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Biomedical subjects

O K Faber

Publications and source records attributed to O K Faber.

At least 37 records · Page 2Linked to original sources
PubMed1983

Hepatic extraction of insulin after carbohydrate hyperalimentation.

Peripheral venous plasma insulin and C-peptide concentrations during oral glucose tolerance tests were measured in 7 normal weight non-diabetic subjects before and after 7 days of sucrose hyperalimentation. This induced a deterioration of the glucose tolerance with higher levels of glucose, insulin and C-peptide. The C-peptide to insulin molar ratio as well as the relation between incremental areas under the plasma curves of the two peptides were used as relative measures of the hepatic insulin extraction. Both estimates of hepatic insulin extraction were unchanged by hyperalimentation, suggesting that the induced decreases in glucose tolerance and insulin receptor function are not followed by a decrease in hepatic insulin extraction as found in obese subjects with similar changes in glucose tolerance and insulin receptor function.

Adult↗
PubMed1982

The transient effect of strict glycaemic control on B cell function in newly diagnosed type 1 (insulin-dependent) diabetic patients.

Within 24h of diagnosis, 15 consecutive Type 1 (insulin-dependent) diabetic patients were allocated at random to one of two treatment groups: group A (n = 9, mean age: 28 years, range: 17-35 years) was treated conventionally with one or two daily doses of insulin; group B (n = 6, mean age: 27 years, range: 21-37 years) was treated with nine daily injections of fast-acting insulin for ten days and there-after conventionally as for group A. The mean diurnal blood glucose concentration during the initial ten days of insulin treatment was 11.7 +/- 0.5 mmol/l (mean +/- SEM) in group A and 6.4 +/- 0.3 mmol/l in group B (p less than 0.01). Pancreatic B cell function was evaluated 1, 7, 14, 90, and 180 days after the start of insulin treatment from the C-peptide response to a standard meal. At one and seven days after diagnosis, no difference was found in B cell function between the two groups. After 14 days, the amount of C-peptide secreted during the test meal was 18.0 +/- 2.6 nmol (mean +/- SEM) in group A compared with 29.0 +/- 3.6 nmol in group B (p less than 0.05). After 90 and 180 days, no difference was demonstrated in B cell function. The maximal B cell function observed was similar in the two groups, but occurred earlier in group B (at 14 days) than in group A (at 90 days) (p less than 0.05). This study indicates that strict initial glycaemic control may lead to an earlier improvement in B cell function, but that this improvement is of short duration.

Adolescent↗
PubMed1982

Hormonal, metabolic and cardiovascular responses to hypoglycaemia in Type 1 (insulin-dependent) diabetes with and without residual B cell function.

Hormonal, metabolic and cardiovascular responses to insulin induced hypoglycaemia were investigated in seven Type 1 (insulin-dependent) diabetic patients with residual B cell function, eight Type 1 diabetic patients without B cell function and six healthy subjects. No differences were found between the diabetic groups regarding nadir of glucose and rate of recovery to normoglycaemia. The patients with residual B cell function had a glucagon response to hypoglycaemia which was close to that of normal subjects. In patients without B cell function, the glucagon response to hypoglycaemia was present, albeit significantly smaller than in the patients with preserved B cell function (0.025 ng/ml, range 0.007-0.042 versus 0.054 ng/ml, range 0.029-0.087). The group without B cell function had signs of an exaggerated rate of lipolysis and ketogenesis compared with the patients with B cell function and the normal subjects.

Adult↗
PubMed1982

B cell function in patients with chronic pancreatitis and its relation to exocrine pancreatic function.

Exocrine pancreatic function was evaluated by a Lundh meal test and a secretin-cholecystokinin test in 16 patients with chronic pancreatitis. B cell function was assessed by measuring the concentration of C-peptide after stimulation with oral glucose and intravenous glucagon. The Cc-peptide response to intravenous glucagon and oral glucose was closely correlated (r = 0.88, p less than 0.01). Plasma C-peptide after glucagon was significantly correlated to the post-prandial concentration of lipase (r = 0.72, p less than 0.001), amylase (r = 0.64, p less than 0.05) and to amylase output (r = 0.64, p less than 0.05). Eight out of nine patients treated with insulin had residual B cell function, but it diminished significantly with increasing duration of diabetes. We conclude that B cell function is correlated to pancreatic enzyme secretion and that patients with insulin-treated diabetes secondary to chronic pancreatitis have a residual insulin secretion similar to that of patients with Type 1 (insulin-dependent) diabetes.

