Correlation between glycemia and glycated hemoglobin.
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Blood Glucose↗
Biomedical subjects
F J Service
Publications and source records attributed to F J Service.
Meal-related insulin requirements.
Postprandial glycemia correlates with meal size in insulin dependent diabetic and nondiabetic persons. Decline in meal tolerance as the day progresses noted in nondiabetics does not occur in IDDM. Meal size correlates with insulin secretion in nondiabetics and amounts of insulin infused by an artificial endocrine pancreas to IDDM. There is no diurnal change in insulin secretion in nondiabetics or insulin infusion into IDDM but not amounts of insulin secretions by nondiabetics. Sequence of meal ingestion influenced amounts of insulin infused into IDDM. It is unclear to what extent variation in carbohydrate contribution or composition affect postprandial events. More precise quantitative measures of meal-related glucose behavior such as mean indices of meal excursions may be useful. CSII used in IDDM has been shown to normalize postprandial endogenous glucose production.
Blood Glucose↗
Hypoglycemia and the postprandial syndrome.
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Blood Glucose↗
Diagnostic interpretation of the intravenous tolbutamide test for insulinoma.
The plasma glucose and insulin responses to intravenous administration of tolbutamide in patients with insulinoma and healthy control subjects were compared to determine the sensitivity and specificity of the intravenous tolbutamide test for the diagnosis of insulinoma. The records of 406 healthy persons without concurrent disease known to affect glucose homeostasis or insulin concentrations and 41 patients with histologically confirmed insulinoma who underwent standard intravenous tolbutamide testing during the period from 1976 to 1986 were reviewed. The 5th percentile of the mean of plasma glucose levels at the 120-, 150-, and 180-minute points (G120-180) after injection of tolbutamide was 55 mg/dl for lean and 62 mg/dl for obese control subjects. With 95% specificity, the sensitivity of these criteria was 95% for lean and 100% for obese patients with insulinoma. Minimal differences were observed between men and women. At 95% specificity, the sensitivities were less for the ratio of the 180-minute plasma glucose to fasting plasma glucose level (64% in lean and 75% in obese patients), for mean of plasma insulin at the 120-, 150-, and 180-minute points (IRI120-180) (53% in lean and 36% in obese patients), for maximal insulin concentration (27% in lean and 31% in obese patients), for increase in insulin concentration above basal (18% in lean and 23% in obese patients), and for the combined criteria of the 5th percentile of G120-180 and the 95th percentile of IRI120-180 (47% in lean and 73% in obese patients).(ABSTRACT TRUNCATED AT 250 WORDS)
Adenoma, Islet Cell↗
Proinsulin levels and insulinomas.
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Adenoma, Islet Cell↗
Potential incretins.
A greater plasma concentration of insulin after isoglycemic enteral than after parenteral administration of glucose is called the incretin effect. The primary mediator of this effect, gastric inhibitory polypeptide, may not account for the complete manifestation of this phenomenon. We evaluated other gastroenteric polypeptides with respect to a differential response to oral ingestion of glucose and intravenous administration of glucose at rates that achieved arterial plasma glucose concentrations matched to those from orally administered glucose. Gastrin, peptide histidine methionine, peptide YY, and neurotensin showed increases in plasma concentrations in response to oral ingestion of glucose but not to intravenous administration of glucose. Vasoactive intestinal polypeptide showed no increased concentration in response to either oral or intravenous administration of glucose. The differential responses to orally and intravenously administered glucose noted in the former gastroenteric polypeptides qualifies them as potential mediators of the incretin effect.
Administration, Oral↗
Management of noninsulin-dependent diabetes mellitus.
Management of the patient with NIDDM requires the skill and patience of the physician and the input of a health team, including the dietitian and nurse educator. With perseverance and careful follow up, most treatment goals can be achieved in these patients. The attitude of neglect and easy treatment goals that previously characterized the care of these patients are not justified.
Continuity of Patient Care↗
Role of gastric inhibitory polypeptide in postprandial hyperinsulinemia of obesity.
