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Biomedical subjects

R Nosadini

Publications and source records attributed to R Nosadini.

At least 73 records · Page 4Linked to original sources
PubMed1990

Age and glucose tolerance in healthy subjects.

An important and still controversial issue is the role played by the aging process itself in the metabolic alterations observed in aged people. We previously reported that a group of normal elderly people exhibited glucose disposal comparable to that of young controls. In the present study we investigated the effect of age on beta-cell secretion, by analyzing C-peptide measurements. Ten elderly men (E, 70 +/- 2 years) with normal oral glucose test and ten young subjects (Y, 27 +/- 1 years) with matching ideal body weight formed the study group. They were studied under highly dynamic conditions by means of a 0.3 g/kg i.v. glucose tolerance test. Fasting glucose and insulin were not different in the two groups (Y: 87 +/- 2 mg/di, E: 88 +/- 3, p greater than 0.1; Y: 50 +/- 7 pM, E: 36 +/- 7, p greater than 0.05). Glucose-insulin data set was analyzed by means of the minimal model of glucose disappearance which provided two parameters for every individual, yielding a quantitative description of glucose utilization: i.e., SI, the index of insulin sensitivity, and SG, the fractional glucose disappearance at basal insulin (glucose effectiveness). Both parameters were unaltered by age (SI = Y: 6.30 +/- 0.41 10(-4)min-1/(microU/ml), E: 7.11 +/- 0.72, p greater than 0.1; SG = Y: 0.020 +/- 0.003 min-1, E: 0.019 +/- 0.002, p greater than 0.1). C-peptide time course in elderly people was systematically lower than in the control group (basal levels: Y: 252 +/- 36 pM, E: 129 +/- 17, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Substrate availability other than glucose in the brain during euglycemia and insulin-induced hypoglycemia in dogs.

Alternative substrates other than glucose could be used by the brain. In this study we hypothesized that lactate and ketone bodies can provide a significant portion of oxidative brain substrates in insulin-dependent diabetes mellitus (IDDM). Six control (C) and six insulin-treated streptozotocin diabetic (IDDM) dogs were studied during euglycemia (EU) and acute insulin induced hypoglycemia (HYPO). During EU for similar plasma glucose concentration (5.5 +/- 0.4 v 5.2 +/- 0.2 mmol/L in IDDM dogs showed a higher baseline lactate concentration (1.5 +/- 0.25 v 0.74 +/- 0.10 mmol/L; P less than .05). The ketone body concentrations were also increased in IDDM dogs but this increase was not statistically significant. The brain glucose uptake was 6.9 +/- 0.6 mumol/kg/min in C and 5.4 +/- 0.7 in IDDM. Lactate was released by the brain both in IDDM dogs (11.36 +/- 1.8 mumol/kg/min) and in C dogs (3.87 +/- 0.9; P less than .05). The brain ketones rate of disappearance (Rd) was 0.3 +/- 0.05 mumol/kg/min in IDDM dogs and 0.19 +/- 0.08 in C dogs. During HYPO the glucose uptake across the brain was 2.88 +/- 0.7 mumol/kg/min in IDDM and 3.12 +/- 0.5 in C dogs. We observed an overall brain lactate release (3.21 +/- 1.7 mol/kg/min) in C dogs and a net uptake (13.44 +/- 1.1; P less than .01) in IDDM (P less than .01). The brain ketones Rd was 0.1 +/- 0.2 mumol/kg/min in IDDM and 0.1 +/- 0.1 in C dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1990

Renal, metabolic and hormonal responses to ingestion of animal and vegetable proteins.

