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Biomedical subjects

R Prager

Publications and source records attributed to R Prager.

At least 73 records · Page 4Linked to original sources

Role of islet amyloid polypeptide secretion in insulin-resistant humans.

Although it is generally accepted that islet amyloid polypeptide is cosecreted with insulin, relatively few data on its kinetics are available. We therefore studied the dynamics of islet amyloid polypeptide release following oral and frequently sampled intravenous glucose tolerance tests in comparison to insulin and C-peptide using mathematical model techniques in 14 control subjects, 10 obese and 11 hypertensive patients. The fractional clearance rate of islet amyloid polypeptide (0.034 +/- 0.004 min-1 in control subjects, 0.058 +/- 0.008 in the obese and 0.050 +/- 0.008 in the hypertensive patients) was significantly different (p < 0.01) in each group compared with that of insulin (0.14 +/- 0.03 min-1) and similar to that of C-peptide (0.061 +/- 0.007 min-1), at least in the insulin-resistant subjects. Based on the insulin sensitivity index derived from the minimal model analysis of intravenous glucose tolerance test data, both the hypertensive (2.4 +/- 0.4 min-1/(microU/ml); p < 0.0005) and the obese (2.7 +/- 0.5; p < 0.001) patients demonstrated severe insulin resistance compared to control subjects (8.1 +/- 1.3). Marked insulin hypersecretion was found in the hypertensive (57.6 +/- 5.2 nmol.l-1 in 180 min; p < 0.001) and obese (60.8 +/- 10.1; p < 0.003) patients in comparison with control subjects (32.4 +/- 3.2). The release of islet amyloid polypeptide was significantly higher in the hypertensive (83.1 +/- 16.6 pmol/l in 180 min; p < 0.02) and obese (78.6 +/- 13.1; p < 0.005) patients than in control subjects (40.5 +/- 6.4). No correlation was found between islet amyloid polypeptide release and the insulin sensitivity index in any group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Psychological moderator variables and metabolic control in recent onset type 1 diabetic patients--a two year longitudinal study.

The relationships between psychosocial adjustment and subsequent glycaemic control were prospectively examined in forty-three adult patients during the first 2 yr after onset of type 1 diabetes mellitus. Decreasing depression was the single psychosocial parameter that changed over time. No correlations were found between the decrease in HbA1c levels and psychological variables at 8- and 16-month follow-ups. Global and specific coping features such as high control attitude, low coping anxiety and low emotional attribution correlated significantly with the decrease in HbA1c levels at the 2-yr follow-up, whereas stressful life events, depression, state-trait anxiety did not correlate. In a regression analysis coping explained 22% variance of the 2 yr decrease in HbA1c levels. We conclude that coping is a better predictor for metabolic control than emotional adaptation and life events. Metabolic control might deteriorate with prolonged stage of the disease being a first sign for psychophysiological coping exhaustion.

Adaptation, Psychological↗

Expression and plasmid transfer of genes coding for the fimbrial antigen F107 in porcine Escherichia coli strains.

Expression of the fimbrial antigen F107 of porcine E. coli strains on agar plates was achieved by microaerobic cultivation. For part of the strains of some types, addition of alizarin yellow and eosin to the agar medium proved to be necessary. Some of these strains reacted distinctly positive only when the small colonies growing between the larger ones on alizarin-yellow agar were tested. The fimbrial antigen of the Swiss strain 107/86 was provisionally designated the F107ab variant and that of the Hungarian strain 2134P and the Czech strain 8813, the F107ac variant. The F107 genetic determinants were found to be often linked with those encoding haemolysin production and are frequently carried by plasmids.

Animals↗

Apolipoprotein (a) levels and atherogenic lipid fractions in relation to the degree of urinary albumin excretion in type 2 diabetes mellitus.