To assess the contribution of gastric inhibitory polypeptide (GIP) to the postprandial hyperinsulinemia of obesity, secretion rates of GIP (generated from kinetic analyses from infusions of porcine GIP) and insulin (from C-peptide applied to a validated kinetic model) to meals of 3 sizes were determined in 10 obese (5 male and 5 female) and 10 lean, sex- and age-matched healthy subjects. Although the postprandial secretion rates of GIP were greater in obese subjects (P = 0.03), postprandial concentrations of GIP were not. The latter may be explained by the greater volume of distribution of GIP in obese subjects (P = 0.036). Secretion rates and volume of distribution of GIP were correlated (r = 0.652, P less than 0.01). Despite excessive integrated postprandial (P = 0.010) insulin concentrations, insulin secretion was not significantly different between obese and lean subjects. We conclude that 1) although postprandial plasma GIP concentrations are normal, GIP secretion is increased in obesity, 2) the postprandial hyperinsulinemia of obesity is not due to excessive insulin secretion but is likely secondary to altered insulin clearance, and 3) GIP cannot account for the hyperinsulinemia of obesity through its insulinotropic action.
Adult↗
Incretin effect due to increased secretion and decreased clearance of insulin in normal humans.
To assess the contribution of changes in insulin secretion and clearance to the incretin effect (greater insulinemia after oral than after intravenous glucose), 10 healthy subjects were studied after oral glucose (1 g/kg body wt) and again when glucose was infused intravenously at rates to match arterialized plasma glucose concentrations after oral glucose. Although basal and integrated plasma glucose did not differ between oral and intravenous glucose, integrated responses of insulin (3.3 +/- 0.5 vs. 1.8 +/- 0.4 mU ml-1.240 min-1, P less than .001), C-peptide (456.5 +/- 58.5 vs. 327.9 +/- 46.3 ng.ml-1.240 min-1, P = .002), gastric inhibitory polypeptide, (16.8 +/- 3.5 vs. -2.8 +/- 1.0 micrograms.ml-1.240 min-1, P less than .001), and insulin secretion (6.6 +/- 1.1 vs. 4.7 +/- 0.7 U.240 min-1, P = .003) were greater with oral than intravenous glucose. However, insulin clearance, whether calculated as the molar ratio of integrated C-peptide to integrated insulin responses (6.9 +/- 0.7 vs. 14.2 +/- 3.8, P = .005) or from the formula insulin clearance equals insulin secretion divided by integrated insulin responses (1.1 +/- 0.2 vs. 2.5 +/- 0.7 L.min-1.m-2, respectively, P = .002), was less for oral than for intravenous glucose. Therefore, the incretin effect is mediated both by increased secretion and decreased clearance of insulin.
Administration, Oral↗
Regulation of whole-body leucine metabolism with insulin during mixed-meal absorption in normal and diabetic humans.
To determine the effects of insulin on dietary and endogenous leucine metabolism, five normal subjects, seven insulin-insufficient insulin-dependent (IDDM) diabetic patients, and five diabetic patients controlled with continuous subcutaneous insulin infusion (CSII) were studied before and for 8 h after ingestion of a chemically defined elemental test meal (10 cal/kg) containing crystalline amino acids. L-[1-14C]leucine was included in the meal to trace the entry and oxidation of the dietary leucine. Total (meal + endogenous) entry of leucine into the circulation was estimated with a constant infusion of [2H3]leucine. Postabsorptive and meal-related increases in the plasma leucine concentration were greater (P less than .05) in the insulin-insufficient IDDM than in the normal subjects but returned to near-normal values with CSII. Baseline leucine flux was approximately 40% greater in the insulin-insufficient IDDM than in normal subjects (2.17 +/- 0.17 vs. 1.55 +/- 0.15 mumol.kg-1.min-1, respectively; .05 less than P less than .01) but were near normal during CSII treatment (1.85 +/- 0.25 mumol.kg-1.min-1). Furthermore, total leucine entry during meal absorption was greater in the insulin-insufficient IDDM (1.41 +/- 0.10 mmol.kg-1.8 h-1) than in either normal (0.96 +/- 0.08 mmol.kg-1.8 h-1, P less than .01) or IDDM subjects during CSII treatment (1.09 +/- 0.11 mmol.kg-1.8 h-1, P less than .05). Fractional oxidation (approximately 40-50%) and entry of dietary leucine were similar in all three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Hypoglycemia.
Hypoglycemia is an abnormally low plasma glucose concentration and not a disease entity. With the exception of the effect of hypoglycemic drugs (insulins and sulfonylureas), hypoglycemia arises from an aberration in one or more mechanisms involved in glucose homeostasis. Progress in our knowledge of glucose homeostasis in the past decade and the development of radioimmunoassay for insulin, the primary hypoglycemic hormone, and C-peptide, a marker of insulin secretion, have facilitated both the understanding and diagnostic precision of hypoglycemic disorders.