Renal and hormonal responses were studied in a group of healthy individuals fed, in random order, for three weeks, a vegetable protein diet (N = 10), an animal protein diet (N = 10), or an animal protein diet supplemented with fiber (N = 7), all containing the same amount of total protein (chronic study). In seven additional subjects the acute renal, metabolic and hormonal response to ingestion of a meat or soya load of equivalent total protein content was investigated (acute study). In the chronic study GRF, RPF and fractional clearance of albumin and IgG were significantly higher on the animal than the vegetable protein diets (GFR: 121 +/- 4 vs. 111 +/- 4 ml/min/1.73 m2, P less than 0.001; RPF: 634 +/- 29 vs. 559 +/- 26 ml/min/1.73 m2, P less than 0.001; theta alb: 19.5 +/- 3.1 vs. 10.2 +/- 1.6 x 10(-7), P less than 0.01; theta IgG: 11.6 +/- 3.1 vs. 7.5 +/- 1.7 x 10(-7), P less than 0.05). Renal vascular resistance was lower on the animal than vegetable protein diet (82 +/- 5 vs. 97 +/- 5 mmHg/min/liter; P less than 0.001). Fiber supplementation to APD did not have any effect on the renal variables measured which were indistinguishable from APD. In the acute study, GFR and RPF both rose significantly by approximately 16% (P less than 0.005) and approximately 14% (P less than 0.05), respectively, after the meat load, while RVR fell by approximately 12% (P less than 0.05). There were no significant changes in these parameters following the soya load.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Reduced beta-cell secretion and insulin hepatic extraction in healthy elderly subjects.

One factor responsible for the altered carbohydrate metabolism in elderly subjects is impaired insulin release; however, difficulties in directly measuring insulin secretion have limited studies on pancreatic activity and on the contribution of the liver to insulin delivery. This study investigated beta-cell performance and insulin hepatic extraction under dynamic conditions in normal elderly subjects. Two strictly comparable groups of 12 young controls (Y, 27 +/- 1 (SE) years, 73 +/- 3 kg) and 12 elderly men (E, 69 +/- 2 years, 73 +/- 3 kg) were chosen on the basis of normal OGTT and normal insulin sensitivity in order to investigate a "pure" age effect. The subjects underwent a 4-hour frequently sampled intravenous glucose tolerance test (FSIGT) (dose 0.3 g/kg). Although no significant differences were found between the fasting levels of glucose and insulin (respectively: E: 89 +/- 3 mg/dL versus Y: 87 +/- 2, P greater than .1; and E: 5.0 +/- 0.5 microU/mL versus Y: 6.8 +/- 1.0, P greater than .05), basal C-peptide was found to be lower in the old subjects: 0.43 +/- 0.06 ng/mL versus 0.70 +/- 0.11 (P less than .025). The patterns of glucose and insulin during the FSIGT were similar, whereas C-peptide concentration in E was systematically lower, suggesting a reduced insulin secretion. To verify this hypothesis, we analyzed FSIGT data with a mathematical model-based method that provides a noninvasive direct measurement of the time courses of insulin secretion and hepatic extraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Myocardial metabolism in insulin-deficient diabetic humans without coronary artery disease.

Eleven insulin-dependent diabetes mellitus (IDDM) patients with angiographically normal coronary arteries and a normal hemodynamic response to an echocardiographic-dipyridamole test and 12 normal controls were studied at rest and after atrial pacing simultaneously sampling arterial and coronary sinus blood. In IDDM patients, despite hyperglycemia [10.0 +/- 2.0 (SE) mmol/l], myocardial glucose uptake was slightly lower than in controls. This process was significantly activated in both groups during atrial pacing. The isotopically calculated net flux of lactate across myocardium, in agreement with the net balance value based on unlabeled lactate-pyruvate arteriovenous differences, showed a net uptake in controls (3.5 +/- 0.6 mumol.min-1.1.73 m-2) and a net release in IDDM (12.4 +/- 2.6; P less than 0.01). Atrial pacing stimulated lactate uptake in both groups. Myocardial uptake of ketone bodies was significantly higher in IDDM (37.0 +/- 6.3 mumol.min-1.1.73 m-2) than in controls (10.1 +/- 3.4 mumol.min-1.1.73 m-2; P less than 0.01). Free fatty acid uptake was also significantly greater in IDDM than in controls (44.1 +/- 7.0 vs. 24.1 +/- 5.1 mumol.min-1.1.73 m-2; P less than 0.01). Alanine and branched amino acids were released by diabetic but not by control hearts at rest. The normalization of blood glucose concentrations restored normal patterns of lactate and ketone body kinetics across diabetic myocardium. In conclusion, 1) at rest, myocardial lactate and amino acid uptake is markedly impaired in IDDM without coronary artery disease, and 2) the metabolic abnormalities of the diabetic myocardium are not a primary phenomenon but rather a consequence of hypoinsulinemia and hyperglycemia because insulin administration, resulting in euglycemia, restored normal patterns of cardiac metabolism.