The relationship between serum lipids, apolipoprotein levels including apolipoprotein (a) to albumin excretion rate (AER) in 52 (17 male, 35 female) type 2 diabetic patients was studied. Patients were classified in groups as follows: (1) patients with normal AER (< 30 mg/24 h); (2) patients with microalbuminuria (AER 30-300 mg/24 h), and (3) patients with macroalbuminuria (AER > 300 mg/24 h). Apolipoprotein B levels were significantly (p < 0.05) elevated in the patients with macroalbuminuria compared to the normoalbuminuric group. Further, we observed a significant correlation between total cholesterol, low-density lipoprotein cholesterol, as well as apolipoprotein B levels to the degree of AER. No correlation between apolipoprotein (a) levels and AER, which is in contrast to recently published data for type 1 diabetic patients, was found. Systolic blood pressure was significantly higher (p < 0.002) in the patients with micro- and macroalbuminuria compared to the group with normal albumin excretion, whereas no relationship between diastolic blood pressure and albuminuria was found. We conclude that elevated increased atherogenic lipid fractions in addition to systolic hypertension may contribute to an increased cardiovascular risk in type 2 diabetic patients with proteinuria.

Aged↗

Increased levels of circulating islet amyloid polypeptide in patients with chronic renal failure have no effect on insulin secretion.

To elucidate the metabolism of islet amyloid polypeptide (IAPP) with respect to a possible renal elimination we investigated IAPP levels in 20 lean, nondiabetic patients with renal failure maintained on chronic hemodialysis (HD) and in 20 healthy controls. The basal levels of IAPP were significantly higher in uremic patients than in controls (15.1 +/- 3.2 vs. 3.2 +/- 0.2 pM, P < 0.001) suggesting renal excretion of IAPP. To investigate the impact of chronically elevated levels of endogenous IAPP on insulin secretion and insulin sensitivity, a frequently sampled intravenous glucose tolerance test (FSIGT) was performed in a subset of patients on hemodialysis and in age-matched healthy controls (C) and obese patients with normal (NGT) and with impaired glucose tolerance (IGT). Insulin sensitivity index (SI) was 8.7 +/- 1.5 in C (P < 0.05 vs. NGT, P < 0.01 vs. IGT), 5.4 +/- 0.9 in HD (P < 0.05 vs. IGT), 3.1 +/- 1.0 in NGT, and 2.0 +/- 0.5 in IGT. First phase insulin secretion was increased in patients on HD compared with those of several control groups. The results of this study therefore indicate a renal route of metabolism of IAPP. Increased endogenous circulating IAPP levels over a long period of time do not lead to a decrease in insulin release in patients on HD and do not cause the insulin resistance commonly seen in obesity and diabetes. Increased levels of circulating IAPP therefore are not likely to be a pathogenetic factor in the development of non-insulin-dependent diabetes mellitus (NIDDM).

Adult↗

Antihypertensive efficacy of cilazapril 2.5 and 5.0 mg once-daily versus placebo on office blood pressure and 24-hour blood pressure profile.

In a double-blind, randomized, multicenter study the antihypertensive efficacy of cilazapril 5.0 and 2.5 mg once daily vs. placebo was examined on 180 ambulatory hypertensive subjects with supine diastolic office blood pressure (OBP) > or = 95 and < or = 115 mm Hg: a 4-week, single-blind, placebo period was followed by a 4-week double-blind treatment period. At the beginning and end of the latter, OBP measurements and ambulatory 24-h BP monitoring (ABPM) were both carried out on two different days (3 +/- 1), whereby each time two 24-h BP recordings were made using SpaceLabs 90202. Measurements were made every 30 min, and actual waking and sleeping phase evaluation was done using diary entries. White coat hypertensive patients were excluded by the ambulatory BP (ABP) inclusion criterion: mean diastolic 24-h BP > or = 85 mm Hg, or frequency of measurements > 90 mm Hg > or = 35%. One-hundred eighty patients were included in the study. Safety was evaluated in 170 of these patients, and efficacy on OBP in 162. Twenty-four-hour BP recordings that were amenable to analysis were available in the case of 146 patients (average age 56 +/- 10 years, 56 women, 90 men). The results of the main target variable for OBP, namely responder rates, were in the three treatment groups: placebo, 39.6%; cilazapril 2.5 mg, 55.6%; and cilazapril 5.0 mg, 65.5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Apolipoprotein (a) levels in patients with type 1 diabetes mellitus are unrelated to metabolic control or vascular disease.