Adult↗
PubMed1982

Hormonal and metabolic changes in hepatic cirrhosis.

The hormonal and metabolic response to 50 g oral glucose has been studied in fifteen patients with hepatic cirrhosis and seven control subjects. Fasting blood glucose concentration was similar in both groups but cirrhotics showed higher glucose levels throughout the glucose tolerance test. Fasting serum insulin concentration was raised in the patient group (0.12 +/- 0.02 vs 0.07 +/- 0.01 nmol/l, p less than 0.05 and hyperinsulinaemia persisted after oral glucose. Blood lactate and pyruvate concentrations were elevated in cirrhotic patients, both fasting and post-glucose, while mean blood lactate correlated with mean serum insulin concentrations (rs 0.55, p less than). Plasma glucagon concentrations although highly variable, did not differ significantly in control and cirrhotic subjects before or after oral glucose. Fasting blood glycerol was increased in the patient group (O.11 +/- 0.01 vs 0.06 +/- 0.01 mmol/l, p less than 0.05) but fasting blood ketone body levels were normal and both glycerol and ketone body concentrations fell normally after glucose. Basal serum cortisol levels were similar in patient and control groups but the expected fall in cortisol concentration found in the control group over the test period was absent in cirrhotics. The hormonal and metabolic abnormalities did not correlate with severity of disease assessed by liver function test and abnormalities were not related to the presence or absence of portal-systemic shunting.

Adult↗
PubMed1981

Effect of strict blood glucose control on residual B-cell function in insulin-dependent diabetics.

In 14 insulin dependent diabetics past their initial remission period B-cell function was evaluated using a test meal before and after 1 week of strict blood glucose control, and again 3 weeks later when the patients were outpatients on conventional therapy. Eight patients with fasting C-peptide above 0.07 nmol/l improved their B-cell function significantly (p Less Than 0.05) during the period of strict blood glucose control. However, the improvement was of short duration and was absent 3 weeks later in most patients. Six patients with fasting C-peptide below or equal to 0.07 nmol/l had no significant improvement in B-cell function during the period of strict control. The study shows that B-cell function and degree of blood glucose control are related in patients with fasting C-peptide above 0.07 nmol/l, and that B-cell function can change within days.

Adolescent↗
PubMed1981

Hepatic insulin extraction in human pregnancy.

The hepatic degradation of insulin in late pregnancy has been estimated by determination of the molar C-peptide: Insulin (C/l) ratio under fasting conditions in 20 normal women in late pregnancy and again 4--8 weeks post-partum. Fasting plasma C-peptide and insulin concentrations were both significantly enhanced in pregnancy. However, since the relative gestational increments in plasma C-peptide and insulin concentrations were of almost the same magnitude, the C/l ratio remained unaffected by pregnancy (7.3 +/- 0.07 (mean +/- S.E.M) (pregnancy) vs. 7.4 +/- 0.8 (post-partum), N.S.). The results suggest that, in pregnancy, peripheral hyperinsulinaemia is due, in general, to pancreatic hypersecretion rather than to diminished hepatic extraction of insulin.

Adult↗
PubMed1981

Practical clinical value of the C-peptide response to glucagon stimulation in the choice of treatment in diabetes mellitus.

In order to discriminate between insulin-dependent and non-insulin-dependent patients, serum C-peptide concentration was determined using antiserum M1230 in the fasting state and 6 min after an i.v. injection of 1 mg glucagon in 215 patients treated with insulin and 53 treated with diet and oral antidiabetics. A patient was considered well controlled without insulin when fasting blood glucose was below 8 mmol/l and when glucosuria was absent. After re-evaluation of therapy in hospital it was found that the majority of patients with a post-stimulatory serum C-peptide concentration above 0.60 pmol/ml appeared to have non-insulin-dependent diabetes mellitus. When fasting C-peptide was used, a great overlap was found between the two treatment groups. During evaluation of therapy in hospital, 6 previously insulin-treated patients could be well treated with diet and tablets and 6 diet- and tablet-treated patients required insulin. The glucagon test seems to be of value in the outpatient clinic to discriminate non-insulin-dependent from insulin-dependent patients.