Adult↗
PubMed1990

Effects of insulin on whole body and forearm leucine and KIC metabolism in type 1 diabetes.

To investigate whole body rates of appearance (Ra) and forearm metabolism of leucine and alpha-ketoisocaproate (KIC) in type 1 diabetes, before and after insulin administration, seven diabetic subjects were studied in the postabsorptive state with primed-constant infusions of L-[4,5-3H]leucine and [1-14C]KIC, and forearm arterial deep-venous catheterization. This combined technique allowed the selective quantitation of the two processes regulating forearm leucine and KIC metabolism (release and uptake) that may occur simultaneously. Before insulin (arterial plasma glucose, 284 +/- 24 mg/dl; leucine, 215 +/- 24 mumol/l; KIC, 42 +/- 3 mumol/l) forearm leucine and KIC release exceeded uptake slightly but significantly (P less than 0.05). During a 180-min insulin infusion, arterial glucose (144 +/- 27 mg/dl) and leucine concentrations (130 +/- 15 mumol/l) decreased (P less than 0.05 or less vs. base line) toward normal, whereas KIC did not change (33 +/- 4 mumol/l, NS). However, no net uptake of either leucine or KIC across the forearm was detected at any time point. In contrast, a significant net release of these substrates occurred throughout the insulin infusion. By the end of the hormone administration, whole body leucine and KIC Ra decreased 17 and 33%, respectively (P less than 0.01). However, forearm uptake and release of leucine and KIC did not significantly change with respect to base line. The fraction of whole body leucine released from estimated total muscle mass did not change (54 to 48%, NS) before vs. after insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Sodium-lithium countertransport in microalbuminuric insulin-dependent diabetic patients.

A familial predisposition to arterial hypertension has recently been suggested as one important component of the susceptibility to diabetic kidney disease. Sodium-lithium countertransport activity, a marker of risk for essential hypertension, has been found to be increased in diabetic patients with overt nephropathy. We have measured red blood cell sodium-lithium counter-transport activity in 36 microalbuminuric insulin-dependent diabetic patients, a group at high risk of progression to clinical nephropathy and cardiovascular disease, and compared it with that of a matched group of 36 normoalbuminuric diabetic patients. Sodium-lithium countertransport was higher in the microalbuminuric (0.43 [95% confidence interval (CI) 0.38-0.47] mmol/l red blood cells [RBC]/hr) than in the normoalbuminuric diabetic patients (0.29 [0.25-0.33] mmol/l RBC/hr, mean difference 0.14 [0.08-0.20]; p less than 0.0001). Microalbuminuric patients had a higher frequency of parental hypertension than normoalbuminuric diabetic patients (56% vs. 28%, p less than 0.05). Sodium-lithium countertransport was related to mean arterial pressure in the microalbuminuric patients (r = 0.54, p less than 0.001) and to daily insulin requirements in both groups (microalbuminuric patients r = 0.39, p less than 0.05; normoalbuminuric patients r = 0.42, p less than 0.01). In a subset of patients in whom lipoproteins were measured, sodium-lithium countertransport activity was related to total and very low density lipoprotein triglycerides (r = 0.41, p less than 0.05 and r = 0.48, p less than 0.05) and to apolipoprotein B (r = 0.56, p less than 0.05), independently of body mass index, albumin excretion rate, glycemic control, and insulin dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Na/H and Li/Na exchange in red blood cells of normotensive and hypertensive patients with insulin dependent diabetes mellitus (IDDM).