Increased serum levels of lipoprotein (a) have been found to be an independent risk factor for coronary heart disease. The major protein constituents of lipoprotein (a) are apolipoprotein B 100 und apolipoprotein (a) (apo(a)). We determined the serum levels of apo(a) and several lipid (cholesterol, HDL- and LDL-cholesterol, triglycerides, apolipoproteins A, A1 and B) and glycaemic (HbA1c, fasting blood glucose) parameters in 40 patients with type 1 diabetes mellitus and in 103 age- and sex-matched control subjects. The median serum levels of apo(a) were significantly increased in the type 1 diabetic patients (142.7 vs. 80.0 U/L; P = 0.03), whilst HDL, LDL-cholesterol, and apolipoprotein A, A1 and B levels were lower (P < 0.01). No significant correlation was found between parameters of metabolic control and apo(a) levels. After subdivision of the diabetic patients according to different stages of diabetic nephropathy (DN), determined by urinary albumin excretion, significant relationships were found between DN and triglycerides (P = 0.04), LDL (P = 0.03) and apolipoprotein B (P = 0.008, Kruskal-Wallis test) levels. Apo(a) levels were significantly higher than normal values in patients without DN (P < 0.05), but unrelated to the degree of DN. Patients with diabetic macroangiopathy had significant higher levels of cholesterol (P = 0.0001), triglycerides (P = 0.026), LDL (P = 0.0003), and apoB (P = 0.002) than patients without. Apo(a) levels were unrelated to diabetic macroangiopathy. The significantly elevated levels of apo(a) even in patients without DN or macroangiopathy are noteworthy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Haemostatic abnormalities persist despite glycaemic improvement by insulin therapy in lean type 2 diabetic patients.

Diabetes mellitus is associated with disturbances of the hemostatic system, which might contribute to the development of diabetic vascular disease. We investigated the effect of metabolic improvement by insulin therapy on the haemostatic system in 61 patients with type 2 diabetes mellitus and secondary sulfonylurea failure compared with 45 healthy control subjects matched for age, sex and BMI. Median age was 65, median diabetes duration 10 years. Median HbA1c (10%) and fructosamine (4.0 mM) levels were elevated before induction of therapy and decreased significantly within 6 months of insulin treatment to 7.5% and 3.0 mM, respectively (p < 0.0001). Compared with control subjects, median plasma levels of fibrinogen (317 vs 286 mg/dl), coagulation factor VII activity (1.1 vs 0.89 U/l), von Willebrand factor (1.6 vs 1.3 U/l), D-dimer (105 vs 86 micrograms/l), protein C:Ag (1.24 vs 0.95 U/l), total protein S:Ag (1.15 vs 0.91 U/l), and antithrombin III activity (1.17 vs 1.08 U/l) were significantly elevated. Levels of free protein S were not different from control values. No significant decline of coagulation parameters could be recorded during insulin therapy. Patients with diabetic vasculopathy had higher levels of D-dimer than those without (133 vs 76 micrograms/l before, 109 vs 88 micrograms/l during therapy), whereas the other haemostatic parameters were not different. Our data indicate a significant activation of the coagulation system in diabetic patients with secondary failure to sulfonylurea drugs, with signs of a prethrombotic state and endothelial cell disturbance.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Phase-specific function of denial in type 1 diabetic patients after disease onset].

In a longitudinal study we examined 43 patients with type 1 diabetes one week after onset as well as 8 and 24 month later in order to analyze the psychological role of denial processes in correlation to metabolic functions. Only depression decreased over the studied period while coping and denial remained stable. However, the adaptive function of denial after onset with low anxiety, good coping and few complaints became maladaptive over the first two years and the correlation of denial with a centripetal kinship behavior loosened. The destructive effect of denial was indicated only by delayed requests for assistance while no correlation could be shown for phase-specific internal restructuring of the psychological function of denial to compliance and metabolic control.

Adaptation, Psychological↗

Effect of dexamethasone on insulin sensitivity, islet amyloid polypeptide and insulin secretion in humans.