Humans↗
Lack of a direct effect of the autonomic nervous system on glucose-stimulated gastric inhibitory polypeptide (GIP) secretion in man.
To determine whether the autonomic nervous system has a direct effect on GIP secretion, six normal subjects received a 4-hr intraduodenal perfusion of glucose (225 mg/min) and polyethylene glycol on four successive days. During the latter 2 hr, either normal saline, propranolol, phentolamine, or atropine were infused intravenously. Glucose absorption was calculated by measuring glucose and polyethylene glycol following luminal aspiration distal to the perfusion site. Basal and peak or nadir values in the saline study of plasma glucose, insulin, glucagon, and GIP were similar to the other three studies prior to autonomic blockade. During the latter 2 hr of the glucose perfusion, the plasma glucose and glucagon responses to saline did not differ from responses to the three blocking agents. Phentolamine but not atropine or propranolol resulted in a greater insulin response compared to saline (3247 +/- 762 vs 1348 +/- 388 microU/ml/120 min, P less than 0.01). GIP was not significantly affected by phentolamine (18,146 +/- 4574), propranolol (7585 +/- 5854), or atropine (15,797 +/- 6297) compared to saline (11,717 +/- 5204 pg/ml/120 min). Glucose absorption was unaffected by infusions of saline, phentolamine, and propranolol, but was increased following atropine infusion (5841 +/- 1120 vs 1044 +/- 808 mg/120 min, P less than 0.02). There appears to be no direct effect of the autonomic nervous system on glucose-induced secretion of GIP.
Adult↗
Neurotensin in diabetes and obesity.
Basal and postprandial concentrations of immunoreactive neurotensin were measured in insulin dependent diabetic patients and lean and obese noninsulin dependent diabetic patients when partially withdrawn from subcutaneous (s.c.) insulin treatment and again when near normoglycemia had been achieved from insulin infusion by an artificial endocrine pancreas (AEP). Neither basal nor postprandial neurotensin differed among the 3 groups of diabetic patients during s.c. insulin treatment nor from weight matched nondiabetic subjects. In addition, AEP resulted in no significant change in postprandial neurotensin responses. No differences in neurotensin levels were observed between lean and obese nondiabetic subjects. In contrast to observations in experimental diabetes, these observations do not support the presence of an abnormality of neurotensin in human diabetes.
Blood Glucose↗
What is "tight control" of diabetes? Goals, limitations, and evaluation of therapy.
Complete normalization of the blood glucose concentration is the ideal goal in patients with diabetes. Because of deficiencies in therapeutic modalities for diabetes, achievement of approximation of normoglycemia is usually a satisfactory result. Generally, blood glucose ranges of 70 to 120 mg/dl preprandially and less than 160 to 180 mg/dl 90 minutes postprandially in nonpregnant patients with diabetes are considered appropriate. Diurnal variations in glycemia can be caused by the size and composition of meals, the time of day a meal is eaten, stress, and exercise. Self-monitoring of blood glucose by the patient and measurement of glycosylated hemoglobin have been useful in achieving control of diabetes.
Blood Glucose↗
Benign pancreatic insulinoma: preoperative and intraoperative sonographic localization.
Twenty-nine patients with surgically proved benign pancreatic insulinoma were studied by preoperative or intraoperative sonography. Twenty-five patients had solitary pancreatic tumors; four had multiple tumors. Six of the patients with solitary insulinomas and one of the patients with multiple insulinomas had undergone previous unsuccessful exploration. Preoperative sonography was performed in 24 patients with solitary insulinomas, and 15 (63%) were localized. Intraoperative sonography was performed in 22 patients with solitary insulinomas, and 19 (86%) were visualized without having been previously located by palpation. Four of these visible solitary tumors (18%) were not detected by palpation at surgery. All the solitary insulinomas were detected with the combination of palpation and intraoperative sonography. In each of the six patients with solitary insulinoma who had undergone previous surgery, the tumor was visible with intraoperative sonography, which also demonstrated nonpalpable insulinomas in two of the four patients with multiple tumors. Preoperative real-time sonography is a sensitive, noninvasive, inexpensive method for localization of insulinoma. Intraoperative high-frequency sonography is a highly sensitive method for the detection of insulinoma. Intraoperative sonography is also valuable to determine the relationship of the insulinoma to pancreatic and bile ducts and thereby facilitate safe enucleation.