It has been shown that red blood cell Li/Na exchange, also called countertransport (Li/Na CTT) is increased in patients with insulin dependent diabetes mellitus (IDDM) with clinical or subclinical nephropathy and elevated blood pressure. Because recent experimental evidence confirms that red cell Li/Na CTT is a mode of functioning of the Na/H exchange (Na/H CTT), we have measured both transport modes in 23 IDDM (16 hypertensive and seven normotensive) and in eight normotensive controls with normal glucose tolerance. Na/H and Li/Na CTT were significantly increased in hypertensive compared to normotensive diabetics and controls. Na/H CTT was 78 +/- 28 mmol/L cell/h in hypertensive IDDM, 50 +/- 21 in normotensive IDDM, and 55 +/- 24 in the controls. Li/Na CTT was 0.37 +/- 0.13 mmol/L cell/h, 0.27 +/- 0.10, and 0.25 +/- 0.11, respectively. Na/H and Li/Na CTT were significantly correlated (r = .38, P less than .05). The proximal tubule sodium reabsorption, measured as the fractional Li+ reabsorption, was significantly correlated to red cell Na/H CTT (r = .38, n = 29, P less than .05), but not to the Li/Na CTT (r = .21, n = 29). In conclusion this work confirms that Na/H and Li/Na CTT are function modes of the same transporter and that an increased activity of Na/H CTT might play a role in the blood pressure increase in IDDM.

Adult↗
PubMed1989

Kidney hemodynamics after ketone body and amino acid infusion in normal and IDDM subjects.

Little information is available on the hemodynamic response (renal reserve) of the diabetic kidney during an acute amino acid infusion, which has been shown to increase glomerular filtration rate (GFR) in normal humans. We recently found that the infusion of ketone bodies is able to raise GFR in both normal subjects and insulin-dependent diabetes mellitus (IDDM) patients. The aim of this study was to evaluate the renal reserve in 15 IDDM patients with a duration of diabetes of greater than 9 yr [8 with albumin excretion rate less than 15 micrograms/min (group 1) and 7 with albumin excretion rate greater than 100 micrograms/min (group 2)] and in 8 normal subjects during amino acid infusion (33 mumol.kg-1.min-1, Travasol 10% wt/vol solution containing 0.154 mM sodium chloride concentration; Travenol, Savage, MD) and during acetoacetic sodium salt (25 mumol.kg-1.min-1) infusion. Blood glucose was clamped at euglycemic levels. The infusion of sodium acetoacetate resulted in a 10- to 15-fold increase in circulating concentrations of ketone bodies, which were similar in magnitude in normal subjects and diabetic patients. The GFR peak increase above baseline after sodium acetoacetate infusion was 28% in normal subjects and 27% in group 1 and 19% in group 2 diabetic patients. The infusion of amino acid solution produced a three- to fivefold increase in plasma concentrations of amino acids in both normal subjects and diabetic patients. The GFR peak increase above baseline after amino acid infusion was significantly lower in diabetic patients (IDDM group 1: 5%, P less than .01; IDDM group 2: 6%, P less than .01) than in normal subjects (38%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Sodium metabolism in insulin dependent diabetic patients. Role of insulin and atrial natriuretic peptide.

Acute insulin administration shows an antinatriuretic effect in normal man. Thus it can be postulated that insulin therapy resulting in circulating hyperinsulinemia can lead to sodium retention and in turn to hypertension in insulin dependent diabetes. Moreover it has been proved that atrial natriuretic peptide (ANP) plays a major role in modulating natriuresis in man. The aim of the present study was to investigate the relationship between insulin and ANP in modulating sodium metabolism in seven insulin dependent diabetic patients in comparison with eight normal control subjects at baseline and during a saline infusion (2 mmol/kg/90 min) at euglycemic blood levels. Diabetics received a subcutaneous insulin infusion (0.015 U/kg/hr) resulting in a two fold higher plasma free insulin levels (16 +/- 2 microU/ml) than in control subjects (7 +/- 2 microU/ml). During saline challenge sodium excretion rate increased by 29 +/- 6% in control patients and only by 6 +/- 0.7% in diabetic patients (p less than 0.01). At baseline ANP plasma concentrations were significantly higher in diabetic patients than in control subjects (diabetics = 37 +/- 8 pg/ml and controls = 21 +/- 3 (p less than 0.01). After saline challenge ANP concentration rose to 71 +/- 9 pg/ml in control subjects, whereas no significant change above baseline values was shown by diabetic patients.

Atrial Natriuretic Factor↗
PubMed1989

Tubular Na+ handling in type I insulin-dependent diabetics during saline and ketone body infusion.