The response of islet amyloid polypeptide and insulin and their molar ratios were investigated in eight healthy volunteers before and after treatment with dexamethasone by oral and frequently-sampled intravenous glucose tolerance tests. Following dexamethasone treatment the insulin sensitivity index decreased significantly from 6.5 +/- 1.3 to 4.1 +/- 1.0 (microU.ml-1).min-1, p < 0.05. The area under the curve representing above-basal levels of insulin during oral glucose tolerance test increased significantly following dexamethasone treatment from 48132 +/- 9736 to 82230 +/- 14846 pmol.l-1 x 3 h-1, p < 0.05, the area under the curve of islet amyloid polypeptide increased from 1308 +/- 183 to 2448 +/- 501 pmol.l-1 x 3 h-1, p < 0.05. The overall insulin/islet amyloid polypeptide molar ratios calculated from the area under the curve during the 3-h period of the oral glucose tolerance test was not significantly different before and after dexamethasone treatment (42 +/- 5 vs 40 +/- 4). During the oral glucose tolerance test the insulin/islet amyloid polypeptide ratio increased significantly from baseline to 30 min (p < 0.05), then declined towards initial values before and after dexamethasone treatment. In conclusion, dexamethasone induced a significant decrease in insulin sensitivity and a significant increase in insulin secretion during the oral glucose tolerance test. However, in contrast to previous animal experiments we did not find a change in the insulin/islet amyloid polypeptide ratio before and after dexamethasone treatment.

Adult↗

Thrombogenic factors are related to urinary albumin excretion rate in type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetic patients.

Parameters of haemostasis, endothelial cell markers and lipid peroxide levels were studied in 64 Type 1 (insulin-dependent) and 94 Type 2 (non-insulin-dependent) diabetic patients according to their urinary albumin excretion rate in comparison with age-matched control subjects. We determined plasma levels of fibrinogen (Clauss' method), coagulation factor VII:activity (clotting assay), factor VII antigen, protein C and S antigen, von Willebrand factor antigen, D-dimer concentration (ELISA), and lipid peroxide levels (thiobarbituric acid) in relation to urinary albumin excretion rate (RIA). Significant positive correlations were found between urinary albumin excretion rate and plasma fibrinogen (p < 0.005, p < 0.02), factor VII activity (p < 0.0002, p < 0.002), factor VII antigen (p < 0.0001, p < 0.001), protein C (p < 0.003, p < 0.05), and lipid peroxides (p < 0.02, p < 0.004) in Type 1 as well as in Type 2 diabetes. Von Willebrand factor (p < 0.001) and protein S (p < 0.0005) correlated with albuminuria only in patients with Type 1 diabetes. Although most of the haemostatic abnormalities are already found in normoalbuminuric patients, the significant positive correlations to urinary albumin excretion indicate that endothelial cell damage and coagulation disorders deteriorate with the progression of diabetic nephropathy.

Adult↗

Hormonal and blood glucose responsiveness as an indicator of specific emotional arousal in type 1 diabetics.

The aim of the present study was to examine, whether individual emotional arousal induced by a specific stress interview may effect growth hormone (GH), cortisol, catecholamine and blood glucose levels in diabetes patients. To test the validity of this hypothesis we subjected 18 Type 1 diabetics and 18 healthy controls to a life event interview which produces individual arousal. During this stress interview catecholamines and plasma cortisol levels showed no significant increase, whereas there was a significant increase of GH over time in both group (p < 0.04), with a trend in diabetics to have a more marked GH response than controls (p < 0.10). Blood glucose levels remained unaffected by the interview. Depressed diabetics showed significantly higher cortisol increases (p < 0.004) than non-depressed diabetics, whereas there was no difference among depressed and non-depressed controls. Depression was not associated with an increase of other hormones or blood glucose levels in both groups. The results of our study confirm specific pathways in which individual emotional arousal and depression may lead to chronic metabolic disturbances as a result of GH and cortisol hypersecretion.

Adaptation, Psychological↗

Dissection of pathogenetic determinants and their genomic positions for the evaluation of epidemic strains and infection routes.

The epidemiology of infectious diseases intends to disclose the infection routes and sources of the respective diseases in order to provide preventive measures. The success of such a task is directly dependent on the knowledge about the special biological quality and the environmental distribution of the causative agents. This will imply extensive laboratory analysis rather than statistical surveys. The laboratory analysis for epidemiological purposes comprises a set of sophisticated methods for the subdifferentiation of the isolates (e.g. serofermentative and electrotyping, genomic fingerprinting). These methods provide circumstantial evidence of genetic and thus, epidemiological relatedness. Also the dissection of the pathogenic personality of the respective infectious agents was shown to have epidemiologic implications. However, the virulence pattern and the pattern of the genomic position of the respective determinants were found to be well conserved. For this reason, the dissection of virulence factors in comparison to other clonal properties must be regarded only as an additional marker for epidemiological discrimination. Moreover, any form of epidemic virulence remains to be detected by future analysis.