Adenoma, Islet Cell↗
Diabetic neuropathy.
The incidence and prevalence of diabetic neuropathies in Insulin Dependent (IDDM) and Non-Insulin Dependent (NIDDM) Diabetes Mellitus is not known because in previous studies the heterogeneity of diabetes and of the neuropathies was not taken into account, criteria for diagnosis and surveillance for neuropathy were variable, and studies were not prospective or population based. We have begun such prospective epidemiologic studies using a uniform algorithm for the classification of the diabetic disorders and uniform and validated approaches for the assessment of symptoms, neurologic deficits and various quantitative end-points of neural dysfunction. As regards cause, a key question which we are trying to answer is whether hyperglycemia and associated metabolic alterations affect neural tissue directly or whether there is an intervening tissue alteration between metabolic derangement and tissue change. Improved control of hyperglycemia does not appear to be associated with rapid neurologic improvement, possibly arguing for an intervening tissue alteration. The recently observed decrease in nerve oxygen tension and blood flow in streptozotocin diabetes suggests that an alteration of the nerve microenvironment may relate importantly to the cause of diabetic neuropathy.
Diabetes Mellitus, Type 1↗
Near normoglycaemia improved nerve conduction and vibration sensation in diabetic neuropathy.
Twelve C-peptide deficient Type 1 (insulin-dependent) diabetic patients with abnormal peripheral nerve function were randomly assigned to continuation of conventional insulin therapy (CIT) or to continuous subcutaneous insulin infusion (CSII). There were no statistically significant differences at entry to the study between the two treatment groups in nerve function assessed by neurologic disability score, computer assisted sensation examination and measurements of amplitudes, distal latencies, F-wave latencies and somatosensory evoked potential latencies over the spine and conduction velocities of motor and sensory fibers of ulnar, median, peroneal, tibial, plantar and sural nerves. In addition, mean plasma glucose from 24 h profiles (12.5 vs 10.6 mmol/l, respectively) and HbA1 (11.0 vs 11.6%, respectively) did not differ significantly between the two treatment groups at entry. Despite improved glycaemia from CSII in 5 patients (one dropped out of the study after 2 months) contrasted to CIT in 6 patients (5.3 vs 9.9 mmol/l, respectively, p = 0.002) and HbA1 (8.5 vs 10.7%, respectively, p = 0.002), there were no significant differences in measurements of peripheral nerve function after 4 months. After 8 months of improved glycaemia (4.4 vs 10.2 mmol/l, p = 0.004) and improved HbA1 (8.3 vs 10.5%, p = 0.002), nerve conduction (p = 0.03) and vibratory sensation threshold (p = 0.002) were significantly better in patients treated with CSII than those who received CIT. The improvements in nerve function, although small, provide further evidence that some clinical endpoints of neuropathy are favorably influenced by improved control of glycaemia.
Adolescent↗
Clinical and neuropathological criteria for the diagnosis and staging of diabetic polyneuropathy.
Scored symptoms, neurological deficits, detection threshold of cutaneous sensation and parameters of nerve conduction were compared with quantitated neuropathological abnormalities in the sural nerve in 47 healthy subjects and 36 diabetic patients, 32 with and 4 without neuropathy. The fifth percentile line of a new Index of Pathology, which combines loss of myelinated fibres and abnormality of the remaining fibres, was found to provide a sensitive and reliable minimum neuropathological criterion for the diagnosis of polyneuropathy. Abnormality, as assessed by two clinical evaluations, similarly separated healthy subjects and diabetic patients into those with and without neuropathy. For the detection of diabetic polyneuropathy, vibration sense was more sensitive than touch-pressure or thermal cooling. Abnormalities of nerve conduction were found to be both sensitive and reliable in the detection of polyneuropathy. Velocity was most frequently abnormal, but only slightly more often than F wave latency and amplitude. We conclude that abnormality, as judged independently from two different types of evaluation, provides a sensitive and reliable minimal criterion for the diagnosis of neuropathy. Although symptoms, neurological deficits and abnormalities of nerve conduction are statistically associated, they should be evaluated separately to provide adequate characterization.
Adolescent↗