It has been reported that patients with type I insulin dependent diabetes mellitus (IDDM) are characterized by reduced Na+ excretion during water immersion and saline infusion and abnormal glomerulo-tubular balance. Aims of the present study were therefore to investigate firstly the fractional tubular Na+ reabsorption during saline infusion to clarify the altered tubular site and secondly the glomerulo-tubular balance during acute increase of glomerular filtration rate induced by sodium acetoacetate infusion in IDDM. During saline and euglycaemic glucose clamp, after an overnight fast, glomerular filtration rate, renal plasma flow, filtration fraction and plasma sodium were 99 +/- 15 ml min-1 1.73 m-2, 452 +/- 109 ml min-1 1.73 m-2, 0.23 +/- 0.04 and 142 +/- 8 mmol l-1 (Mean +/- SD) in 10 type I insulin dependent diabetic patients and 96 +/- 18, 452 +/- 87, 0.21 +/- 0.02, 143 +/- 2 in five matched normal subjects, respectively. The lithium and sodium clearances were significantly lower in diabetic patients than in normal subjects (23 +/- 5 ml min-1 1.73 m-2 vs 28 +/- 6, p less than 0.05 and 1.1 +/- 0.4 vs 1.6 +/- 0.3, p less than 0.01 respectively). The fractional lithium reabsorption was greater (0.77 +/- 0.04 vs 0.72 +/- 0.03, p less than 0.05) and the distal fractional sodium reabsorption smaller (0.22 +/- 0.04 vs 0.27 +/- 0.03, p less than 0.01) in the diabetic patients compared to the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetoacetates↗
PubMed1988

Insulin sensitivity and beta-cell responsivity are not decreased in elderly subjects with normal OGTT.

Glucose intolerance has been observed often in elderly subjects, but it is not yet clear whether this impaired metabolic state is due to the aging process itself or is secondary to the appearance of other age-related variables. This study attempts to elucidate the effect of age in itself on factors controlling glucose tolerance. Several metabolic parameters were measured in 10 young male controls (23-29 yr) and 17 nonhospitalized, healthy, nonobese, old (60-80 yr) male subjects. Insulin binding to circulating cells was performed along with the intravenous glucose tolerance test, and the data were analyzed by the minimal model method. This approach yields the following measures: tissue insulin sensitivity (SI), fractional glucose disappearance at basal insulin (glucose effectiveness, SG), and first (phi 1) and second (phi 2) phase beta-cell responsiveness to glucose. Insulin-binding capacity to monocytes and erythrocytes was respectively 6.03% +/- 0.57% and 5.96% +/- 0.53% (elderly), 5.97% +/- 0.39% and 5.36% +/- 0.57% (young); SI was 6.20 +/- 0.59 X 10(4) min-1/(microU/mL) (elderly) and 6.35 +/- 0.30 (young); SG was 0.016 +/- 0.002 min-1 (elderly) and 0.019 +/- 0.003 (young); phi 1 was 1.84 +/- 0.29 min-1 (microU/mL)/(mg/dL) (elderly) and 3.37 +/- 0.84 (young); phi 2 was 13.80 +/- 1.78 X 10(4) min-2 (microU/mL)/(mg/dL) (elderly) and 9.59 +/- 2.65 (young). These results show no change with aging of tissue insulin sensitivity and an intact beta-cell activity, suggesting that age per se does not contribute to the deterioration of glucose tolerance when the effect of other age-related variables, eg, obesity and physical inactivity, is precluded.

Adult↗
PubMed1988

Porcine and human insulin absorption from subcutaneous tissues in normal and insulin-dependent diabetic subjects: a deconvolution-based approach.