Bacteria↗

Left ventricular diastolic impairment in type 1 diabetic patients with microalbuminuria.

The high incidence of cardiac mortality in type 1 diabetic patients is further increased when diabetic nephropathy is present. Since microalbuminuria (albumin excretion rate > 30 mg/day) represents an incipient stage of diabetic nephropathy, we decided to investigate whether incipient renal changes correlate with early diastolic cardiac dysfunction, known to preceed systolic dysfunction. To test this hypothesis, 13 normotensive type 1 diabetics with incipient nephropathy (mean age 37.8 +/- 3.5, diabetes duration 18.8 +/- 2.6 years), 13 type 1 diabetics without nephropathy (matched for age, diabetes duration and metabolic control) or other microangiopathic changes and 13 normal controls were studied. Diseases known to affect left ventricular performance were ruled out before investigation. Right and left ventricular parameters were assessed by M-mode and Doppler echocardiography. While parameters for left ventricular systolic function stayed within the normal range and did not differ between the two diabetic groups (ejection fraction 69.3 +/- 2.4 vs. 69.6 +/- 1.4%; fractional shortening 40.3 +/- 2.2 vs. 38.5 +/- 1.1%), diastolic function was significantly impaired in diabetic patients with microalbuminuria. This is expressed by an inversed early and late peak flow velocity ratio in patients with microalbuminuria (0.988 +/- 0.04 vs. 1.362 +/- 0.1; p < 0.05) and a significant percentual increase in late (atrial) filling (39.1 +/- 1.7 vs. 29.9 +/- 1.4% when compared to whole filling; p < 0.05) despite a similar rate-corrected isovolumetric relaxation period in both diabetic groups (98.4 +/- 5.8 vs. 95.5 +/- 6.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Elevated hepatic insulin extraction in essential hypertension.

Insulin resistance, hyperinsulinemia, and dyslipidemia are common characteristics of patients with untreated hypertension. However, the link between the vascular and metabolic disturbances is still unclear. To provide further insights into the metabolic picture of subjects with hypertension, we evaluated insulin resistance, pancreatic secretion, and hepatic extraction of the hormone in 16 untreated patients with essential hypertension before and after 12-16 weeks of drug treatment in comparison with 16 age-, sex-, and body weight-matched normotensive control subjects. All subjects underwent an oral and a frequently sampled intravenous glucose tolerance test. Metabolic parameters were calculated by the minimal model technique. The hypertensive patients exhibited a highly reduced tissue insulin sensitivity (2.6 +/- 0.4 versus 9.6 +/- 1.9 10(4) min-1/[microunits/mL]; p < 0.001). The basal secretion rate (70 +/- 11 versus 35 +/- 5 pmol/L per minute) and the total amount of prehepatically secreted insulin (32 +/- 4 versus 16 +/- 2 nmol/L in 4 hours) were significantly increased in the hypertensive patients compared with the control subjects (p < 0.01), whereas the posthepatic insulin delivery rate was not significantly different between the two groups (4.9 +/- 0.6 versus 3.5 +/- 0.3 nmol/L in 4 hours). Hepatic insulin extraction was found to be significantly elevated in the hypertensive patients compared with control subjects (81 +/- 4% versus 69 +/- 3%, p < 0.04). Increased hepatic insulin extraction partially ameliorated B cell hypersecretion in hypertensive patients. After 12-16 weeks of drug treatment, the blood pressure was normalized, but the metabolic profile of the patients remained unchanged. We conclude that elevated insulin extraction in the liver is a specific characteristic of individuals with essential hypertension and partially compensates pancreatic B cell hypersecretion.

Adult↗

[Diabetes and sports].