Adult↗
PubMed1981

Very early changes in circulating T3 and rT3 during development of metabolic derangement in diabetic patients.

Alterations in circulating iodothyronines were studied in 15 juvenile type diabetic patients during the development of metabolic derangement after withdrawal of insulin. By means of measurements of circulating C peptide, one group of patients with and one without residual beta-cell function had been selected. In both groups there was a gradual decrease in serum T3 during the 12-hour period studied after withdrawal of insulin, while an increase in serum rT3 was observed after 4-6 hours. The alterations in serum T3 and the metabolic derangement were significantly more pronounced in patients without than with residual beta-cell function.

C-Peptide↗
PubMed1981

Development of bone mineral loss in insulin-treated diabetes: a 1 1/2 years follow-up study in sixty patients.

The change in bone mass during 1 1/2 years was determined in a longitudinal study of sixty adult insulin-treated diabetic out-patients. During the study period the mean bone mass decreased by 1.30 +/- 0.28 (SEM)% (P less than 0.001), to a mean value of 91.0 +/- 1.7% of normal (P less than 0.001). The rate of bone loss was significantly higher in patients with 1-6 years of diabetes (n = 29, bone loss: 1.96 +/- 0.32%/1 1/2 years) than in patients with longer duration of the disease (n = 31, bone loss: 0.61 +/- 0.44%/1 1/2 years, P less than 0.02). The endogenous insulin secretion estimated with the glucagon-stimulated serum C-peptide concentration decreased during the observation period in 58.6% of the patients with 1-6 years of diabetes compared to 16.1% among patients with 7-11 years of diabetes (P less than 0.002). The rate of bone mineral loss was almost 3 times higher in the twenty-two patients in whom endogenous insulin secretion had deteriorated (2.12 +/- 0.30%/1 1/2 years) than in the thirty-eight patients without as well as with unchanged or increased insulin secretion (0.78 +/- 0.39%/1 1/2 years, P less than 0.01). In twenty patients with an increased insulin dose during the study period the mean bone mineral loss was 2.05 +/- 0.36%/1 1/2 years compared to a mean bone mineral loss of 0.91 +/- 0.38%/1 1/2 years in the forty patients with unchanged or decreased insulin dosage (P less than 0.05). This longitudinal study further supports the hypothesis that the bone mineral loss in insulin-treated diabetic patients begins with the onset of clinical diabetes and that its development is associated with the deterioration of the beta-cell function and with the increment in insulin dosage. The rate of bone mineral loss is high during the first few years of clinical diabetes, but levels off with increasing duration of the disease.

Adult↗
PubMed1981

Decreased insulin removal contributes to hyperinsulinemia in obesity.

Peripheral plasma insulin and C-peptide concentrations during oral glucose tolerance tests were measured in 7 severely obese and 12 normal weight nondiabetic subjects. The insulin and C-peptide levels as well as incremental areas under the plasma curves were 2--5 times higher in the obese subjects (P less than 0.05). The C-peptide to insulin molar ratios as well as the relation between incremental areas under the plasma curves of the two peptides were used as relative measures of the hepatic insulin extraction. They were both reduced in the obese subjects, which suggests that decreased insulin removal may contribute to the hyperinsulinemia of obesity. Sixty minutes after the oral glucose load, all of the obese patients had higher peripheral venous insulin concentrations compared with those found in normal subjects with similar C-peptide levels. This suggests that the reduced insulin extraction is not entirely explained by increased beta-cell secretory activity, but is also a specific consequence of obesity.

Blood Glucose↗
PubMed1981

Sensitivity of insulin secretion to feedback inhibition by hyperinsulinaemia.