The mechanisms of sc insulin absorption are not understood, and models for interpreting in vivo data cannot be developed without gross simplification. To overcome this difficulty we developed a new approach which makes use of deconvolution analysis and does not require any model of the sc tissue. In five normal subjects and seven insulin-dependent diabetic (IDDM) patients endogenous insulin secretion was suppressed by means of a hypoglycemic glucose clamp procedure (approximately 2.8 mmol/L) sustained by a continuous insulin infusion (approximately 4 pmol/min.kg). A bolus injection of insulin (5.4 nmol) was administered iv, and plasma insulin concentrations were measured frequently for 2 h to assess iv insulin kinetics. Insulin then was injected sc in the abdominal region, and plasma insulin concentrations were measured for 8 h. Each subject was studied twice, with porcine and semisynthetic human insulin (Actrapid, Novo). The rate of insulin absorption was reconstructed by deconvolution from the plasma concentrations and iv insulin kinetic data. Linearity of the iv insulin kinetics, essential for deconvolution analysis, was confirmed by a dose-response study in the range of the measured concentrations (150-1800 pmol/L). In most instances, a two-compartment model was adequate to describe the iv response. The mean plasma insulin clearance rates were 15.5 +/- 1.9 (+/- SD) mL/min.kg (porcine) and 17.2 +/- 6.0 (human) in normal subjects and 20.7 +/- 8.8 (porcine) and 20.9 +/- 9.1 (human) in the IDDM patients. The rate of appearance of human insulin from sc tissue was faster than that of porcine insulin in both normal and IDDM subjects, but no significant differences were found in bioavailability, which was 55 +/- 12% (+/- SD; porcine) and 61 +/- 34% (human) in the normal subjects, and 84 +/- 28% (porcine) and 86 +/- 23% (human) in the IDDM patients. The rate of absorption and bioavailability were higher in the IDDM patients than in the normal subjects, a difference possibly related to increased sc blood flow in the IDDM patients. No differences were found with regard to glucose requirement values, normalized to plasma insulin concentrations, in agreement with the finding that the bioavailability of the two insulin species was similar.

Adolescent↗
PubMed1987

Ketone bodies increase glomerular filtration rate in normal man and in patients with type 1 (insulin-dependent) diabetes mellitus.

The purpose of this study was to investigate whether the administration of acetoacetic and hydrochloric acids in a group of control and Type 1 (insulin-dependent) diabetic patients influenced renal haemodynamics. Renal plasma flow increased from 657 +/- 88 to 762 +/- 81 ml X min-1. 1.73 m-2 in diabetic patients (p less than 0.01) and from 590 +/- 71 to 691 +/- 135 in control subjects (p less than 0.01). Glomerular filtration rate increased from 135 +/- 9 to 180 +/- 8 ml X min-1. 1.73 m-2 in diabetic patients (p less than 0.001) and from 117 +/- 8 to 145 +/- 7 in control subjects (p less than 0.01). Similar effects on renal haemodynamics, even if less pronounced, were observed with low dose acetoacetic but not with hydrochloric acid infusion. Total protein, beta 2-microglobulin but not albumin excretion rates were increased by acetoacetic acid. We conclude that an acute increase in blood concentration of ketone bodies within the range found in diabetic patients with poor metabolic control increases renal plasma flow and glomerular filtration rate both in control subjects and diabetic patients and causes a tubular proteinuria.

Acetoacetates↗
PubMed1987

Insulin receptors on circulating blood cells from patients with pancreatogenic diabetes: a comparison with type I diabetes and normal subjects.

We studied 125I-insulin binding to erythrocytes from 14 patients with diabetes secondary to chronic pancreatitis or pancreatectomy and compared the results with those found in 10 patients with type I diabetes and 25 normal controls. Patients with pancreatogenic diabetes had higher 125I-insulin binding and enhanced tissue sensitivity to exogenous insulin measured with the glucose clamp technique as compared with patients with type I diabetes. Similar binding data were obtained with monocytes from 3 patients with pancreatogenic diabetes. The increase in insulin binding seemed due mainly to an increase in receptor number. The increase in insulin binding to cells from patients with pancreatogenic diabetes in comparison with cells from normal subjects was also seen in young-erythrocyte-rich fractions and in old-erythrocyte-rich fractions obtained from the mixed population of circulating erythrocytes by centrifugation in density gradient of Percoll-Pielografin. These data, in the absence of any sign of major hematological disorders, suggest that the increase in insulin receptors seen in erythrocytes and in monocytes from patients with pancreatogenic diabetes, can mirror a general phenomenon on tissues throughout the body, including major target cells for insulin and correlate with the heightened sensitivity to insulin characteristic of these patients. In conclusion, patients with pancreatogenic diabetes have increased insulin binding as compared to controls and to patients with type I diabetes with chronic hypoinsulinemia of the same degree. Thus, in addition to insulin deficiency, other factor (s), such as glucagon deficiency, are responsible for the clinical and metabolic differences between these two conditions of insulin deficiency.

Blood Cells↗