Through better understanding of the physiology of physical exercise in normal and diabetic subjects we can more closely define the significance of regular physical exercise in the treatment of diabetes. Although patients with type I and type II diabetes can obtain different advantages from regular physical exercise, this activity is in turn connected with different risks. The introduction of self-monitoring of blood glucose has though considerably eased management in relation to physical activity by type I diabetics. Essentially the risk to type I diabetics is that of developing hypoglycemia during or after exercise as well as the danger of a worsening of metabolic levels with the development of ketoacidosis. In type II diabetics the risk of hypoglycemia is less pronounced and in patients treated solely by dietary means the regulation of blood glucose presents no great problem. With these individuals regular physical activity can be implemented as a further therapeutic tool towards the normalisation of body weight and an improvement in insulin sensitivity. With appropriate training and self-control the potential hypoglycemia in type I diabetic patients can easily be avoided. For this reason regular physical exercise can be recommended as a cornerstone of therapy, both in the management of type I as well as type II diabetes. The positive effect of exercise is significantly better defined in regard to type II diabetics than with type I diabetics. In particular, regular physical exercise can be implemented as a supplement to caloric restriction for weight reduction and as a means to improve insulin sensitivity in the obese insulin-resistant individual.

Blood Glucose↗

[Diabetes mellitus and carbohydrate metabolism in primary hyperparathyroidism].

It is generally known that patients with primary hyperparathyroidism (pHPT) feature disturbances in carbohydrate metabolism and hypertension. The incidence and prevalence of frank diabetes mellitus is significantly increased in these patients. The etiology and pathogenesis of the vascular and metabolic aberrations in this condition are still unclear. Glucose intolerance in pHPT is characterized by severe insulin resistance associated with pancreatic beta cell hypersecretion of insulin. Hypercalcemia is thought to be mainly responsible for the impaired glucose metabolism. However, several studies demonstrated that hypophosphatemia can also induce insulin hypersecretion and impair peripheral glucose uptake. Hypertension in primary hyperparathyroidism is mainly attributed to hypercalcemia. However, high peripheral insulin levels are also proposed to contribute to the development of essential hypertension and hyperinsulinemia per se is regarded as an important independent cardiovascular risk factor. After parathyroidectomy and decrease of the calcium levels to within the normal range, the blood pressure levels of the patients with pHPT normalised very quickly, whereas normalization of the high peripheral insulin levels was only found in a subgroup of patients. Thus, hypercalcemia seems to be mainly responsible for hypertension in primary hyperparathyroidism. Another important, yet unresolved issue is the question as to whether or to which extent the disturbances in glucose homeostasis are reversible after surgical correction of pHPT. At an early stage of the disease, insulin resistance and insulin hypersecretion are fully reversible after parathyroidectomy, whereas in patients with long-standing primary hyperparathyroidism and severely impaired glucose tolerance the metabolic disturbances will only partially improve. These results argue for improved screening to identify asymptomatic patients with primary hyperparathyroidism and for early surgical intervention in this disease.

Blood Glucose↗

Beta-cell hypersecretion and not reduced hepatic insulin extraction is the main cause of hyperinsulinemia in obese nondiabetic subjects.

Obesity is characterized by peripheral hyperinsulinemia, for which either beta-cell hypersecretion, diminished hepatic insulin extraction, or both may be responsible. To clarify this issue, we investigated insulin secretion and hormone hepatic extraction in 18 nondiabetic obese patients (body mass index [BMI], 39 +/- 1.3 kg/m2) and 18 healthy, lean control subjects (BMI, 21.3 +/- 0.7 kg/m2). Body fat distribution was calculated by measuring the waist to hip ratio (WHR). A highly reduced tissue insulin sensitivity (2.4 +/- 0.5 v 9.5 +/- 1.5 10(4).min-1/[microU/mL], P > .0005) and glucose effectiveness, ie, glucose's ability to stimulate its own disappearance at basal insulin (16 +/- 2 v 30 +/- 3 10(3).min-1, P > .005), were found in the overweight subjects compared with the controls. The basal (76 +/- 14 v 37 +/- 4 pmol/L/min) and total (377,848 +/- 5,562 v 16,864 +/- 1,850 pmol/L) prehepatic insulin secretion and the basal (15 +/- 2 v 7 +/- 0.7 pmol/L/min) and total (8,286 +/- 2,009 v 2,840 +/- 210 pmol/L) posthepatic insulin delivery were significantly higher in the overweight subjects compared with the controls (P < .005), whereas the mean hepatic insulin extraction did not differ (77.8% +/- 2.6% v 79.5% +/- 2.6%). A significant inverse correlation was found between the hepatic insulin extraction and the WHR (r = .5, P > .04), signifying the importance of fat distribution in insulin metabolism. The obese patients were subdivided into two subgroups according to their glucose tolerance; eight patients exhibited a normal tolerance and the remaining 10 were intolerant.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