and 18 ng X kg-1 X min-1 at 60-min intervals was compared with either saline or beta-adrenergic blockade (propranolol infusion). In uremics, plasma glucose increased by 20-25% and by 40-50% at the 3 and 6 ng X kg-1 X min-1 glucagon doses, respectively, with no further increases at higher infusion rates. Glucose production increased transiently and in tandem with glucose uptake at each glucagon increment (P less than 0.0001). During beta-adrenergic blockade, the effect of glucagon in stimulating glucose production was blunted by 14-24% at the 6-18 ng X kg-1 X min-1 doses (P less than 0.05). During saline infusion, plasma insulin concentrations increased progressively to peak levels fourfold above basal at the 18 ng X kg-1 X min-1 dose. This increase in plasma insulin was virtually abolished by concomitant beta-adrenergic blockade (P = 0.0002). In contrast to uremic subjects, normal controls exhibited lesser degrees of hyperglycemia and hyperinsulinemia at all glucagon infusion rates. Propranolol infusion had no effect on the increments in glucose production and uptake nor on the plasma insulin response. These results suggest that in uremic humans propranolol independently reduces the hepatic response to glucagon and the insulin secretory response to hyperglycemia and/or hyperglucagonemia. These observations provide a possible mechanism for the adrenergic regulation of glucose homeostasis in uremia.

Adult↗