The ability of insulin to inhibit its own secretion was examined in 15 normal subjects given an intravenous infusion of insulin in a dose of 0.25, 0.50, 1.0, 5.0 or 10.0 mU/kg/min for two hours. Arterial plasma insulin concentration achieved during the infusion segregated into three levels of hyperinsulinaemia: 35 +/- 1 (mean +/- SEM), 87 +/- 15 and 828 +/- 210 muU/ml. Plasma glucose concentration was kept constant at the basal level by a variable glucose infusion. Fasting C-peptide (0.29 +/- 0.02 pmol/ml) fell significantly in all subjects during hyperinsulinaemia and reached a concentration of 0.19 +/- 0.03 pmol/ml at 60 min and 0.14 +/- 0.03 at 120 min after the start of the insulin infusion. The C-peptide response was not related to the infusion dose nor to the steady state plasma insulin concentration. It is concluded that (a) basal insulin secretion as evaluated from C-peptide measurements is inhibited by small (24 +/- 3 muU/ml) physiological elevations in plasma insulin concentration independent of changes in plasma glucose, and (b) supraphysiological or even pharmacological elevations in plasma insulin do not result in a further decrease in endogenous insulin secretion above that achieved with mild hyperinsulinaemia.

Adult↗
PubMed1980

Islet-cell antibodies and beta-cell function in insulin-dependent diabetics.

Residual insulin secretion and islet-cell antibodies were studied in 399 insulin-dependent diabetics with age at onset of between 10--19.9 years (248 patients) or 30--39.9 years (151 patients). We found the prevalence of islet-cell antibodies to be independent of residual beta-cell function as measured by serum C-peptide and age at onset. The cause and role of the persistence of islet-cell antibodies in insulin-dependent diabetics remain obscure.

Adolescent↗
PubMed1980

Importance of insulin absorption, subcutaneous blood flow, and residual beta-cell function in insulin therapy.

The interaction between variation in insulin absorption and beta-cell function was studied as well as the possible relation between subcutaneous blood flow through the region of injection and the variability in insulin absorption. The results indicate that the dose of insulin, the type of insulin preparation and the local blood flow influence the insulin absorption. Residual endogenous insulin secretion, governed by the blood glucose values, serves as a modulator.

Adult↗
PubMed1980

Hepatic extraction and renal production of 3,3'-diiodothyronine and 3',5'-diiodothyronine in man.

The sequential deiodination of thyroxine (T4) gives rise to several iodothyronine analogs including 3,3'-diiodothyronine (3,3'-T2) and 3',5'-diiodothyronine (3',5'-T2). In vitro animal studies suggest that the liver and the kidneys are the main sites of both formation and degradation of 3,3'-T2 and 3',5'-T2. To determine the metabolism of 3,3'-T2 and 3',5'-T2 in human liver and kidneys plasma samples were obtained from (a) a brachial artery and a hepatic vein in 20 normal subjects, and from (b) a femoral artery and a renal vein in 11 normal subjects. Further, the hepatic plasma flow (a) and the renal plasma flow (b) were determined. Both plasma 3,3'-T2 and 3',5'-T2 levels were reduced in the hepatic venous blood as compared to arterial values (1.09 +/- 0.40 vs. 1.75 +/- 0.74 ng/dl (P < 0.02)) (mean +/- 1 SD). This resulted in a hepatic extraction of both, 3,3'-T2 and 3',5'-T2, which averaged 8.2 and 5.2 microgram/d, respectively. Plasma 3,3'-T2 as well as 3'5'-T2 levels were higher in the renal vein as compared to arterial values, 1.49 +/- 0.42 vs. 1.39 +/- 0.45 ng/dl (P < 0.05) and 2.35 +/- 0.83 vs. 2.09 +/- 0.81 ng/dl (P < 0.05), respectively. This positive venoarterial difference implies a net production of 3,3'-T2 and 3',5'-T2 in the kidneys of 1.2 and 3.0 microgram/d, respectively. It is concluded that the liver is an important site of 3,3'-T2 and 3',5'-T2 extraction in normal man. In contrast, the renal production of 3,3'-T2 as well as 3'5'-T2 exceeds the degradation and urinary excretion.

Adolescent↗